Drugs online research references
Acta Anaesthesiol Scand. 1980 Apr;24(2):102-8.
Effects of hydrocortisone, phenoxybenzamine and propranolol on the blood plasma levels of adrenaline and noradrenaline during hemorrhagic hypotension in the dog.
Hellman A, Haggendal E, Haggendal J, Lundberg D.
The adrenergic aspects of the mechanism(s) of the vasodilating action of phenoxybenzamine and massive doses of hydrocortisone were studied in anesthetized dogs subjected to controlled hemorrhagic shock. During the predrug hypotension period with decreased cardiac output and heart rate, the plasma adrenaline and noradrenaline levels were both increased. Phenoxybenzamine injected alone augmented the cardiac output and heart rate and reduced the plasma adrenaline without changing the plasma noradrenaline concentration. However, if the adrenergic alpha-receptor blocker was administered in combination with massive doses of hydrocortisone, the degree of vasodilation increased further with a concomitant increase in the concentrations of the two plasma catecholamines. Thus there seems to be no clear-cut relationship between hemodynamic changes and plasma catecholamines. The present findings illustrate the extreme complexity of plasma catecholamine kinetics during hypovolemic shock.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7386142&dopt=Abstract
Masui. 1994 Apr;43(4):557-64.
[Anesthetic management for pheochromocytoma resection: a comparison of epinephrine predominant and norepinephrine predominant pheochromocytoma]
[Article in Japanese]
Doi M, Ikeda K.
Department of Anesthesiology and Intensive Care, Hamamatsu University School of Medicine.
Eleven patients with pheochromocytoma were divided into two groups; epinephrine predominant group (n = 4) and norepinephrine predominant group (n = 7). In each case, anesthesia was given using only inhalational anesthetics and adenosine triphosphate (ATP); and the same strategy was used to control cardiovascular variables. If arterial blood pressure, pulmonary artery pressure, central venous pressure or heart rate failed to be controlled with the strategy before the tumor resection, phentolamine, trinitroglycerine or propranolol was used. After the tumor resection, if decreasing the anesthetic concentration, cessation of ATP infusion and rapid intravenous infusion could not maintain the systolic arterial blood pressure above 80 mmHg, norepinephrine was infused. Maximum heart rate and arterial blood pressure during the tumor exploration were similar in both groups. No ventricular arrhythmias were recognized in any case. The frequency of usage of the cardiovascular depressants was not different between the two groups. In the norepinephrine predominant group, five cases required norepinephrine infusion after the tumor resection, but in the epinephrine predominant group, none required the norepinephrine infusion. Desensitization of alpha 1 adrenergic receptor induced by continuous high plasma norepinephrine concentration, was considered to decrease vascular resistance. In conclusion, except for the hypotension after the tumor resection in the norepinephrine predominant pheochromocytoma, both epinephrine predominant and norepinephrine predominant pheochromocytoma could be managed with similar anesthetic risks.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8189622&dopt=Abstract
Scand J Immunol. 1993 Aug;38(2):197-200.
Interferon-gamma induces a phospholipase D-dependent release of arachidonic acid from endothelial cell membranes: a mechanism for protein kinase C activation.
Mattila P, Ustinov J, Renkonen R.
Department of Bacteriology and Immunology, University of Helsinki, Finland.
Interferon-gamma (IFN-gamma) induces MHC class II expression on endothelial cells in a protein kinase C (PKC)-dependent manner. Here we show that IFN-gamma induces a sixfold arachidonic acid (AA) release from cultured rat microvascular endothelial cell membranes compared with non-treated cells. Since this result suggests that AA could act as a second messenger for IFN-gamma, we analysed its capacity to directly activate PKC. We have previously shown that IFN-gamma induces a transient, multiphasic activation of PKC via the action of the phospholipase D (PLD) pathway. Here we show that AA is able to activate PKC. In an attempt to characterize the source of the liberated AA after IFN-gamma induction in endothelial cells we used a panel of enzyme inhibitors. The IFN-gamma-induced release of AA could not be modified by interfering either with the phospholipase A2 (PLA2) pathway using bromophenacyl bromide (BPB), or with the phospholipase C (PLC) pathway using neomycin. The phosphatidic acid phosphatase (PAPase) inhibitor propranolol, inhibiting the generation of diacylglycerol (DAG) and further AA from phosphatidic acid (PA), could totally down-regulate the IFN-gamma-induced release of AA. Since PA is produced solely by the action of PLD from phosphatidylcholine (PC) we conclude that the AA originated from the cell membrane-associated PC. In summary, we show here that IFN-gamma causes the liberation of cell membrane-associated, PC-linked AA. This AA could directly activate PKC in a similar multiphasic manner to IFN-gamma, suggesting that it is a true second messenger for IFN-gamma in cultured endothelial cells.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8346419&dopt=Abstract
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