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Biomedical subjects

H Wernze

Publications and source records attributed to H Wernze.

At least 37 records · Page 2Linked to original sources
PubMed1986

Tyrosine loading in patients with hepatic cirrhosis: lack of effect on plasma catecholamines.

Plasma norepinephrine concentrations are often elevated in patients with hepatic cirrhosis in relation to the stage of disease and possibly in response to a decrease in "effective" arterial blood volume. Since tyrosine, the precursor for catecholamines, is said to influence the rate of catecholamine biosynthesis within the central nervous system and peripheral sympathetic structures, we tested whether basal hypertyrosinemia and increased plasma tyrosine levels after oral loading with l-tyrosine are associated with elevated plasma catecholamine concentrations. Baseline norepinephrine (NE) and epinephrine (E) were significantly higher in 17 patients with decompensated cirrhosis, as compared with 11 healthy controls (NE: 809 +/- 108 pg/ml vs 295 +/- 16 pg/ml; E: 69 +/- 9 pg/ml vs 36 +/- 8 pg/ml). No significant correlation between the basal plasma tyrosine and norepinephrine level could be demonstrated in patients with cirrhosis (r = 0.04). Oral tyrosine loading (100 mg/kg b.w.) administered in six equal doses did not change the level of catecholamines, whereas plasma tyrosine increased two- to three-fold. Even a large single dose (14 g l-tyrosine) failed to alter plasma catecholamines in six cirrhotic patients with marked ascites. We therefore conclude that the enhanced availability of tyrosine in cirrhotics does not influence catecholamine biosynthesis in peripheral sympathetic neurons.

Blood Pressure↗
PubMed1986

Atrial natriuretic peptide in hepatic cirrhosis: relation to stage of disease, sympathoadrenal system and renin-aldosterone axis.

58 patients (mean age 51 years) with cirrhosis of the liver were studied. 16 patients were compensated, 18 decompensated with ascites, and 24 decompensated and treated with diuretics. Basal plasma levels of atrial natriuretic peptide were not different between any groups of cirrhotic patients and 17 control subjects (mean age 43 years). In contrast, the sympathoadrenal system (plasma noradrenaline, plasma adrenaline) and renin/aldosterone were significantly activated in decompensated cirrhotics. Circulating ANP was not related to plasma noradrenaline and adrenaline, plasma renin activity, plasma aldosterone, blood pressure, heart rate, or urinary sodium/potassium excretion in any cirrhotic group. Despite established sodium and volume retention in decompensated cirrhosis, the results indicate that diminished effective blood volume fails to release atrial natriuretic peptide in a larger amount due to insufficient atrial stretching. After insertion of a peritoneovenous shunt in one patient for treatment of refractory ascites, plasma atrial natriuretic peptide, urinary volume and sodium excretion increased, whereas elevated plasma levels of noradrenaline, renin activity and aldosterone decreased markedly.

Adult↗
PubMed1985

Catecholamines in arterial and venous umbilical blood: placental extraction, correlation with fetal hypoxia, and transcutaneous partial oxygen tension.

In 34 parturient women the levels of free epinephrine (E), norepinephrine (NE), and dopamine (D) were determined by a radioenzymatic method using maternal venous and umbilical arterial and venous blood. The study was conducted to investigate the relationship between fetal catecholamines and hypoxia, fetal heart rate (FHR), and transcutaneous pO2 (tcpO2). The placental catecholamine extraction rates were also calculated. Results The NE concentrations (10,200 pg/ml) and the E concentrations (1,120 pg/ml) in the fetal arterial blood were highly elevated with mean values increased 4-fold over umbilical vein values. Compared with the maternal venous blood, NE values were increased 20-fold, and E values 10-fold. Free D concentrations in fetal arterial blood (130 pg/ml) had risen 2.5-fold over maternal levels. These results suggest that the catecholamines measured in cord blood are of fetal origin and that the placenta has a high capacity for inactivation of free catecholamines. The placental extraction rate is 77 +/- 14% for NE, 76 +/- 16% for E, and 33 +/- 25% for D. The placental extraction rates for E and NE were virtually identical; in agreement with morphological studies they demonstrated absence of sympathetic innervation on the fetal side of the placenta. Highly significant correlations were found between fetal arterial NE concentrations and the 1-minute APGAR score, pH and base deficit in the umbilical artery and alterations of the FHR (deceleration area, baseline FHR). Further analysis of FHR alterations reveals that an increase in deceleration area without tachycardia is not correlated with an increase of fetal arterial NE concentration. A significant rise in NE was only found with additional tachycardia which is often associated with a loss of oscillation amplitude. Fetal arterial E concentrations were found to correlate with the fetal parameters indicating increased adrenal secretion of the hormone during fetal stress. However, correlation coefficients were lower than those obtained for NE. A significant effect of fetal hypoxia on arterial and venous D levels could not be demonstrated. Fetal tcpO2 varies between 0-25 mm Hg during the last two hours before delivery. In most cases tcpO2 was lower than the arterial pO2. Besides epidermal thickness and artifacts, skin perfusion is a major factor influencing the tcpO2 (transcutaneous arterial pO2 difference). Vasoconstriction of the cutaneous vessels induced by increased NE secretion during hypoxia may obviously produce a fall in tcpO2.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1983

Alpha-receptor restriction of coronary blood flow during atrial fibrillation.

The effects of atrial fibrillation (AF) on coronary circulation before and after alpha-receptor blockade were studied in 14 anesthetized, open-chest dogs. AF was induced by electrical stimulation of the left atrial appendage; identical rhythmic heart rates were adjusted by left atrial pacing. During atrial pacing, coronary vascular resistance (CVR) was 0.97 +/- 0.10 mm Hg X min X 100 g/ml (resistance units [RU]), coronary blood flow (CBF) 125 +/- 14 ml/min X 100 g, and oxygen saturation 30 +/- 2%; plasma epinephrine was 193 +/- 42 pg/ml and norepinephrine 584 +/- 111 pg/ml. During AF, CVR was higher (1.16 +/- 0.11 RU, p less than 0.0005), whereas CBF (92 +/- 9 ml/min X 100 g, p less than 0.001) and coronary sinus oxygen saturation (24 +/- 2%, p less than 0.0025) were lower than during atrial pacing. When AF was induced, epinephrine increased to 333 +/- 98 pg/ml (p less than 0.05) and norepinephrine to 1,005 +/- 214 pg/ml (p less than 0.005). The large increase in plasma catecholamines suggested an activation of the sympathoadrenal system during AF. In addition, the alpha-receptor blocker phenoxybenzamine (10 mg/kg, intravenously) abolished the differences in CVR, CBF and oxygen saturation between AF and atrial pacing. The data suggest that the decrease in CBF and increase in CVR during experimentally induced AF are caused by coronary vasoconstriction, mediated by sympathetic activation of alpha receptors in the coronary vascular bed.

Animals↗
PubMed1983

The renin-angiotensin-aldosterone system in fulminant hepatic failure.

The relationship of the renin-angiotensin-aldosterone system to blood pressure and sodium homeostasis and to renal function was investigated serially in 12 patients with fulminant hepatic failure. The plasma concentrations of renin, angiotensin II, and aldosterone were, in most instances, markedly increased. Systolic blood pressure, which was often very low, showed a significant inverse relationship to the plasma renin concentration, suggesting that the marked stimulation of the system is a homeostatic response to hypotension. However, the plasma renin substrate concentration was markedly decreased, and the conversion of angiotensin II to inactive peptides increased, both of which may have severely limited the full 'expression' of the stimulated system. Renin and angiotensin II levels were both related to creatinine clearance, which was often reduced, but it is not clear as to which was cause and which effect. No relationship between the plasma aldosterone concentration and renal sodium excretion could be detected.

Adult↗
PubMed1981

[Renin-angiotensin system in acute hepatitis (author's transl)].

Plasma renin activity (PRA) and plasma concentrations of angiotensin II (A.II) were measured radioimmunologically in 31 patients suffering from acute virus hepatitis during the course of the disease. Average PRA and A II values did not differ from values of normal persons, neither during the acute phase of the disease nor during the recovery phase though there were deviations from the normal in single cases. PRA and A II were correlated significantly (r = 0,86, p < 0,001), but there was no correlation to the levels of transaminases. There was no indication, that A II plasma levels were lowered because of increased activity of angiotensinases. In some cases PRA and A II were elevated; this however was probably due to increased renin secretion following changes in water and electrolyte balance rather than to decreased hepatic metabolism of renin.

Adolescent↗
PubMed1980

Relationship between urinary prostaglandin (PGE2 and PGF2 alpha) and sodium excretion in various stages of chronic liver disease.

A. No consistent changes in the urine PGE2 and PGF2 alpha related to sodium excretion could be found in hepatic cirrhosis with and without ascites. B. Intensive renal sodium retention in cirrhosis with ascites (urine Natless than 20 mEq/24 hr) is very often associated with increasing PGF/PGE ratio, whereas absolute urine PGE2 can be found low or normal. The PG shift is possibly due to a stimulation of the PGE2-9-keto-reductase. C. Application of saluretics and spironolactone in cirrhosis with ascites normalizes the PGF/PGE ratio in accordance with increasing sodium excretion. D. PG changes observed cannot be considered as a primary factor accounting for deranged renal sodium handling in cirrhosis. Anomalous PG pattern possibly reflects enchanced intrarenal vascular resistance.

Adult↗
PubMed1979

Plasma renin, renin substrate and angiotensin II changes following experimental endotoxinaemia.

The effect of a single dose of endotoxin (B. coli, 1.5 mg/kg intravenously) on plasma renin concentration (PRC), renin substrate (PRSC), and angiotensin II (AT II) was studied in rats over a period of 48 hours. All determinations were performed by specific radioimmunoassay. Six and nine hours following endotoxin administration, renin secretion was decreased, whereas at 48 hours a slight increase in the PRC was found. In contrast, a three-fold elevation of the PRSC occurred during the first 24 hour period, attributable to a stimulation of the hepatic biosynthesis as result of corticosterone oversecretion. According to the observed changes in PRC and PRSC, AT II remains unchanged after six and nine hours, whereas a significant increase was detected after 24 and 48 hours. Based on the actual AT II level, the findings emphasize that in the rat the RAS does participate in the later stages of endotoxin stress only.

Angiotensin II↗
PubMed1979

Changes of serum angiotensin I converting enzyme in patients with viral hepatitis and liver cirrhosis.

Serum angiotensin I converting enzyme, identical with kininase II, was measured fluorometrically in patients with acute viral hepatitis (n=18), liver cirrhosis without (n=44) and with (n=19) ascites. In all groups of patients the enzyme was significantly elevated as compared to 44 healthy controls (p less than 0.001). No correlation could be found between angiotensin I converting enzyme activity and liver function tests (serum glutamic oxalacetic transaminase, serum glutamic pyruvic transaminase, total protein, albumin, bilirubin) or other parameters (serum potassium, serum sodium). High serum converting enzyme activity in chronic liver diseases might originate primarily from an altered pulmonary circulation and indicates higher conversion rate of angiotensin I by passage through the lungs as well as increased bradykinin degradation. The reason for the enzyme liberation in acute viral hepatitis is as yet uncertain.

Adult↗
PubMed1978

Studies on the activity of the renin-angiotensin-aldosterone system (RAAS) in patients with cirrhosis of the liver.

Plasma renin activity (PRA), plasma renin concentration (PRC), angiotensinogen, angiotensin II (AT II) and plasma aldosterone were determined by radioimmunoassay in 77 patients with cirrhosis of the liver [group I: with ascites, untreated (n=23); group II: patients with ascites during treatment (n=32); group III: after removal of fluids, but under further spironolactone therapy (n=10); group IV: untreated subjects without ascites (n=12)]. With the exception of decreased angiotensinogen values in all groups ranging between 39% (group IV) and 73% (group III) no significant changes of the other parameters of the RAAS were found in untreated patients. A highly significant increase of PRA, PRC, AT II and plasma aldosterone was observed in treated cirrhotics with (group II) or without (group III) ascites. In the total series of patients AT II was closely related to PRA, PRC and aldosterone emphasizing aldosterone secretion. Plasma sodium was inversely correlated to PRA, PRC, AT II and aldosterone, but no relationship was detected between these parameters of the RAAS and plasma potassium. Our results indicate that hyperaldosteronism in cirrhosis appears unlikely to be the major determinant of avid renal sodium retention and ascites formation. An increased activity of the RAAS is most often initiated by therapeutic factors and/or markedly altered electrolyte metabolism. Therefore, basal conditions of the patients to be studied must be well defined to exclude any artificially induced stimulation of the RAAS.

Adult↗
PubMed1977

[Critical analysis of the saralasintest in the diagnosis of hypertension (author's transl)].

The reliability of the angiotensin II (AT II)-antagonist Saralasin in the diagnosis of AT II-dependent forms of hypertension was investigated in 61 cases of hypertension of different etiology. In 14 patients, lowering of blood pressure by Saralasin suggested an AT II-dependent hypertension which could be ascertained in 8 patients (5 had undergone successful surgery) by increased levels of plasma-renin-activity (PRA), AT II, PRA-ratio in renal vein blood and by angiography. Besides, depressor reactions by Saralasin yielded additional information in three patients with renovascular hypertension but normal levels of PRA and AT II, in two patients with high renin essential hypertension and one patient with pheochromocytoma. This test seems to be valuable in the diagnosis of renin-dependent hypertension.

Angiotensin II↗
PubMed1977

Plasma prolactin and prolactin release in liver cirrhosis.

A significant increase of basal plasma prolactin levels (radioimmunoassayed) in 75 patients with liver cirrhosis was found in comparison to 50 male controls (8.5+/-4.5 (SD) vs. 5.5+/-1.7 ng/ml p less than 0.001). The extent and incidence of hyperprolactinaemia in 48 patients with alcoholic cirrhosis was more pronounced than in 27 cases of cirrhosis of non-alcoholic aetiologies (mean 9.7+/-4.8 vs. 5.7+/-2.1 ng/ml). No relation to ascites formation as well as to the development of gynaecomastia was apparent. Prolactin release following thyrotropin-releasing hormone was markedly enhanced in alcoholic as compared to non-alcoholic cirrhosis. Possibly hyperprolactinaemia and increased pituitary hormone reserve reflects hyperoestrogenism but changes of the hypothalamic regulation cannot be excluded as yet.

Alcoholism↗