Search

Lipids from erythrocyte membranes of normal and cholesterol fed animals were isolated and the various fractions were analyzed quantitatively. Erythrocyte membrane lipid composition of animals fed with an atherogenic diet for 2 months revealed marked elevations in cholesterol followed by significant alterations in phospholipids, free fatty acids and triglycerides. These findings were discussed from the point of view of the role of membrane lipids in the maintenance of cell integrity, shape, and homeostasis.

An expression for the pulse wave velocity in a non-linear elastic pressurized arterial tube is derived; in terms of the arterial constitutive (experimentally derived strain energy density function) parameters and the undeformed and deformed arterial diameters. The pulse wave velocity expression is then employed for developing the analysis for invivo determination of the arterial constitutive parameters from arterial imaging data. The analysis provides a method to non-invasively determine the values of the non-linear elastic parameters of the artery by using the invivo monitored values of its diameter and the pulse wave velocity. This Information on the elastic parameters of an artery could characterize the state of the artery and hence a diagnostic indication of the atheromatous involvement of the blood vessel. ? 1981, Walter de Gruyter. All rights reserved ? 1981, Walter de Gruyter. Alle Rechte vorbehalten.

The receptors involved in the pressor and tachycardic effects of catecholamines applied systemically or released from sympathetic nerve endings were compared. Intravenously administered (-)-epinephrine activated alpha-1, alpha-2, beta-1 and beta-2 adrenoceptors as demonstrated in pithed rats, using the alpha-1 sympatholytic drug prazosin, the alpha-2 adrenoceptor blocking substance rauwolscine, the beta-1 and beta-2 sympatholytic agent(-)-propranolol, the predominantly beta-1 adrenoceptor antagonist atenolol and the selective beta-2 adrenoceptor blocking agent ICI 118,551 as tools. (-)-Norepinephrine given i.v. proved to be an alpha-1, alpha-2 and beta-1 adrenoceptor agonist. 1,1-Dimethyl-4-phenylpiperazine iodide (DMPP) releases catecholamines from noradrenergic neurons and the adrenal medulla. The i.v. injection of DMPP into pithed rats caused an increase in diastolic pressure and heart rate by this indirect effect, which has been confirmed by pretreatment with reserpine and removal of the adrenals. After bilateral adrenalectomy, there occurred a release of mainly norepinephrine, only from the neurons. Catecholamines liberated by DMPP activated alpha-1 and beta-1 receptors and, at high doses of DMPP, alpha-2 and beta-2 adrenoceptors as well. Removal of both adrenal glands abolished the alpha-2 and beta-2 adrenoceptor-mediated effects. (-)-Norepinephrine released from neurons stimulated alpha-1 and beta-1 adrenoceptors only, although after i.v. administration of this catecholamine alpha-2 adrenoceptors were also activated. There was no indication for a beta-2 adrenoceptor-mediated vasodilation by neuronally released catecholamines. A beta-2 adrenoceptor-mediated effect, however, could be demonstrated by i.v. injection of (-)-epinephrine. The results can be explained by the presence of predominantly alpha-1 and beta-1 adrenoceptors in the postganglionic sympathetic synapses and an extrasynaptic location of alpha-2 and beta-2 adrenoceptors. The extrasynaptic receptors are possibly controlled by epinephrine from the adrenals.

In a group of 21 cats, the middle cerebral artery pressure (MCAP) was recorded by means of a catheter introduced into the artery at its origin, just distal to the occlusion. The effects of hypertension, hypercapnia, and hypocapnia were studied. In a group of five cats, both middle cerebral arteries (MCA) were catheterized and the pressure was recorded simultaneously on both sides. In another group of five cats, O2 tension measurements were made with the aid of oxygen electrodes in the brain tissue, the occluded MCA, and the common carotid artery. Some of the results obtained in this study are compared with the results of a previous study where monkeys were used as experimental animals. Chemicals/CAS: carbon dioxide, 124-38-9, 58561-67-4; Oxygen, 7782-44-7

An integrating sphere technique has been applied to assess the reflectivity of different skin sites on the body, in male subjects of various complexion and of differing form. The measured reflectance and absorbance with helium-neon laser is shown to vary with skin colour, tissue composition and the blood flow through the organs. ? 1981 IFMBE.

The decrease in apparent viscosity of blood with decreasing tube radius (Fahraeus-Lindqvist effect) under steady flow conditions, is well known. The question naturally arises: what is the effect of tube size on the apparent viscosity of blood under oscillatory conditions? The purpose of this study was to answer this question.

272 patients admitted to coronary care unit (C.C.U.) for acute myocardial infarction were subdivided into two age groups; group A: 83 patients over 65 years old (mean age 69.3), group B: 189 patients under 65 years old (mean age 59.3). Mortality rate was significantly higher in group A compared with group B (40.9% and respectively 12.2%: p

The local EEG, the local cerebral blood flow (lCBF), and the flow in the distal stump of the occluded middle cerebral artery were simultaneously recorded in 28 acute experiments in cats. Nembutal anesthesia was used eleven times, and Halothane anaesthesia 17 times. The recordings were made via platinum electrodes: 12 in the ischaemic hemisphere, and 2-3 in the opposite non-ischaemic hemisphere. The flow in the occluded middle cerebral artery was recorded via a platinum electrode introduced into this artery via the transorbital approach. The changes in lEEG, lCBF, and middle cerebral artery flow were studied during normotension, hypertension, and hypotension. A beneficial effect of hypertension was noted in the acute phase of brain ischaemia. Hypertension counteracted also the 'diaschisis' in the non-ischaemic part of the ischaemic hemisphere and in the opposite non-ischaemic hemisphere. A correlation between lEEG changes and lCBF changes were noted. In addition an interesting discrepancy was observed between the rapid H2 clearance in the middle cerebral artery stump and the much slower H2 clearance in the ischaemic brain area. Significant differences between experiments under Halothane and experiments under Nembutal anaesthesia were noted. In the acute phase those changes are probably the result of the different levels of blood pressure in those two groups. Chemicals/CAS: Metaraminol, 54-49-9; Nitroprusside, 15078-28-1

Clinical, neuropathological, and immunohistochemical (PAP) findings are reported in a 7 month-old girl with Tuberous sclerosis (TS). Polycystic kidneys and massive cardiomegaly constituted the prominent pathological features. The neuropathology of the syndrome was characterized by Megalencephaly, Subependymal giant cell astrocytoma, Very large protoplasmic astrocytes in Golgi-rapid method preparations of cortical tubers and Glial fibrillary acidic protein (GFAP)-negative giant cells in the subependymal nodules as well as in the cortical tubers. The identity of these giant cells is discussed.

Confluent cultures of endothelial cells from human umbilical cord were used to study the effect of activated human protein C (APC) on the production of plasminogen activators, plasminogen activator-inhibitor, and factor VIII-related antigen. Addition of APC to the cells in a serum-free medium did not affect the production of tissue-type plasminogen activator (t-PA) or factor VIII-related antigen; under all measured conditions, no urokinase activity was found. However, less plasminogen activator-inhibitor activity accumulated in the conditioned medium in the presence of APC. This decrease was dose dependent and could be prevented by specific anti-protein C antibodies. No decrease was observed with the zymogen protein C or with diisopropylfluorophosphate-inactivated APC. APC also decreased the t-PA inhibitor activity in endothelial cell-conditioned medium in the absence of cells, which suggests that the effect of APC is at least partly due to a direct effect of APC on the plasminogen activator-inhibitor. High concentrations of thrombin - but not of factor Xa or IXa - had a similar effect on the t-PA inhibitor activity. The effect of APC on the plasminogen activator-inhibitor provides a new mechanism by which APC may enhance fibrinolysis. The data suggest that activation of the coagulation system may lead to a secondary increase of the fibrinolytic activity by changing the balance between plasminogen activator(s) and its (their) fast-acting inhibitor. Chemicals/CAS: plasminogen activator inhibitor, 105844-41-5; plasminogen activator, 9039-53-6; protein C, 60202-16-6; Antigens; Blood Proteins; Culture Media; Factor VIII, 9001-27-8; Glycoproteins; Isoantigens; Plasminogen Activators, EC 3.4.21.-; Plasminogen Inactivators; Protein C; Urinary Plasminogen Activator, EC 3.4.21.73; urokinase inhibitor; von Willebrand Factor

In a group of 21 cats, the middle cerebral artery pressure (MCAP) was recorded by means of a catheter introduced into the artery at its origin, just distal to the occlusion. The effects of hypertension, hypercapnia, and hypocapnia were studied. In a group of five cats, both middle cerebral arteries (MCA) were catheterized and the pressure was recorded simultaneously on both sides. In another group of five cats, O2 tension measurements were made with the aid of oxygen electrodes in the brain tissue, the occluded MCA, and the common carotid artery. Some of the results obtained in this study are compared with the results of a previous study where monkeys were used as experimental animals. Chemicals/CAS: carbon dioxide, 124-38-9, 58561-67-4; Oxygen, 7782-44-7

Confluent cultures of endothelial cells from human umbilical cord were used to study the effect of activated human protein C (APC) on the production of plasminogen activators, plasminogen activator-inhibitor, and factor VIII-related antigen. Addition of APC to the cells in a serum-free medium did not affect the production of tissue-type plasminogen activator (t-PA) or factor VIII-related antigen; under all measured conditions, no urokinase activity was found. However, less plasminogen activator-inhibitor activity accumulated in the conditioned medium in the presence of APC. This decrease was dose dependent and could be prevented by specific anti-protein C antibodies. No decrease was observed with the zymogen protein C or with diisopropylfluorophosphate-inactivated APC. APC also decreased the t-PA inhibitor activity in endothelial cell-conditioned medium in the absence of cells, which suggests that the effect of APC is at least partly due to a direct effect of APC on the plasminogen activator-inhibitor. High concentrations of thrombin - but not of factor Xa or IXa - had a similar effect on the t-PA inhibitor activity. The effect of APC on the plasminogen activator-inhibitor provides a new mechanism by which APC may enhance fibrinolysis. The data suggest that activation of the coagulation system may lead to a secondary increase of the fibrinolytic activity by changing the balance between plasminogen activator(s) and its (their) fast-acting inhibitor. Chemicals/CAS: plasminogen activator inhibitor, 105844-41-5; plasminogen activator, 9039-53-6; protein C, 60202-16-6; Antigens; Blood Proteins; Culture Media; Factor VIII, 9001-27-8; Glycoproteins; Isoantigens; Plasminogen Activators, EC 3.4.21.-; Plasminogen Inactivators; Protein C; Urinary Plasminogen Activator, EC 3.4.21.73; urokinase inhibitor; von Willebrand Factor

Platelet-activating factor (PAF-acether; 1-O-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine) induced the release of plasminogen activator in rat, both in vivo and in perfused hind legs. The released plasminogen activator was shown by immunologic and functional criteria to be tissue-type plasminogen activator (t-PA). Release of t-PA by PAF-acether could be inhibited by phospholipase inhibitors and by lipoxygenase inhibitors, but not by cyclooxygenase inhibitors. It is suggested that PAF-acether induces the release of t-PA from vascular endothelial cells by the (calcium-dependent) activation of a phospholipase-lipoxygenase pathway. Chemicals/CAS: 3 amino 1 (3 trifluoromethylphenyl) 2 pyrazoline, 66000-40-6; 4 bromophenacyl bromide, 99-73-0; acetylsalicylic acid, 493-53-8, 50-78-2, 53663-74-4, 53664-49-6, 63781-77-1; diethylcarbamazine, 1642-54-2, 1851-24-7, 90-89-1; docebenone, 80809-81-0; edetic acid, 150-43-6, 60-00-4; indometacin, 53-86-1, 74252-25-8, 7681-54-1; mepacrine, 69-05-6, 83-89-6; nordihydroguaiaretic acid, 500-38-9; plasminogen activator, 9039-53-6; thrombocyte activating factor, 64176-80-3, 65154-06-5; tissue plasminogen activator, 105913-11-9; Calcium, 7440-70-2; Cyclooxygenase Inhibitors; Lipoxygenase Inhibitors; Phospholipases, EC 3.1.-; Plasminogen Activators, EC 3.4.21.-; Platelet Activating Factor

The local EEG, the local cerebral blood flow (lCBF), and the flow in the distal stump of the occluded middle cerebral artery were simultaneously recorded in 28 acute experiments in cats. Nembutal anesthesia was used eleven times, and Halothane anaesthesia 17 times. The recordings were made via platinum electrodes: 12 in the ischaemic hemisphere, and 2-3 in the opposite non-ischaemic hemisphere. The flow in the occluded middle cerebral artery was recorded via a platinum electrode introduced into this artery via the transorbital approach. The changes in lEEG, lCBF, and middle cerebral artery flow were studied during normotension, hypertension, and hypotension. A beneficial effect of hypertension was noted in the acute phase of brain ischaemia. Hypertension counteracted also the 'diaschisis' in the non-ischaemic part of the ischaemic hemisphere and in the opposite non-ischaemic hemisphere. A correlation between lEEG changes and lCBF changes were noted. In addition an interesting discrepancy was observed between the rapid H2 clearance in the middle cerebral artery stump and the much slower H2 clearance in the ischaemic brain area. Significant differences between experiments under Halothane and experiments under Nembutal anaesthesia were noted. In the acute phase those changes are probably the result of the different levels of blood pressure in those two groups. Chemicals/CAS: Metaraminol, 54-49-9; Nitroprusside, 15078-28-1

In nine patients with non-malignant diseases undergoing major upper abdominal surgery, the mechanism of the postoperative fibrinolytic shut-down was investigated because of its potential significance for postoperative deep vein thrombosis by employing new and specific methods for assessing and stimulating the fibrinolytic system. The shut-down was found to result from an impairment of the balance between tissue-type plasminogen activator, t-PA, and its recently discovered fast-acting inhibitor. In this balance, the t-PA antigen concentrations both in resting conditions and after stimulation evoked by desamino-D-arginine vasopressin (DDAVP) were found to be unchanged by surgery. However, there was a significant postoperative increase in t-PA inhibitor levels. The release of t-PA under the stimulus of DDAVP infusion overcame the postoperative shut-down of t-PA activity. However, DDAVP infusion was associated with potentially unfavourable increases in the Factor VIII/von Willebrand factor complex. The discovery of increased t-PA inhibitor in the postoperative period opens new possibilities for a rational approach to reduce or abolish the postoperative fibrinolytic shut-down. Chemicals/CAS: blood clotting factor 8, 9001-27-8; desmopressin, 16679-58-6; plasminogen activator inhibitor, 105844-41-5; tissue plasminogen activator, 105913-11-9; Desmopressin, 16679-58-6; Factor VIII, 9001-27-8; Glycoproteins; Plasminogen Inactivators; Tissue Plasminogen Activator, EC 3.4.21.68; von Willebrand Factor

The effect of intravenously injected endotoxin on inflammatory cells within solid Meth A tumours was studied and central hyperaemia, necrosis and early collapse were observed macroscopically at 4, 24 and 48 h, respectively. The effects were studied in semithin sections and cytocentrifuge preparations of the tumours. The inflammatory cell reaction evoked by the tumours in untreated animals was relatively slight. It was located predominantly around the lateral margins of the tumours and only a few inflammatory cells were found inside the tumour. Prominent effects of endotoxin included a transient increase of mononuclear inflammatory cells in the centre of the tumour by 4 h and a reduction of the influx of lymphocytes, observed in and around the margin of control tumours, by 48 h. Mast cells formed an important part of the inflammatory cell infiltrate, but no distinct changes in number and appearance were observed with time or following treatment. Total host cell numbers within tumours did not increase significantly upon endotoxin-treatment. Results suggest that a direct cytotoxic action of host cells cannot account for the extensive tumour damage observed. Rather, endotoxin-induced regression seems to be related to decreased lymphocyte numbers. Chemicals/CAS: Endotoxins

Binding and metabolism of low density lipoprotein (LDL) and acetylated LDL were examined in endothelial cells from human umbilical cord arteries and veins. Both high and low affinity LDL interactions were observed. High affinity LDL binding and catabolism were increased five- to sevenfold after preincubation for 18 hours in LPDS containing medium. Subconfluent cells degraded, endocytosed, and bound 1.5 to 2.7 times more LDL by high affinity interaction than confluent cells, when endothelial cell growth supplement (ECGS) was present in the culture system. In the absence of ECGS, these ratios were somewhat less. Low affinity LDL metabolism was less affected by the state of confluency. Binding of LDL and acetylated LDL by venous endothelial cells was more than two- and threefold, respectively, than that by comparable arterial cells. However, the difference in LDL binding was not reflected in an altered LDL catabolism. There apparently is a population of low affinity binding sites not involved in LDL catabolism. LDL metabolism was identical in cells, which were cultured in medium supplemented with 20% to 100% serum or hirudin- or heparin-treated platelet-poor plasma. Without preincubation in LPDS, high affinity adsorptive endocytosis mediated the main part of LDL uptake only at low LDL concentrations (5 to 20 ??g protein/ml). However, at physiological LDL concentrations (550 ??g/ml), we estimated that this process mediated only 17% of the LDL uptake. We calculated that fluid endocytosis and low affinity adsorptive endocytosis of LDL accounted for the remaining 12% and 70%, respectively, of the LDL uptake at physiological LDL concentrations. Chemicals/CAS: acetyl-LDL receptor; Growth Substances; Lipoproteins, LDL; Receptors, Cell Surface; Receptors, LDL

[No abstract available]

The clinical and laboratory features of 47 patients with primary Sjogren's syndrome, confirmed by lip biopsy, were analyzed in this study. The majority of our patients had the classical signs and symptoms of Sjogren's syndrome at the time of diagnosis. An average of 8 years had elapsed, however, before the diagnosis was made. The progressive appearance of new signs and symptoms during the course of the disease and the predilection for premenopausal women were found to be characteristic. Extraglandular extension of the disease was most frequently manifested by renal involvement and vasculitis. 9 5 685 690

The effect of intravenously injected endotoxin on inflammatory cells within solid Meth A tumours was studied and central hyperaemia, necrosis and early collapse were observed macroscopically at 4, 24 and 48 h, respectively. The effects were studied in semithin sections and cytocentrifuge preparations of the tumours. The inflammatory cell reaction evoked by the tumours in untreated animals was relatively slight. It was located predominantly around the lateral margins of the tumours and only a few inflammatory cells were found inside the tumour. Prominent effects of endotoxin included a transient increase of mononuclear inflammatory cells in the centre of the tumour by 4 h and a reduction of the influx of lymphocytes, observed in and around the margin of control tumours, by 48 h. Mast cells formed an important part of the inflammatory cell infiltrate, but no distinct changes in number and appearance were observed with time or following treatment. Total host cell numbers within tumours did not increase significantly upon endotoxin-treatment. Results suggest that a direct cytotoxic action of host cells cannot account for the extensive tumour damage observed. Rather, endotoxin-induced regression seems to be related to decreased lymphocyte numbers. Chemicals/CAS: Endotoxins

The effects of administration of cholesterol alone and of cholesterol and fresh whole onion extract, on the shape of erythrocytes, were studied in albino rabbits. In animals on a cholesterol-enriched diet, the erythrocytes changed shape and showed an increased tendency to aggregate, whereas they retained their normal appearance in animals on cholesterol and onion extract, and did not differ from those of normal control rabbits. ? 1980.

Platelet-activating factor (PAF-acether; 1-O-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine) induced the release of plasminogen activator in rat, both in vivo and in perfused hind legs. The released plasminogen activator was shown by immunologic and functional criteria to be tissue-type plasminogen activator (t-PA). Release of t-PA by PAF-acether could be inhibited by phospholipase inhibitors and by lipoxygenase inhibitors, but not by cyclooxygenase inhibitors. It is suggested that PAF-acether induces the release of t-PA from vascular endothelial cells by the (calcium-dependent) activation of a phospholipase-lipoxygenase pathway. Chemicals/CAS: 3 amino 1 (3 trifluoromethylphenyl) 2 pyrazoline, 66000-40-6; 4 bromophenacyl bromide, 99-73-0; acetylsalicylic acid, 493-53-8, 50-78-2, 53663-74-4, 53664-49-6, 63781-77-1; diethylcarbamazine, 1642-54-2, 1851-24-7, 90-89-1; docebenone, 80809-81-0; edetic acid, 150-43-6, 60-00-4; indometacin, 53-86-1, 74252-25-8, 7681-54-1; mepacrine, 69-05-6, 83-89-6; nordihydroguaiaretic acid, 500-38-9; plasminogen activator, 9039-53-6; thrombocyte activating factor, 64176-80-3, 65154-06-5; tissue plasminogen activator, 105913-11-9; Calcium, 7440-70-2; Cyclooxygenase Inhibitors; Lipoxygenase Inhibitors; Phospholipases, EC 3.1.-; Plasminogen Activators, EC 3.4.21.-; Platelet Activating Factor

Binding and metabolism of low density lipoprotein (LDL) and acetylated LDL were examined in endothelial cells from human umbilical cord arteries and veins. Both high and low affinity LDL interactions were observed. High affinity LDL binding and catabolism were increased five- to sevenfold after preincubation for 18 hours in LPDS containing medium. Subconfluent cells degraded, endocytosed, and bound 1.5 to 2.7 times more LDL by high affinity interaction than confluent cells, when endothelial cell growth supplement (ECGS) was present in the culture system. In the absence of ECGS, these ratios were somewhat less. Low affinity LDL metabolism was less affected by the state of confluency. Binding of LDL and acetylated LDL by venous endothelial cells was more than two- and threefold, respectively, than that by comparable arterial cells. However, the difference in LDL binding was not reflected in an altered LDL catabolism. There apparently is a population of low affinity binding sites not involved in LDL catabolism. LDL metabolism was identical in cells, which were cultured in medium supplemented with 20% to 100% serum or hirudin- or heparin-treated platelet-poor plasma. Without preincubation in LPDS, high affinity adsorptive endocytosis mediated the main part of LDL uptake only at low LDL concentrations (5 to 20 ??g protein/ml). However, at physiological LDL concentrations (550 ??g/ml), we estimated that this process mediated only 17% of the LDL uptake. We calculated that fluid endocytosis and low affinity adsorptive endocytosis of LDL accounted for the remaining 12% and 70%, respectively, of the LDL uptake at physiological LDL concentrations. Chemicals/CAS: acetyl-LDL receptor; Growth Substances; Lipoproteins, LDL; Receptors, Cell Surface; Receptors, LDL

Since two different types of α-adrenoceptors (α1- and α2-) subserve vasoconstriction in pithed rats and noradrenaline behaves as a non-selective agonist of both receptors (for review see Timmerman and van Zwieten, 1981), we have investigated this interaction between noradrenaline and captopril in more detail to identify the class of α-adrenoceptor involved. This study confirms the findings reported recently (Antonaccio and Kerwin, 1981; Clough et al., 1981) that captopril inhibits postjunctional vasocontrictor responses to noradrenaline in pithed rats. However, captopril interfered with the vasoconstriction elicited by noradrenaline only in those animals in which the vascular postsynaptic α2-adrenoceptor system could be triggered (saline-and prazosin-treated rats). Captopril was without effect after removal of the contribution of post-synaptic α2-adrenoceptor stimulation to the in vivo vascular smooth muscle contraction due to (-)-noradrenaline (rauwolscine-treated rats). These results indicate that captopril selectively impairs the vasoconstriction subserved in vivo by postjunctinal α2-adrenoceptors. The vasoconstrictor process initiated by α1-adrenoceptor activation is not affected by captopril.