Search

Physiological and biochemical studies have provided indirect evidence for a membrane-associated carbonic anhydrase (CA) isoform, similar to mammalian type IV CA, in the gills of dogfish (Squalus acanthias). This CA isoform is linked to the plasma membrane of gill epithelial cells by a glycosylphosphatidylinositol anchor and oriented toward the plasma, such that it can catalyze the dehydration of plasma HC[O.sup.-.sub.3] ions. The present study directly tested the hypothesis that CA IV is present in dogfish gills in a location amenable to catalyzing plasma HC[O.sup.-.sub.3] dehydration. Homology cloning techniques were used to assemble a 1,127 base pair cDNA that coded for a deduced protein of 306 amino acids. Phylogenetic analysis suggested that this protein was a type IV CA. For purposes of comparison, a second cDNA (1,107 base pairs) was cloned from dogfish blood; it encoded a deduced protein of 260 amino acids that was identified as a cytosolic CA through phylogenetic analysis. Using real-time PCR and in situ hybridization, mRNA expression for the dogfish type IV CA was detected in gill tissue and specifically localized to pillar cells and branchial epithelial cells that flanked the pillar cells. Immunohistochemistry using a polyclonal antibody raised against rainbow trout type IV CA revealed a similar pattern of CA IV immunoreactivity and demonstrated a limited degree of colocalization with [Na.sup.+]-[K.sup.+]-ATPase immunoreactivity. The presence and localization of a type IV CA isoform in the gills of dogfish is consistent with the hypothesis that branchial membrane-bound CA with an extracellular orientation contributes to C[O.sub.2] excretion in dogfish by catalyzing the dehydration of plasma HC[O.sup.-.sub.3] ions. carbon dioxide excretion; gill

African lungfish Protopterus annectens utilized both respiratory and metabolic compensation to restore arterial pH to control levels following the imposition of a metabolic acidosis or alkalosis. Acid infusion (3 mmol kg-1 NH4Cl) to lower arterial pH by 0.24 units increased both pulmonary (by 1.8-fold) and branchial (by 1.7-fold) ventilation frequencies significantly, contributing to 4.8-fold and 1.9- fold increases in, respectively, aerial and aquatic CO2 excretion. This respiratory compensation appeared to be the main mechanism behind the restoration of arterial pH, because even though net acid excretion (JnetH+) increased following acid infusion in 7 of 11 fish, the mean increase in net acid excretion, 184.5±1185 µmol H+ kg-1 h-1 (mean ± s.e.m., N=11), was not significantly different from zero. Base infusion (3 mmol kg-1 NaHCO3) to increase arterial pH by 0.29 units halved branchial ventilation frequency, although pulmonary ventilation frequency was unaffected. Correspondingly, aquatic CO2 excretion also fell significantly (by 3.7-fold) while aerial CO2 excretion was unaffected. Metabolic compensation consisting of negative net acid excretion (net base excretion) accompanied this respiratory compensation, with JnetH+ decreasing from 88.5±75.6 to -337.9±199.4 µmol H+ kg-1 h-1 (N=8). Partitioning of net acid excretion into renal and extra-renal (assumed to be branchial and/or cutaneous) components revealed that under control conditions, net acid excretion occurred primarily by extra-renal routes. Finally, several genes that are involved in the exchange of acid-base equivalents between the animal and its environment (carbonic anhydrase, V-type H+-ATPase and Na+/HCO3-cotransporter) were cloned, and their branchial and renal mRNA expressions were examined prior to and following acid or base infusion. In no case was mRNA expression significantly altered by metabolic acid-base disturbance. These findings suggest that lungfish, like tetrapods, alter ventilation to compensate for metabolic acid-base disturbances, a mechanism that is not employed by water-breathing fish. Like fish and amphibians, however, extra-renal routes play a key role in metabolic compensation. [ABSTRACT FROM AUTHOR]

Background: Transfusion-related acute lung injury (TRALI) is a well-characterized, serious complication of blood component therapy in hospitalized patients. The signs and symptoms are often attributed to other clinical aspects of a patient's condition, and therefore TRALI may go unrecognized. IVIG is a pooled plasma derivative commonly used in the outpatient setting. Respiratory complications of IVIG infusion have typically been attributed to volume overload or allergic and vasomotor reactions. TRALI has never been documented to occur after IVIG infusion.Case Report: A 23-year-old man with multifocal motor neuropathy developed noncardiogenic pulmonary edema 6 hours after receiving 90 g of IVIG by a rapid-infusion protocol. He fully recovered in 5 days with nasal oxygen and bed rest. Granulocyte-associated IgG was detected in his blood 14 and 27 weeks after the event. The lots of IVIG that he received were found to contain a low-titer, panreactive, granulocyte antibody, mostly IgG.Conclusion: This is the first documented case of TRALI after IVIG infusion. An autoimmune syndrome, including autoantibody-coated granulocytes, may have been a priming stimulus for granulocyte interaction with pulmonary capillary endothelium. Rapid infusion of a large quantity of granulocyte antibody may have precipitated TRALI. A pooled plasma product or derivative may result in TRALI. [ABSTRACT FROM AUTHOR]

Mattresses designed for clinical applications are deceptively simple pieces of equipment. Their primary function is to comfortably support the patient in an appropriate position. However, there are many other technical factors that affect the quality of the support surfaces. In this paper we discuss the basic functions that mattresses should fulfil, explain some of the underlying mechanics and discuss CE marking and other standards. [ABSTRACT FROM AUTHOR]