44 results on '"Tegazzin, V."'
Search Results
2. European Malignant Hyperthermia Group guidelines for investigation of malignant hyperthermia susceptibility
- Author
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Hopkins, P. M., Rüffert, H., Snoeck, M. M., Girard, T., Glahn, K. P. E., Ellis, F. R., Müller, C. R., Urwyler, A., Bandschapp, O., Gillies, R., Glauber, V., Heytens, L., Islander, G., Klingler, W., Kraft, B., Krivosic-Horber, R., Pollock, N., Schuster, F., Silva, H., Sorrentino, V., Street, N., Tegazzin, V., and Tzanova, I.
- Published
- 2015
- Full Text
- View/download PDF
3. A Multicenter Study of 4-Chloro-m-cresol for Diagnosing Malignant Hyperthermia Susceptibility
- Author
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Baur, C. P., Bellon, L., Felleiter, P., Fiege, M., Fricker, R., Glahn, K., Heffron, J. J. A., Herrmann-Frank, A., Jurkat-Rott, K., Klingler, W., Lehane, M., Ørding, H., Tegazzin, V., Wappler, F., Georgieff, M., and Lehmann-Horn, F.
- Published
- 2000
- Full Text
- View/download PDF
4. In vitro contracture test for diagnosis of malignant hyperthermia following the protocol of the European MH Group: Results of testing patients surviving fulminant MH and unrelated low-risk subjects
- Author
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Ørding, H., Brancadoro, V., Cozzolino, S., Ellis, F. R., Glauber, V., Gonano, E. F., halsall, P. J., Hartung, E., Heffron, J.J. A., Heytens, L., Kozak-Ribbens, G., Kress, H., Krivosic-Horber, R., Lehmann-Horn, F., Mortier, W., Nivoche, Y., Ranklev-Twetman, E., Sigurdsson, S., Snoeck, M., Stieglitz, P., Tegazzin, V., Urwyler, A., and Wappler, F.
- Published
- 1997
5. European Malignant Hyperthermia Group guidelines for investigation of malignant hyperthermia susceptibility
- Author
-
Hopkins, P. M., Rüffert, H., Snoeck, M. M., Girard, T., Glahn, K. P. E., Ellis, F. R., Müller, C. R., Urwyler, A., Hardman, J. G., Bandschapp, O., Gillies, R., Glauber, V., Heytens, L., Islander, G., Klingler, W., Kraft, B., Krivosic-Horber, R., Pollock, N., Schuster, F., Silva, H., Sorrentino, V., Street, N., Tegazzin, V., and Tzanova, I.
- Abstract
It is 30 yr since the British Journal of Anaesthesia published the first consensus protocol for the laboratory diagnosis of malignant hyperthermia susceptibility from the European Malignant Hyperthermia Group. This has subsequently been used in more than 10 000 individuals worldwide to inform use of anaesthetic drugs in these patients with increased risk of developing malignant hyperthermia during general anaesthesia, representing an early and successful example of stratified medicine. In 2001, our group also published a guideline for the use of DNA-based screening of malignant hyperthermia susceptibility. We now present an updated and complete guideline for the diagnostic pathway for patients potentially at increased risk of developing malignant hyperthermia. We introduce the new guideline with a narrative commentary that describes its development, the changes to previously published protocols and guidelines, and new sections, including recommendations for patient referral criteria and clinical interpretation of laboratory findings
- Published
- 2017
6. Undiagnosed myopathy before surgery and safe anaesthesia table
- Author
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Trevisan, C. P., Accorsi, A., Morandi, L. O., Mongini, T., Savoia, G., Gravino, E., Corrado Angelini, and Tegazzin, V.
- Subjects
Adult ,anaesthesia complications ,Drug-Related Side Effects and Adverse Reactions ,hyperCKemia ,Contraindications ,Patient Harm ,Original Articles ,Muscular Diseases ,safe anaesthesia ,Asymptomatic Diseases ,Preoperative Care ,Humans ,Anesthesia ,undiagnosed myopathy ,Diagnostic Errors ,Drug Monitoring ,Child ,Anesthetics - Abstract
Patients with muscle pathology are a challenge for anaesthesiologists because of possible life-threatening general anaesthesia complications. A review of the current medical literature on the issue clearly indicates that increasing awareness by anaesthesiologists in recent years has led to a reduction in the occurrence of adverse events in patients with diagnostically well-defined muscle disease. On the other hand, the current emerging aspect is that the great majority of complications concern subjects with clinically non-overt (silent to mildly symptomatic) and thus undiagnosed myopathy. With a view to improving prevention of possible critical anaesthesia complications in such patients, we present a "Safe Anaesthesia Table", listing both the anaesthetic drugs to be avoided and those considered harmless for myopathic patients, irrespective of age and type of pathology. In addition, a brief outline about the clinical aspects suggestive of a possible muscle pathology is also provided. Using "safe drugs" during routine surgical procedures in subjects with suspected undiagnosed myopathy will enable the anaesthesiologist to avoid delaying surgery, while protecting them from anaesthesia complications. By following this approach the presumed myopathy can be properly investigated after surgery.
- Published
- 2013
7. Chlorocresol: an activator of ryanodine receptor mediated Ca2+ release
- Author
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Zorzato, Francesco, Scutari, E., Tegazzin, V., Clementi, E., and Treves, Susan Nella
- Subjects
agonist ,ryanodine receptor - Published
- 1993
8. G.P.13.09 Identification of a point mutation in the skeletal muscle ryanodine receptor gene associated in the homozygous state to central core disease
- Author
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Melli, G., primary, Colleoni, L., additional, Bernasconi, P., additional, Romaggi, S., additional, Tegazzin, V., additional, Mantegazza, R., additional, and Morandi, L., additional
- Published
- 2008
- Full Text
- View/download PDF
9. A truncation in the RYR1 gene associated with central core lesions in skeletal muscle fibres
- Author
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Rossi, D., primary, De Smet, P., additional, Lyfenko, A., additional, Galli, L., additional, Lorenzini, S., additional, Franci, D., additional, Petrioli, F., additional, Orrico, A., additional, Angelini, C., additional, Tegazzin, V., additional, Dirksen, R., additional, and Sorrentino, V., additional
- Published
- 2006
- Full Text
- View/download PDF
10. Multicentre evaluation of in vitro contracture testing with bolus administration of 4-chloro-m-cresol for diagnosis of malignant hyperthermia susceptibility
- Author
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Wappler, F., primary, Anetseder, M., additional, Baur, C. P., additional, Censier, K., additional, Doetsch, S., additional, Felleiter, P., additional, Fiege, M., additional, Fricker, R., additional, Halsall, P. J., additional, Hartung, E., additional, Heffron, J. J. A., additional, Heytens, L., additional, Hopkins, P. M., additional, Klingler, W., additional, Lehmann-Horn, F., additional, Nivoche, Y., additional, Tegazzin, V., additional, Tzanova, I., additional, Urwyler, A., additional, Weißhorn, R., additional, and Schulte am Esch, J., additional
- Published
- 2005
- Full Text
- View/download PDF
11. Multicentre evaluation of in vitro contracture testing with bolus administration of 4-chloro-m-cresol for diagnosis of malignant hyperthermia susceptibility
- Author
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Wappler, F., primary, Anetseder, M., additional, Baur, C. P., additional, Censier, K., additional, Doetsch, S., additional, Felleiter, P., additional, Fiege, M., additional, Fricker, R., additional, Halsall, P. J., additional, Hartung, E., additional, Heffron, J. J. A., additional, Heytens, L., additional, Hopkins, P. M., additional, Klingler, W., additional, Lehmann-Horn, F., additional, Nivoche, Y., additional, Tegazzin, V., additional, Tzanova, I., additional, Urwyler, A., additional, Weihorn, R., additional, and Schulte Esch, J., additional
- Published
- 2003
- Full Text
- View/download PDF
12. Recent advances in the diagnosis of malignant hyperthermia susceptibility: How confident can we be of genetic testing?
- Author
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Robinson, R L, primary, Anetseder, M J, additional, Brancadoro, V, additional, van Broekhoven, C, additional, Carsana, A, additional, Censier, K, additional, Fortunato, G, additional, Girard, T, additional, Heytens, L, additional, Hopkins, P M, additional, Jurkat-Rott, K, additional, Klinger, W, additional, Kozak-Ribbens, G, additional, Krivosic, R, additional, Monnier, N, additional, Nivoche, Y, additional, Olthoff, D, additional, Rueffert, H, additional, Sorrentino, V, additional, Tegazzin, V, additional, and Mueller, C R, additional
- Published
- 2003
- Full Text
- View/download PDF
13. Mutations in the RYR1 gene in Italian patients at risk for Malignant Hyperthermia: evidence for a cluster of novel mutations in the C-terminal region
- Author
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Galli, L, primary, Orrico, A, additional, Cozzolino, S, additional, Pietrini, V, additional, Tegazzin, V, additional, and Sorrentino, V, additional
- Published
- 2002
- Full Text
- View/download PDF
14. Postanaesthetic myoglobinuric renal failure: an isolated expression of malignant hyperthermia
- Author
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Acquarone, N., primary, Garibotto, G., additional, Tegazzin, V., additional, Sofia, A., additional, and Gurreri, G., additional
- Published
- 1994
- Full Text
- View/download PDF
15. Halothane, Enflurane, and Isoflurane Stimulate Calcium Leakage from Rabbit Sarcoplasmic Reticulum
- Author
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Blanck, T. J. J., primary, Peterson, C. V., additional, Baroody, B., additional, Tegazzin, V., additional, and Lou, Jun, additional
- Published
- 1992
- Full Text
- View/download PDF
16. Muscle biopsy and in vitro contracture test in subjects with idiopathic hyperCKemia.
- Author
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Malandrini A, Orrico A, Gaudiano C, Gambelli S, Galli L, Berti G, Tegazzin V, Dotti MT, Federico A, and Sorrentino V
- Published
- 2008
- Full Text
- View/download PDF
17. Mutation screening of the RYR1 gene and identification of two novel mutations in Italian malignant hyperthermia families
- Author
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Barone, V., Massa, O., Sorrentino, V., Intravaia, E., Bracco, A., Martino, A. Di, Cozzolino, S., and Tegazzin, V.
- Abstract
Point mutations in the ryanodine receptor (RYR1) gene are associated with malignant hyperthermia, an autosomal dominant disorder triggered in susceptible people (MHS) by volatile anaesthetics and depolarising skeletal muscle relaxants. To date, 17 missense point mutations have been identified in the human RYR1 gene by screening of the cDNA obtained from muscle biopsies. Here we report single strand conformation polymorphism (SSCP) screening for nine of the most frequent RYR1 mutations using genomic DNA isolated from MHS patients. In addition, the Arg163Cys mutation was analysed by restriction enzyme digestion. We analysed 57 unrelated patients and detected seven of the known RYR1 point mutations. Furthermore, we found a new mutation, Arg2454His, segregating with the MHS phenotype in a large pedigree and a novel amino acid substitution at position 2436 in another patient, indicating a 15.8% frequency of these mutations in Italian patients. A new polymorphic site in intron 16 that causes the substitution of a G at position -7 with a C residue was identified.
- Published
- 1999
18. Chlorocresol: an activator of ryanodine receptor-mediated Ca2+ release.
- Author
-
Zorzato, F, Scutari, E, Tegazzin, V, Clementi, E, and Treves, S
- Abstract
In the present study we investigated the effect of the compound chlorocresol on intracellular Ca2+ homeostasis. Three different systems that have been shown to express the ryanodine receptor Ca2+ channel were chosen, i.e., skeletal muscle sarcoplasmic reticulum, cerebellar microsomes, and PC12 cells. In skeletal muscle sarcoplasmic reticulum, 4-chloro-m-cresol was found to be a potent activator of Ca2+ release mediated by a ruthenium red/caffeine-sensitive Ca2+ release channel. In cerebellar microsomes, this compound released Ca2+ from an inositol-1,4,5-trisphosphate-insensitive store, suggesting that there too it was acting at the ryanodine receptor level. When tested on PC12 cells, chlorocresol released Ca2+ from a caffeine- and thapsigargin-sensitive intracellular store. In addition, the compound was capable of releasing Ca2+ after pretreatment of PC12 cells with bradykinin, suggesting that it acts on a channel contained within an intracellular Ca2+ store that is distinct from that sensitive to inositol-1,4,5-trisphosphate. Structure-activity relationship analyses suggest that the chloro and methyl groups in chlorocresols are important for the activation of the ryanodine receptor Ca2+ release channel.
- Published
- 1993
19. Recommendations for anesthesia and perioperative management of patients with neuromuscular disorders
- Author
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Racca, F., Mongini, T., Wolfler, A., Vianello, A., Renato Cutrera, Del Sorbo, L., Capello, E. C., Gregoretti, C., Massa, R., Luca, D., Conti, G., Tegazzin, V., Toscano, A., Ranieri, V. M., Racca F, Mongini T, Wolfler A, Vianello A, Cutrera R, Del Sorbo L, Capello EC, Gregoretti C, Massa R, De Luca D, Conti G, Tegazzin V, Toscano A, and Ranieri VM
- Subjects
Neurologic Examination ,Postoperative Care ,Airway Management ,Anesthesia ,Heart Function Tests ,Humans ,Intraoperative Care ,Neuromuscular Diseases ,Patient Care ,Perioperative Care ,Preoperative Care ,Respiratory Function Tests ,Insufflation ,Neuromuscular diseases ,Noninvasive ventilation ,Recommendations for anesthesia and perioperative management of patients with neuromuscular disorders ,Settore MED/26 - Neurologia - Abstract
Patients with neuromuscular disorders are at high risk of intraoperative and postoperative complications. General anesthesia in these patients may exacerbate respiratory and cardiovascular failure due to a marked sensitivity to several anesthetic drugs. Moreover, succinylcholine and halogenated agents can trigger life-threatening reactions, such as malignant hyperthermia, rhabdomyolysis and severe hyperkalemia. Therefore, regional anesthesia should be used whenever possible. If general anesthesia is unavoidable, special precautions must be taken. In particular, for patients at increased risk of respiratory complications (i.e., postoperative atelectasis, acute respiratory failure, nosocomial infections), noninvasive ventilation associated with aggressive airway clearance techniques can successfully treat upper airway obstruction, hypoventilation and airway secretion retention, avoiding prolonged intubation and tracheotomy. Anesthesia and perioperative management of patients with neuromuscular disorders are described in this article. To grade the strength of recommendations and the quality of evidence we adopted the GRADE approach. In case of low-quality evidence, these recommendations represent the collective opinion of the expert panel.
20. Pathogenesis of late asthmatic reactions induced by exposure to isocyanates
- Author
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Mapp, C. E., Boschetto, P., Milani, G. F., Pivirotto, F., Tegazzin, V., Leonardo Fabbri, and Zocca, E.
- Published
- 1987
21. Mutation screening of the RYR1 gene and identification of two novel mutations in Italian malignant hyperthermia families
- Author
-
Barone, V., Massa, O., Intravaia, E., Bracco, A., Di Martino, A., Tegazzin, V., Cozzolino, S., and Vincenzo Sorrentino
- Subjects
Male ,Polymorphism, Genetic ,Nemaline ,Muscles ,Single-Stranded Conformational ,Ryanodine Receptor Calcium Release Channel ,Original Articles ,Myopathies, Nemaline ,Pedigree ,Italy ,Genetic ,Caffeine ,Humans ,Point Mutation ,Female ,genetics ,Myopathies ,Polymorphism ,metabolism, DNA Primers, Female, Halothane ,metabolism, Humans, Italy, Male, Malignant Hyperthermia ,genetics, Muscles ,metabolism, Myopathies ,genetics, Pedigree, Point Mutation, Polymorphism ,Genetic, Polymorphism ,Single-Stranded Conformational, Ryanodine Receptor Calcium Release Channel ,Halothane ,Malignant Hyperthermia ,metabolism ,Polymorphism, Single-Stranded Conformational ,DNA Primers - Abstract
Point mutations in the ryanodine receptor (RYR1) gene are associated with malignant hyperthermia, an autosomal dominant disorder triggered in susceptible people (MHS) by volatile anaesthetics and depolarising skeletal muscle relaxants. To date, 17 missense point mutations have been identified in the human RYR1 gene by screening of the cDNA obtained from muscle biopsies. Here we report single strand conformation polymorphism (SSCP) screening for nine of the most frequent RYR1 mutations using genomic DNA isolated from MHS patients. In addition, the Arg163Cys mutation was analysed by restriction enzyme digestion. We analysed 57 unrelated patients and detected seven of the known RYR1 point mutations. Furthermore, we found a new mutation, Arg2454His, segregating with the MHS phenotype in a large pedigree and a novel amino acid substitution at position 2436 in another patient, indicating a 15.8% frequency of these mutations in Italian patients. A new polymorphic site in intron 16 that causes the substitution of a G at position -7 with a C residue was identified. Keywords: malignant hyperthermia; central core disease; ryanodine receptor; in vitro contracture test
22. An experimental model of myasthenia myopathy
- Author
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Tegazzin V, ENRICO FACCO, Caldesi Valeri V, Bresólin N, and Gp, Gíron
- Subjects
Male ,Muscular Diseases ,Electromyography ,Freund's Adjuvant ,Animals ,Fluorescent Antibody Technique ,Rabbits ,Thymus Gland ,Muscle, Skeletal ,Thymectomy ,Autoantibodies ,Myasthenia Gravis, Autoimmune, Experimental - Abstract
Normal and thymectomised rabbits been have immunized by means of a thymic extract emulsified with Freund's Complete Adjuvant. The experiment was conducted over a three month period, in order to reproduce an experimental model of chronic myasthenia. During this period immunological, electromyographic and histologic studies were undertaken. Typical findings of partial neuromuscular block were invariably obtained from all the non thymectomized animals, while such signs were constantly absent both in non-treated control rabbits and in the immunized thymectomized ones. This neuromuscular block was intermittent. The compromised neuromuscular conduction was associated to an histological pattern of autoimmune myopathy. Evidence was put on antibodies directed against the thymus, muscular and nervous tissue. The results indicate the important role of the thymus gland both in altering conduction at the neuromuscular junction level and causing histopathologic muscle lesions.
23. European Malignant Hyperthermia Group guidelines for investigation of malignant hyperthermia susceptibility
- Author
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Hopkins, P. M., Rüffert, H., Snoeck, M. M., Girard, T., Glahn, K. P. E., Ellis, F. R., Müller, C. R., Urwyler, A., Hardman, J. G., Bandschapp, O., Gillies, R., Glauber, V., Heytens, L., Islander, G., Klingler, W., Kraft, B., Krivosic-Horber, R., Pollock, N., Schuster, F., Silva, H., Sorrentino, V., Street, N., Tegazzin, V., Tzanova, I., Hopkins, P. M., Rüffert, H., Snoeck, M. M., Girard, T., Glahn, K. P. E., Ellis, F. R., Müller, C. R., Urwyler, A., Hardman, J. G., Bandschapp, O., Gillies, R., Glauber, V., Heytens, L., Islander, G., Klingler, W., Kraft, B., Krivosic-Horber, R., Pollock, N., Schuster, F., Silva, H., Sorrentino, V., Street, N., Tegazzin, V., and Tzanova, I.
- Abstract
It is 30 yr since the British Journal of Anaesthesia published the first consensus protocol for the laboratory diagnosis of malignant hyperthermia susceptibility from the European Malignant Hyperthermia Group. This has subsequently been used in more than 10 000 individuals worldwide to inform use of anaesthetic drugs in these patients with increased risk of developing malignant hyperthermia during general anaesthesia, representing an early and successful example of stratified medicine. In 2001, our group also published a guideline for the use of DNA-based screening of malignant hyperthermia susceptibility. We now present an updated and complete guideline for the diagnostic pathway for patients potentially at increased risk of developing malignant hyperthermia. We introduce the new guideline with a narrative commentary that describes its development, the changes to previously published protocols and guidelines, and new sections, including recommendations for patient referral criteria and clinical interpretation of laboratory findings
24. Functional and genetic characterization of clinical malignant hyperthermia crises: a multi-centre study.
- Author
-
Klingler W, Heiderich S, Girard T, Gravino E, Heffron JJ, Johannsen S, Jurkat-Rott K, Rüffert H, Schuster F, Snoeck M, Sorrentino V, Tegazzin V, and Lehmann-Horn F
- Subjects
- Adolescent, Adult, Child, Child, Preschool, Female, Humans, Infant, Male, Middle Aged, Mutation, Ryanodine Receptor Calcium Release Channel genetics, Succinylcholine therapeutic use, Young Adult, Malignant Hyperthermia drug therapy, Malignant Hyperthermia genetics
- Abstract
Background: Malignant hyperthermia (MH) is a rare pharmacogenetic disorder which is characterized by life-threatening metabolic crises during general anesthesia. Classical triggering substances are volatile anesthetics and succinylcholine (SCh). The molecular basis of MH is excessive release of Ca2+ in skeletal muscle principally by a mutated ryanodine receptor type 1 (RyR1). To identify factors explaining the variable phenotypic presentation and complex pathomechanism, we analyzed proven MH events in terms of clinical course, muscle contracture, genetic factors and pharmocological triggers., Methods: In a multi-centre study including seven European MH units, patients with a history of a clinical MH episode confirmed by susceptible (MHS) or equivocal (MHE) in vitro contracture tests (IVCT) were investigated. A test result is considered to be MHE if the muscle specimens develop pathological contractures in response to only one of the two test substances, halothane or caffeine. Crises were evaluated using a clinical grading scale (CGS), results of IVCT and genetic screening. The effects of SCh and volatile anesthetics on Ca2+ release from sarcoplasmic reticulum (SR) were studied in vitro., Results: A total of 200 patients met the inclusion criteria. Two MH crises (1%) were triggered by SCh (1 MHS, 1 MHE), 18% by volatile anesthetics and 81% by a combination of both. Patients were 70% male and 50% were younger than 12 years old. Overall, CGS was in accord with IVCT results. Crises triggered by enflurane had a significantly higher CGS compared to halothane, isoflurane and sevoflurane. Of the 200 patients, 103 carried RyR1 variants, of which 14 were novel. CGS varied depending on the location of the mutation within the RyR1 gene. In contrast to volatile anesthetics, SCh did not evoke Ca2+ release from isolated rat SR vesicles., Conclusions: An MH event could depend on patient-related risk factors such as male gender, young age and causative RyR1 mutations as well as on the use of drugs lowering the threshold of myoplasmic Ca2+ release. SCh might act as an accelerant by promoting unspecific Ca2+ influx via the sarcolemma and indirect RyR1 activation. Most MH crises develop in response to the combined administration of SCh and volatile anesthetics.
- Published
- 2014
- Full Text
- View/download PDF
25. Undiagnosed myopathy before surgery and safe anaesthesia table.
- Author
-
Trevisan CP, Accorsi A, Morandi LO, Mongini T, Savoia G, Gravino E, Angelini C, and Tegazzin V
- Subjects
- Adult, Anesthesia methods, Asymptomatic Diseases, Child, Contraindications, Drug Monitoring methods, Humans, Patient Harm prevention & control, Preoperative Care methods, Anesthetics administration & dosage, Anesthetics adverse effects, Anesthetics classification, Diagnostic Errors prevention & control, Drug-Related Side Effects and Adverse Reactions classification, Drug-Related Side Effects and Adverse Reactions etiology, Drug-Related Side Effects and Adverse Reactions physiopathology, Drug-Related Side Effects and Adverse Reactions prevention & control, Muscular Diseases complications, Muscular Diseases diagnosis, Muscular Diseases physiopathology
- Abstract
Patients with muscle pathology are a challenge for anaesthesiologists because of possible life-threatening general anaesthesia complications. A review of the current medical literature on the issue clearly indicates that increasing awareness by anaesthesiologists in recent years has led to a reduction in the occurrence of adverse events in patients with diagnostically well-defined muscle disease. On the other hand, the current emerging aspect is that the great majority of complications concern subjects with clinically non-overt (silent to mildly symptomatic) and thus undiagnosed myopathy. With a view to improving prevention of possible critical anaesthesia complications in such patients, we present a "Safe Anaesthesia Table", listing both the anaesthetic drugs to be avoided and those considered harmless for myopathic patients, irrespective of age and type of pathology. In addition, a brief outline about the clinical aspects suggestive of a possible muscle pathology is also provided. Using "safe drugs" during routine surgical procedures in subjects with suspected undiagnosed myopathy will enable the anaesthesiologist to avoid delaying surgery, while protecting them from anaesthesia complications. By following this approach the presumed myopathy can be properly investigated after surgery.
- Published
- 2013
26. Recommendations for anesthesia and perioperative management of patients with neuromuscular disorders.
- Author
-
Racca F, Mongini T, Wolfler A, Vianello A, Cutrera R, Del Sorbo L, Capello EC, Gregoretti C, Massa R, De Luca D, Conti G, Tegazzin V, Toscano A, and Ranieri VM
- Subjects
- Airway Management, Heart Function Tests, Humans, Intraoperative Care, Neurologic Examination, Patient Care, Postoperative Care, Preoperative Care, Respiratory Function Tests, Anesthesia standards, Neuromuscular Diseases therapy, Perioperative Care standards
- Abstract
Patients with neuromuscular disorders are at high risk of intraoperative and postoperative complications. General anesthesia in these patients may exacerbate respiratory and cardiovascular failure due to a marked sensitivity to several anesthetic drugs. Moreover, succinylcholine and halogenated agents can trigger life-threatening reactions, such as malignant hyperthermia, rhabdomyolysis and severe hyperkalemia. Therefore, regional anesthesia should be used whenever possible. If general anesthesia is unavoidable, special precautions must be taken. In particular, for patients at increased risk of respiratory complications (i.e., postoperative atelectasis, acute respiratory failure, nosocomial infections), noninvasive ventilation associated with aggressive airway clearance techniques can successfully treat upper airway obstruction, hypoventilation and airway secretion retention, avoiding prolonged intubation and tracheotomy. Anesthesia and perioperative management of patients with neuromuscular disorders are described in this article. To grade the strength of recommendations and the quality of evidence we adopted the GRADE approach. In case of low-quality evidence, these recommendations represent the collective opinion of the expert panel.
- Published
- 2013
27. A truncation in the RYR1 gene associated with central core lesions in skeletal muscle fibres.
- Author
-
Rossi D, De Smet P, Lyfenko A, Galli L, Lorenzini S, Franci D, Petrioli F, Orrico A, Angelini C, Tegazzin V, Dirksen R, and Sorrentino V
- Subjects
- Aged, Animals, Biopsy, Calcium metabolism, Cell Line, Cytosol metabolism, DNA blood, DNA genetics, DNA isolation & purification, Exons, Genetic Carrier Screening, Genetic Predisposition to Disease, Humans, Kidney, Leukocytes physiology, Male, Malignant Hyperthermia genetics, Mice, Mice, Knockout, Muscle Contraction, Muscle Fibers, Skeletal physiology, Muscle, Skeletal physiopathology, Mutation, RNA, Messenger genetics, Ryanodine Receptor Calcium Release Channel deficiency, Ryanodine Receptor Calcium Release Channel physiology, Muscle Fibers, Skeletal pathology, Muscle, Skeletal pathology, Ryanodine Receptor Calcium Release Channel genetics, Sequence Deletion
- Abstract
A novel single-nucleotide deletion in exon 100 of the RYR1 gene, corresponding to deletion of nucleotide 14,510 in the human RyR1 mRNA (c14510delA), was identified in a man with malignant hyperthermia and in his two daughters who were normal for malignant hyperthermia. This deletion results in a RyR1 protein lacking the last 202 amino acid residues. All three subjects heterozygotic for the mutated allele presented with a prevalence of type 1 fibres with central cores, although none experienced clinical signs of myopathy. Expression of the truncated protein resulted in non-functional RYR1 calcium release channels. Expression of wild-type and RyR1(R4836fsX4838) proteins resulted in heterozygotic release channels with overall functional properties similar to those of wild-type RyR1 channels. Nevertheless, small differences in sensitivity to calcium and caffeine were observed in heterotetrameric channels, which also presented an altered assembly/stability in sucrose-gradient centrifugation analysis. Altogether, these data suggest that altered RYR1 tetramer assembly/stability coupled with subtle chronic changes in Ca2+ homoeostasis over the long term may contribute to the development of core lesions and incomplete malignant hyperthermia susceptibility penetrance in individuals carrying this novel RYR1 mutation.
- Published
- 2007
- Full Text
- View/download PDF
28. Frequency and localization of mutations in the 106 exons of the RYR1 gene in 50 individuals with malignant hyperthermia.
- Author
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Galli L, Orrico A, Lorenzini S, Censini S, Falciani M, Covacci A, Tegazzin V, and Sorrentino V
- Subjects
- Cohort Studies, DNA Mutational Analysis, Female, Gene Frequency, Genetic Predisposition to Disease, Genetic Testing, Humans, Male, Malignant Hyperthermia diagnosis, Exons, Malignant Hyperthermia genetics, Mutation, Missense, Ryanodine Receptor Calcium Release Channel genetics
- Abstract
Malignant hyperthermia (MH) is a dominantly inherited pharmacogenetic condition that manifests as a life-threatening hypermetabolic reaction when a susceptible individual is exposed to common volatile anesthetics and depolarizing muscle relaxants. Although MH appears to be genetically heterogeneous, RYR1 is the main candidate for MH susceptibility. However, since molecular analysis is generally limited to exons where mutations are more frequently detected, these are routinely found only in 30-50% of susceptible subjects. In this study the entire RYR1 coding region was analyzed in a cohort of 50 Italian MH susceptible (MHS) subjects. Thirty-one mutations, 16 of which were novel, were found in 43 individuals with a mutation detection rate of 86%, the highest reported for RYR1 in MH so far. These data provide clear evidence that mutations in the RYR1 gene are the predominant cause of MH.
- Published
- 2006
- Full Text
- View/download PDF
29. Correlations between genotype and pharmacological, histological, functional, and clinical phenotypes in malignant hyperthermia susceptibility.
- Author
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Monnier N, Kozak-Ribbens G, Krivosic-Horber R, Nivoche Y, Qi D, Kraev N, Loke J, Sharma P, Tegazzin V, Figarella-Branger D, Roméro N, Mezin P, Bendahan D, Payen JF, Depret T, Maclennan DH, and Lunardi J
- Subjects
- Calcium metabolism, Calcium Channels genetics, Calcium Channels, L-Type, Cell Line, Chromosome Mapping, DNA Mutational Analysis, Female, Genetic Testing, Genotype, Haplotypes, Humans, Male, Malignant Hyperthermia diagnosis, Malignant Hyperthermia pathology, Muscle Contraction drug effects, Muscle, Skeletal metabolism, Muscle, Skeletal pathology, Pedigree, Protein Structure, Tertiary, Ryanodine Receptor Calcium Release Channel chemistry, Ryanodine Receptor Calcium Release Channel genetics, Genetic Predisposition to Disease, Malignant Hyperthermia genetics
- Abstract
Malignant hyperthermia susceptibility (MHS) is a subclinical pharmacogenetic disorder caused by an impairment of skeletal muscle calcium homeostasis in response to triggering agents. While in vitro contracture testing (IVCT) is the gold standard for defining MHS, molecular analysis is increasingly used to diagnosis MHS. Mutations associated with MHS have been reported in two genes: RYR1 and CACNA1S. Mutations in RYR1 are also responsible for central core disease (CCD), a myopathy that can be associated with a positive IVCT response. We report here the results of correlation studies performed with molecular, pharmacological, histological, and functional data obtained in 175 families (referred to as confirmed (129) or potential (46) MHS families). Extensive molecular analysis allowed us to identify a variant in 60% of the confirmed MHS families, and resulted in the characterization of 11 new variants in the RYR1 gene. Most mutations clustered to MH1 and MH2 domains of RYR1. Functional analysis allowed us to assign a causative role for seven MHS mutations that we propose to add to the panel of MHS mutations used for genetic testing. The use of genetic data to determine MHS status led to a 99.5% sensitivity for IVCT. IVCT-positive/mutation-negative diagnoses were analyzed not only in terms of specificity for IVCT, but also to assess the presence of a second MHS trait in families, and the genetic heterogeneity of the disease. Histological analyses revealed the presence of cores in more than 20% of muscle biopsies originating from 242 genotyped and tested MHS patients who did not present with clinical symptoms. This indicates that these patients must be considered as MHS patients with cores, and are clearly differentiated from CCD patients who have been tested positive for MHS., (Copyright 2005 Wiley-Liss, Inc.)
- Published
- 2005
- Full Text
- View/download PDF
30. Identification of novel mutations in the ryanodine-receptor gene (RYR1) in malignant hyperthermia: genotype-phenotype correlation.
- Author
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Manning BM, Quane KA, Ording H, Urwyler A, Tegazzin V, Lehane M, O'Halloran J, Hartung E, Giblin LM, Lynch PJ, Vaughan P, Censier K, Bendixen D, Comi G, Heytens L, Monsieurs K, Fagerlund T, Wolz W, Heffron JJ, Muller CR, and McCarthy TV
- Subjects
- Female, Genotype, Humans, Male, Pedigree, Phenotype, Malignant Hyperthermia genetics, Mutation, Ryanodine Receptor Calcium Release Channel genetics
- Abstract
Malignant hyperthermia (MH) is a pharmacogenetic disorder of skeletal muscle that is triggered in genetically predisposed individuals by common anesthetics and muscle relaxants. The ryanodine receptor (RYR1) is mutated in a number of MH pedigrees, some members of which also have central core disease (CCD), an inherited myopathy closely associated with MH. Mutation screening of 6 kb of the RYR1 gene has identified four adjacent novel mutations, C6487T, G6488A, G6502A, and C6617T, which result in the amino acid alterations Arg2163Cys, Arg2163His, Val2168Met, and Thr2206Met, respectively. Collectively, these mutations account for 11% of MH cases and identify the gene segment 6400-6700 as a mutation hot spot. Correlation analysis of the in vitro contracture-test data available for pedigrees bearing these and other RYR1 mutations showed an exceptionally good correlation between caffeine threshold and tension values, whereas no correlation was observed between halothane threshold and tension values. This finding has important ramifications for assignment of the MH-susceptible phenotype, in genotyping studies, and indicates that assessment of recombinant individuals on the basis of caffeine response is justified, whereas assessment on the basis of halothane response may be problematic. Interestingly, the data suggest a link between the caffeine threshold and tension values and the MH/CCD phenotype.
- Published
- 1998
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- View/download PDF
31. Novel mutations at a CpG dinucleotide in the ryanodine receptor in malignant hyperthermia.
- Author
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Manning BM, Quane KA, Lynch PJ, Urwyler A, Tegazzin V, Krivosic-Horber R, Censier K, Comi G, Adnet P, Wolz W, Lunardi J, Muller CR, and McCarthy TV
- Subjects
- Amino Acid Substitution genetics, Arginine genetics, Cysteine genetics, Female, Genotype, Histidine genetics, Humans, Male, Pedigree, Phenotype, CpG Islands, Malignant Hyperthermia genetics, Malignant Hyperthermia metabolism, Mutation, Ryanodine Receptor Calcium Release Channel genetics
- Published
- 1998
- Full Text
- View/download PDF
32. Chlorocresol, an additive to commercial succinylcholine, induces contracture of human malignant hyperthermia-susceptible muscles via activation of the ryanodine receptor Ca2+ channel.
- Author
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Tegazzin V, Scutari E, Treves S, and Zorzato F
- Subjects
- Animals, Caffeine pharmacology, Calcium metabolism, Dose-Response Relationship, Drug, Humans, In Vitro Techniques, Rabbits, Ryanodine Receptor Calcium Release Channel, Calcium Channels drug effects, Cresols pharmacology, Malignant Hyperthermia physiopathology, Muscle Contraction drug effects, Muscle Proteins drug effects, Neuromuscular Depolarizing Agents pharmacology, Succinylcholine pharmacology
- Abstract
Background: A defect in the ryanodine (Ry1) receptor Ca2+ channel has been implicated as one of the possible underlying causes of malignant hyperthermia (MH), a pharmacogenetic disorder characterized by sustained muscle contracture. The disease is triggered by common halogenated anesthetics and skeletal muscle relaxants, such as succinylcholine. This study tested whether the functional properties of the Ry1 receptor Ca2+ channel are affected by chlorocresol, a preservative added to a commercial preparation of succinylcholine (Midarine) and other parenteral compounds., Methods: In vitro contracture testing was carried out on muscle biopsies from malignant hyperthermia-susceptible (MHS) and -negative (MHN) individual according to the protocol of the European MH group. Ca2+ flux studies on isolated rabbit sarcoplasmic reticulum fractions were measured spectrophotometrically by following the A710-790 of the Ca2+ indicator antipyrylazo III., Results: Chlorocresol causes muscle contracture in MHS muscles at a concentration of 25-50 microM and potentiates the caffeine contracture response in human MHS muscles. Sub-threshold (20 microM) concentrations of chlorocresol increase both the Kd and the Vmax of caffeine-induced Ca2+ release from isolated rabbit terminal cisternae., Conclusions: These data suggest that, in muscle from MHS individuals, the enhanced Ca2+ released from the sarcoplasmic reticulum may not be due to the effect of succinylcholine alone but rather to the action of the preservative chlorocresol added to the drug.
- Published
- 1996
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33. Ryanodine receptor gene point mutation and malignant hyperthermia susceptibility.
- Author
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Moroni I, Gonano EF, Comi GP, Tegazzin V, Prelle A, Bordoni A, Bresolin N, and Scarlato G
- Subjects
- Adolescent, Adult, Amino Acid Sequence, Base Sequence, Biopsy, Female, Genetic Predisposition to Disease, Humans, Male, Malignant Hyperthermia diagnosis, Molecular Sequence Data, Muscle Contraction, Muscles pathology, Muscles physiopathology, Pedigree, Ryanodine Receptor Calcium Release Channel, Calcium Channels genetics, Malignant Hyperthermia genetics, Muscle Proteins genetics, Point Mutation
- Abstract
Malignant hyperthermia (MH) is a rare clinical syndrome, triggered in susceptible subjects by a variety of anaesthetic agents and muscle relaxants, and is the commonest cause of death due to general anaesthesia. Previous studies have reported that inherited mutations in the ryanodine receptor (RYR1) gene co-segregated, in some families, with MH susceptibility; lack of linkage between MH and the RYR1 gene in some other families indicates a heterogenous genetic basis for the syndrome. The in vitro contracture test (IVCT) on muscle biopsy specimens is considered to be the most reliable test for establishing the diagnosis of MH. With the identification of RYR1 point mutations this might in turn result in non-invasive methods for the presymptomatic diagnosis of MH. In the present study we investigated four families suspected to be at risk of MH susceptibility; in all subjects histopathological examination and IVCT were performed on muscle biopsy specimens. We undertook a mutation analysis of RYR1 gene testing for the presence of five point mutations; in one pedigree a C1840-->T point mutation was detected, strictly segregating with in vitro MH susceptibility.
- Published
- 1995
- Full Text
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34. [Susceptibility to malignant hyperthermia: diagnostic aspects and practical implications].
- Author
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Tegazzin V
- Subjects
- Humans, Malignant Hyperthermia diagnosis, Malignant Hyperthermia etiology
- Published
- 1992
35. [The role of intra- and extracellular Ca++ in coronary vessel contraction induced in vitro by noradrenaline following a beta-adrenergic block].
- Author
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Bettini V, Bettini MB, Ceccherelli F, Costa L, Marigonda MG, Montin S, Pulliero G, Rizzotti A, and Tegazzin V
- Subjects
- Animals, Cattle, Coronary Vessels drug effects, Coronary Vessels physiology, In Vitro Techniques, Muscle Contraction drug effects, Muscle, Smooth, Vascular drug effects, Perfusion methods, Adrenergic beta-Antagonists pharmacology, Calcium physiology, Muscle Contraction physiology, Muscle, Smooth, Vascular physiology, Norepinephrine pharmacology
- Abstract
Previous studies reported that norepinephrine (NE) induces contraction of the calf isolated coronary arteries after beta-adrenergic blockade with propranolol (PR), and that the effect disappeared after phentolamine. An higher Ca++ concentration increased the response of preparation to NE, whereas the reduction of the concentration reduced the response. In isolated coronary arteries the baseline tone and contractile response to NE after PR were studied as influenced by DA and nicardipine (NI). NI always induced vessel relaxation and DA induced a contraction followed by relaxation. The NE contraction was not abolished in calcium-free medium but in presence of DA and was reduced by NI in the medium containing Ca++. We conclude that NE induces contractions by facilitating the influx of the extracellular Ca++ and by promoting the liberation of intracellular bound Ca++.
- Published
- 1990
36. Vagal stimulation and exogenous acetylcholine in isolated rat stomach: calcitonin effect on contractile activity.
- Author
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Aragno R, Bettini V, Ceccherelli F, Lo Castro G, and Tegazzin V
- Subjects
- Animals, Electric Stimulation, In Vitro Techniques, Muscle, Smooth drug effects, Muscle, Smooth innervation, Rats, Rats, Inbred Strains, Stomach drug effects, Stomach innervation, Acetylcholine pharmacology, Calcitonin pharmacology, Muscle Contraction drug effects, Muscle, Smooth physiology, Stomach physiology, Vagus Nerve physiology
- Abstract
Calcitonin induces contraction in the vascular and extravascular smooth muscle and facilitates the transmission of the excitation in somatic motor nerve endings. These actions are Ca2(+)-dependent. The calcitonin effect on autonomic nerve endings has been studied here by testing influence of calcitonin on the contractile responses of the isolated rat stomach. The organ was submitted to electrical vagal stimulation or, after denervation, to exogenous acetylcholine. Calcitonin invariably increased the muscular tone and reduced the contractile responses to vagal stimulation. Opposite effects were noted after a serotoninergic block with nicergoline. Calcitonin also increased the contractile response evoked by exogenous acetylcholine and the Ca(2)-antagonist nicardipine counteracted the facilitatory effects. We suggest that the inhibitory action of calcitonin is serotonine-dependent while the facilitatory one is Ca2(+)-dependent.
- Published
- 1990
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37. An experimental model of myasthenia myopathy.
- Author
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Tegazzin V, Facco E, Caldesi Valeri V, Bresólin N, and Gíron GP
- Subjects
- Animals, Autoantibodies analysis, Electromyography, Fluorescent Antibody Technique, Freund's Adjuvant, Male, Muscle, Skeletal pathology, Muscular Diseases etiology, Muscular Diseases pathology, Myasthenia Gravis, Autoimmune, Experimental complications, Myasthenia Gravis, Autoimmune, Experimental pathology, Rabbits, Thymus Gland immunology, Muscular Diseases physiopathology, Myasthenia Gravis, Autoimmune, Experimental physiopathology, Thymectomy
- Abstract
Normal and thymectomised rabbits been have immunized by means of a thymic extract emulsified with Freund's Complete Adjuvant. The experiment was conducted over a three month period, in order to reproduce an experimental model of chronic myasthenia. During this period immunological, electromyographic and histologic studies were undertaken. Typical findings of partial neuromuscular block were invariably obtained from all the non thymectomized animals, while such signs were constantly absent both in non-treated control rabbits and in the immunized thymectomized ones. This neuromuscular block was intermittent. The compromised neuromuscular conduction was associated to an histological pattern of autoimmune myopathy. Evidence was put on antibodies directed against the thymus, muscular and nervous tissue. The results indicate the important role of the thymus gland both in altering conduction at the neuromuscular junction level and causing histopathologic muscle lesions.
- Published
- 1979
38. Pathogenesis of late asthmatic reactions induced by exposure to isocyanates.
- Author
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Mapp CE, Boschetto P, Zocca E, Milani GF, Pivirotto F, Tegazzin V, and Fabbri LM
- Subjects
- Anti-Inflammatory Agents therapeutic use, Asthma physiopathology, Bronchi pathology, Humans, Inflammation, Neutrophils physiology, Occupational Diseases physiopathology, Time Factors, Asthma chemically induced, Bronchi drug effects, Cyanates adverse effects, Occupational Diseases chemically induced, Toluene 2,4-Diisocyanate adverse effects
- Abstract
The importance of airways inflammation for the development of bronchial hyperresponsiveness and for exacerbation of asthma was investigated in subjects with occupational asthma. We examined subjects sensitized to isocyanates, a small molecular weight compound that causes occupational asthma. Studies in asthmatic subjects sensitized to toluene diisocyanate (TDI) demonstrated that late, but not early, asthmatic reactions induced by TDI were associated with an acute increase in bronchial responsiveness, and with a marked infiltration of neutrophils and a slight infiltration of eosinophils into the airways, both prevented by steroids. As the late asthmatic reactions and the increase in responsiveness induced by TDI were prevented by steroids, but not by indomethacin, we speculated that cell membrane phospholipid metabolites, which are inhibited by steroids but not by indomethacin, may be involved in TDI induced hyperresponsiveness. The results of these studies suggest that bronchial hyperresponsiveness and exacerbation of asthma may be related to inflammation of the airways and that cell membrane phospholipid metabolites may be involved.
- Published
- 1987
39. Carnitine and acyltransferase in experimental neurogenic atrophies: changes with treatment.
- Author
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Bresolin N, Freddo L, Tegazzin V, Bet L, Armani M, and Angelini C
- Subjects
- Adult, Animals, Carnitine pharmacology, Denervation, Humans, Infant, Infant, Newborn, Male, Muscular Atrophy enzymology, Muscular Atrophy etiology, Muscular Atrophy pathology, Nerve Regeneration, Rats, Rats, Inbred Strains, Acyltransferases metabolism, Carnitine metabolism, Muscular Atrophy metabolism
- Abstract
Carnitine level and carnitine palmityl transferase (CPT) activity were investigated in muscles of patients with infantile and juvenile spinal muscular atrophy and polyneuropathies. A significant decrease of both carnitine and CPT was found in the infantile spinal muscular atrophy, but not in the other neurogenic muscle atrophies. These findings were compared with the experimental effect of denervation and reinnervation upon the lipid metabolism in soleus and extensor digitorum longus (EDL) of adult and newborn rats. Twenty-one days after denervation free and total carnitine decreased significantly in both EDL (P less than 0.001) and soleus (P less than 0.05) of adult animals. CPT activity was significantly decreased in the soleus 50 days after denervation (P less than 0.005). Long-term reinnervation restored the level of carnitine fraction and CPT activity. L-carnitine treatment for 21 days restored the level of free carnitine to normal in the soleus of denervated adult animals. Denervation in newborn rats influenced carnitine concentration in soleus and EDL to a lesser extent; the treatment with L-carnitine raised short-chain acylcarnitines in denervated muscles, while reinnervation restored carnitine level within 50 days.
- Published
- 1984
- Full Text
- View/download PDF
40. Sciatic nerve block by the anterior and posterior approach for operations on the lower extremity. A comparative study.
- Author
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Manani G, Angel A, Civran E, Tegazzin V, Dal Vecchio AD, and Giron GP
- Subjects
- Adolescent, Adult, Aged, Anthropometry, Female, Humans, Male, Middle Aged, Preanesthetic Medication, Tourniquets, Leg surgery, Nerve Block methods, Sciatic Nerve
- Abstract
The results of the analgesic block of the lower extremity by means of an anterior (150 patients) or a posterior (114 patients) approach to the sciatic nerve, associated to a "3 in 1 block" were compared. The anterior approach technique was associated with a higher incidence of failures, insufficient analgesia and hence a higher demand for intraoperative analgesic and sedative drugs. Also tolerance to a pneumatic tourniquet over the proximal thigh was less than with the posterior approach. However, the sciatic nerve block by anterior approach granted a more prolonged analgesia. This technique was suitable for trauma patients immobilized in the supine position, for patients with skeletal traction on Zupinger frame, both for surgery and for closed reduction of lower extremity fractures.
- Published
- 1982
41. [Changes in acetylcholine contractions induced by carnitine in coronary vessels isolated "in vitro"].
- Author
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Bettini V, Catozzo C, Martino R, Mayellaro F, Munari L, Tegazzin V, and Ton P
- Subjects
- Animals, Atropine pharmacology, Calcium metabolism, Cattle, Coronary Vessels drug effects, Fendiline pharmacology, In Vitro Techniques, Kinetics, Muscle Contraction drug effects, Pyrrolidines pharmacology, Receptors, Muscarinic physiology, Verapamil pharmacology, Acetylcholine pharmacology, Carnitine pharmacology, Coronary Vessels physiology
- Abstract
As suggested by literature about the carnitine's choline-mimetic effects, it has been studied the influence of this substance on the response to Ach of the isolated coronary arteries. It has been seen that Ach has often induced the contraction of the preparation that was preceded or abolished by atropine or prifinium bromide, or reduced by fendiline and verapamil. It resulted also that carnitine has always increased the entity of the contraction of the preparation treated with Ach and that the raising was abolished by fendiline or verapamil. Taking such results and suggestions from the literature as a basis, it has been concluded that the carnitine increased the response of the preparation to Ach, sensitizing muscarinic receptors which cause the entry of Ca++ throught the cell membrane.
- Published
- 1985
42. [Contractile response of segments of the coronary arteries to histamine and angiotensin II in the presence of anthocyanosides of myrtillus].
- Author
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Bettini V, Martino R, Tegazzin V, and Ton P
- Subjects
- Animals, Aspirin analogs & derivatives, Aspirin pharmacology, Cattle, Coronary Vessels physiology, Indomethacin pharmacology, Lysine analogs & derivatives, Lysine pharmacology, Plants, Angiotensin II antagonists & inhibitors, Anthocyanins pharmacology, Coronary Vessels drug effects, Histamine Antagonists pharmacology, Vasoconstriction drug effects
- Published
- 1987
43. Caffeine sensitivity of sarcoplasmic reticulum of fast and slow fibers from normal and malignant hyperthermia human muscle.
- Author
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Salviati G, Betto R, Ceoldo S, Tegazzin V, and Della Puppa A
- Subjects
- Humans, In Vitro Techniques, Sarcoplasmic Reticulum pathology, Caffeine pharmacology, Malignant Hyperthermia physiopathology, Sarcoplasmic Reticulum drug effects
- Abstract
We have carried out a comparative study of caffeine sensitivity of the sarcoplasmic reticulum (SR) of fast and slow normal human fibers chemically skinned. Human slow-fiber SR is more sensitive to caffeine than fast fiber SR; however, it releases less calcium and at a lower rate than the SR of fast fibers when exposed to threshold concentrations of caffeine. These results indicate that the SR calcium release mechanisms of SR of fast and slow human fibers are homologous but not identical. An increased sensitivity of SR to caffeine is found in both fast and slow fibers from human malignant hyperthermia muscle. However, fast fibers seem to be the most affected, since their caffeine threshold for contraction is very close to that of slow fibers.
- Published
- 1989
- Full Text
- View/download PDF
44. [Possibilities of control of regulation of the function of arteriovenous anastomoses and of capillary blood flow by means of acupuncture].
- Author
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Tegazzin V, Buchberger R, and Ferramosca A
- Subjects
- Adult, Arteriovenous Anastomosis, Arthritis, Rheumatoid complications, Capillaries, Humans, Leg blood supply, Male, Vascular Diseases etiology, Acupuncture Therapy, Arthritis, Rheumatoid therapy, Blood Flow Velocity, Vascular Diseases therapy, Vasodilation
- Abstract
Acupuncture was carried out on a patient with rheumatoid arthritis and microangiopathy of the lower limbs. Photoplethysmographic waves appeared at the right inferior limb where before they had been absent; at the left inferior limb normalization of postural reflexes was achieved, suggesting that acupuncture is effective in vasodilatation of capillaries and preterminal arterioles and in the reactivation of the arterio-venous blood flow.
- Published
- 1979
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