Effect of vasopressor substances on the thoracic duct lymph flow.
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Angiotensin II↗
Biomedical subjects
H Wernze
Publications and source records attributed to H Wernze.
[Hepatic inactivation and pressor action of angiotensin].
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Angiotensin II↗
Release of prostanoids into the portal and hepatic vein in patients with chronic liver disease.
Arterial and hepatovenous concentrations of circulating prostaglandin E2 and prostaglandin F2 alpha, the stable metabolites of prostacyclin and thromboxane A2 were measured in patients with chronic liver disease and compared with those in control patients with coronary artery disease but without hepatic dysfunction. Specific radioimmunoassays were used after extraction on octadecyl C 18-silica gel columns and thin-layer chromatography. While low levels of all cyclooxygenase products were found in hepatic arterial blood in patients with proven cirrhosis (n = 10) and fibrosis (n = 8), significantly higher concentrations were detected in the hepatic vein. A similar concentration profile was observed in controls (n = 4). Thus, there is a marked but comparable release of prostanoids from the normal as well as the diseased liver. Hepatovenous prostaglandin E2 was 11.6-fold, prostaglandin F2 alpha was 7.5-fold, prostacyclin was 12.2.-fold and thromboxane B2 was 3.9-fold above the level in the artery in both groups of patients. The hepatovenous concentrations of all arachinodate metabolites were unrelated to changes of liver morphology, biochemical abnormalities or the presence of ascites. No correlation could be demonstrated between hepatic venous pressure gradient and the concentration of prostanoids in the hepatic vein with the exception of thromboxane B2 (r = 0.55, p less than 0.05). The occurrence of esophageal varices was not associated with a specific pattern of circulating prostanoids in the posthepatic vasculature. Moreover, the portal-venous concentrations of all prostanoids (five patients: two with fibrosis, three with cirrhosis) exceeded the level in the hepatic vein substantially.(ABSTRACT TRUNCATED AT 250 WORDS)
6-Ketoprostaglandin F1 alpha↗
Drug-induced changes in prolactin secretion. Clinical implications.
Prolactin secretion is affected by various diseases as well as by many drugs in humans and animals. While marked hyperprolactinaemia suggests the presence of a pituitary tumor, moderate changes may also occur in various endocrine or non-endocrine disorders. Drugs can interfere with prolactin regulation via complex mechanisms at the hypothalamus or at the pituitary site, but possible changes in prolactin metabolism are poorly understood as yet. This survey of the literature up to June 1986 covers the influence of various groups of drugs and agents on the plasma prolactin level under various conditions. It contains information that will facilitate evaluation of whether hyper- or hypoprolactinaemia may result from therapeutic intervention or must be related to an underlying disease. It is obvious that more subtle changes can be revealed by the use of dynamic tests either to stimulate or to suppress prolactin secretion.
Drug-Related Side Effects and Adverse Reactions↗
[Metabolic, cardiovascular and sympathoadrenal reactions of the fetus to progressive hypoxia--animal experiment studies].
During delivery a reduction of placental blood flow in relation to uterine contractions resulting in repetitive decelerations of the fetal heart rate is frequently encountered. In this context the question arises whether a critical threshold of oxygen saturation (SO2) in fetal arterial blood can be defined, below which a severe fetal acidosis and a fetal shock syndrome may develope. In chronically instrumented ewes (8 experiments) a slowly progressive fetal hypoxia was induced by stepwise reduction of uterine blood flow via occlusion of the maternal aorta. Fetal arterial blood pressure and heart rate were continuously monitored and fetal arterial blood samples were taken intermittently from a catheter placed in the fetal aorta. The stepwise decrease of fetal arterial SO2 was 10% at time intervals of 15-30 minutes. With SO2-values above 15%, lactate increased 0.01-0.03 mmol/l/min and the pH decreased 0.003-0.0012/min. A significant increase of lactate concentration (0.1-0.3 mmol/l/min) and decrease of the pH (0.003-0.009/min) was encountered when the fetal arterial SO2 was below 15%. With progressive desoxygenation systolic and diastolic blood pressure as well as pulse pressure increased. There was no uniform reaction pattern of the basal fetal heart rate to progressive hypoxia; while in some experiments tachycardia prevailed, bradycardia was encountered in other experiments. Plasma free catecholamines exhibited an inverse relationship to SO2 with an exponential increase of catecholamine concentrations when SO2 fell below 15-20%. During almost complete desoxygenation (SO2 below 5%), catecholamine concentrations were increased 100 fold (norepinephrine), 1000 fold (epinephrine) and 50 fold (dopamine) as compared to control values. In comparison to free catecholamines increases of the concentrations of cortisol and aldosterone were only small. The increase of cortisol with progressive hypoxia may explain the endogenous stimulation of lung maturity during fetal stress. Our experiments suggest that a SO2 level of 15-20% represents a critical threshold for development of severe fetal acidosis and a fetal shock syndrome. However, even during severe hypoxia (SO2 below 10%) the sheep fetus is able to maintain blood pressure for at least 30 minutes with the help of an excessive catecholamine secretion. Only with anoxia a breakdown of fetal circulation has to be anticipated within a few minutes.
Acid-Base Equilibrium↗
[Effect of the beta-blocker metoprolol on the cardiovascular system and plasma catecholamines of the fetus in normoxia and acute hypoxia--animal experiment studies].
Metoprolol, a beta 1 blocking agent, is being used with increasing frequency during pregnancy for treatment of disorders such as hypertension or beta-mimetic induced tachycardia. Since it is well documented that beta-blocking agents are able to cross the placenta, the question arises whether these drugs have any adverse effect on the fetal metabolic or cardiovascular system. It was the aim of this animal experimental study to investigate the following questions: 1. Does metoprolol exert a negative influence on fetal metabolic and cardiovascular functions during normoxia? 2. Is the fetal reaction to an acute short period of hypoxemia altered by metoprolol? To answer these questions, experiments were carried out in 6 pregnant sheep at 110-130 days of gestation. In 8 experiments metoprolol was infused into a fetal vein in increasing dosage (0,04-0,32 mg/min). In a second series of experiments (n = 8), an acute hypoxemia was induced by complete reduction of uterine blood flow for 1 minute, and the results obtained with or without metoprolol were compared. Metoprolol does not exert a negative influence on fetal oxygenation, acid-base balance, lactate concentration and blood pressure, although the metoprolol concentration measured in fetal plasma was relatively high (two - to threefold above therapeutic metoprolol levels). Thus, definitive adverse effects on the fetus induced by metoprolol are not recognizable. The fetal sympathoadrenal reaction to an acute hypoxemia, as measured by the concentration of the free catecholamines epinephrine, norepinephrine and dopamine in the fetal plasma, is also unchanged by metoprolol.(ABSTRACT TRUNCATED AT 250 WORDS)
Acid-Base Equilibrium↗