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Biomedical subjects

C Taube

Publications and source records attributed to C Taube.

At least 91 records · Page 5Linked to original sources
PubMed1982

Electrically induced tachyarrhythmia and the effect of propranolol on the release of cyclic AMP and prostaglandin E by the canine left ventricle.

In anesthetized open-chest dogs, tachyarrhythmia (TA) was electrically induced by above-threshold stimuli via the right ventricle. During TA, a significant increase in the release of PGE and cAMP was observed in the canine coronary sinus blood (CSB). The efflux of cAMP corresponded with a concomitant increase in the left ventricular tissue level of this nucleotide. Pretreatment with propranolol (1.0 mg/kg i.v.) prevented the TA-induced changes in the level of PGE as well as cAMP in the CSB and in the tissue levels of cAMP. There was an increase in the activity of phosphorylase a in the myocardial tissue during TA which could be abolished by propranolol pretreatment. These results suggest possible interrelationships among catecholamines, cAMP, and PGE.

Animals↗
PubMed1982

Augmented acute hypotensive effect of dihydralazine and clonidine after linoleic acid rich diet in normotensive conscious rats.

The influence of dietary linoleic acid (LA) content on the cardiovascular effects of dihydralazine and clonidine was investigated in conscious rats. Male normotensive rats were fed either a diet rich in linoleic acid (LA) (13.3 cal-% LA) or a diet deficient in LA (0.5 cal-% LA) for a period of 5 months beginning in the pregnant mothers. Dihydralazine (1 mg/kg iv) or clonidine (10 micrograms/kg iv) were injected into conscious rats and blood pressure and heart rate were studied during a 20 min investigation period. The blood pressure lowering effects were higher in the rats fed the LA rich diet than in those fed the LA deficient diet 2, 5, 10 and 20 min after dihydralazine and 5 min after clonidine injection. The increase in heart rate per 10 mmHg blood pressure reduction after dihydralazine injection was lower in the rats fed on the diet rich in LA. We assume that the change in the cardiovascular effects of dihydralazine and clonidine by dietary LA may be caused by alterations of endogenous prostaglandin biosynthesis and sympathetic activity.

Animals↗
PubMed1982

Influence of mental stress on plasma level of prostaglandins, thromboxane B2 and on circulating platelet aggregates in man.

In two groups of medical students (group A n=13, group B n=9, aged 23 to 28 years) we estimated the levels of PGE, PGF2 alpha, 6-keto-PGF1 alpha and thromboxane(TX)B2 by means of radioimmunoassay in the peripheral venous blood immediately before (BES) and 15-30 min after (AES) examination stress and compared these to control levels. Furthermore we determined the circulating platelet aggregates, the heart rate and blood pressure changes. Heart rate and systolic blood pressure increased in the BES period expressing a stressful situation. In BES the plasma level of PGE increased from 84 to 249 pg/ml (p less than 0.001), whereas PGF2 alpha was unchanged. The increase of PGE level seems to be an expression of the increased sympathetic nervous activity existing in the stressful situation. The level of 6-keto-PGF1 alpha, the stable metabolite of prostacyclin, behaved differently in the two groups. In group A there was a statistically significant increase (p less than 0.05), whereas in group B the 6-keto-PGF1 alpha level was unchanged. In AES the TXB2 level increased from 113 to 167 pg/ml (p less than 0.01), whereas under BES conditions the TXB2 level was not changed. Simultaneously with the increased TXB2 level the circulating platelet aggregates were increased. The increase in TXB2 level occurring only after the end of the examination may offer a possible explanation of the frequent appearance of heart attacks after stressful situations.

Adult↗
PubMed1982

Alterations in renal and aortic prostaglandin E and F formation correlate with blood pressure dietary linoleate deficiency.

Male Wistar rats received for 4 weeks a linoleic acid (LA) rich (13.3 cal. % LA) or an LA deficient (0.5 cal. % LA) diet as well as 1.5% sodium chloride as drinking fluid. Compared with the LA rich diet the LA deficient diet caused an increase in blood pressure of about 10 mmHg. Indomethacin treatment (2 X 1 mg/kg/day s.c.) increased the blood pressure in the LA rich but not in the LA deficient fed rats. The flow rate of isolated perfused kidneys was reduced after 4 weeks LA deficient diet as were aortic and renal PGE formation, whereas PGF formation was only slightly diminished. PGE2 degradation in the kidney was not influenced by the LA content of the diet. We postulate that the prohypertensive effect of LA deficient diet in salt loaded rats is mediated via a reduction of endogenous PGE formation and a shift towards PGF.

Animals↗
PubMed1981

Chemical sympathectomy abolishes the increase in blood pressure of linoleic acid deficient fed rats induced by salt loading.

In previous experiments an altered PG biosynthesis as well as an increase in blood pressure, heart rate and plasma epinephrine could be found after a linoleic acid deficient diet compared with a linoleic acid rich diet in rats with a high salt intake. We injected rats with 200 micrograms 6-hydroxydopamine into the right and left cerebral ventricles 17 days before a four-week linoleic acid deficient diet (0.5 J% linoleic acid) and salt loading (1.5% NaCl). In these rats the elevation of blood pressure and plasma epinephrine compared with linoleic acid rich fed rats (13.3 J+ linoleic acid) was abolished and heart rate was reduced. PG biosynthesis in aorta and kidney medulla homogenate (PGE and PGF) and stomach fundus homogenate (6-Keto-PGF1 alpha) was not influenced by chemical sympathectomy, neither were the food and fluid intakes. We conclude that an enhanced adrenergic activity (via alterations in PG metabolism?) is involved in the blood pressure increase after a linoleic acid deficient diet under high salt intake.

Animals↗
PubMed1981

Influence of electrically induced tachyarrhythmia on the release of cyclic AMP and PGE in canine coronary sinus blood and on the level of cyclic AMP in myocardial tissue.

In anaesthetized open-chest dogs tachyarrhythmia (TA) was electrically induced by above-threshold stimuli via the right ventricle. During TA a significant increase in the release of PGE and cyclic AMP of 20% and 40% of the control levels, respectively, was observed in the canine coronary sinus blood (CSB), whereas the level of PGF2 alpha remained nearly unchanged under these conditions. The efflux of cyclic AMP corresponded with a concomitant increase in the left ventricular tissue level of this nucleotide by 59% during TA. Pretreatment with the beta-adrenergic blocking agent propranolol (1.0 mg/kg i.v.) prevented the TA induced changes in the level of PGE as well as cyclic AMP in the CSB and in the tissue levels of cyclic AMP. Propranolol alone was without any effect on the efflux of cyclic AMP, but decreased significantly the efflux of PGE by 32%. There was an increase in the activity of phosphorylase a in the myocardial tissue from 10% to 20% of the total (a + b) activity of this enzyme during TA, which could be abolished by propranolol pretreatment. The results suggest possible interrelationships between catecholamines, cyclic AMP and PGE.

Adenosine Triphosphate↗
PubMed1981

Influence of cardiac rhythm disturbances and antiarrhythmic drugs on the efflux of PGE, PGF2 alpha, cyclic AMP, and cyclic GMP in canine coronary sinus blood.

In anaesthetized open-chest dogs, cardiac arrhythmias (CA) were induced by cumulative intravenous doses of aconitine or ouabain. Aconitine in a dose which did not induce CA had no influence on the PGE and PGF2 alpha effluxes into coronary sinus blood (CSB), whereas the PGE efflux into CSB increased after a subtoxic dose of ouabain. However, both PGE and PGF2 alpha effluxes were increased, when CA had developed. During aconitine induced CA, the PGE efflux was 6.5-fold and that of PGF2 alpha had increased by 80%. During ouabain induced CA, the effluxes of both PGs were about 3-fold. Propranolol and lidocaine decreased the PGF2 alpha efflux into CSB by about 50% and the PGE efflux was doubled after lidocaine and decreased after propranolol by about a third. The increased PGE efflux into CSB during CA was normalized after propranolol and quinidine if the CA was abolished or the cardiac rhythm improved. Lidocaine did not modify the increase in PGE efflux, despite the abolishment of CA. The increase in PGF2 alpha efflux was not influenced by antiarrhythmic drugs. The cyclic AMP and cyclic GMP in CSB remained unchanged during ouabain induced arrhythmias or after propranolol. The increased efflux of PGE into CSB during aconitine and ouabain induced CA and its abolishment by propranolol support the hypothesis that PGE participates in the modulation of increased sympathetic tone during CA.

Aconitine↗
PubMed1978

Influence of linoleic acid content of the diet on arterial pressure of salt loaded rats. I. Effects on prostaglandin metabolism and sympathetic nervous system.

1. Compared with linoleic acid rich and pellet diet linoleic acid free diet causes an increase in blood pressure in salt loaded rats. The blood pressure increasing effect of linoleic acid poor diet could not be augmented by linoleic acid free diet. 2. The blood pressure was increased by indomethacin in linoleic acid rich and pellet fed rats. In linoleic acid free fed animals indomethacin shows only a brief augmentation of blood pressure. 3. Prostaglandin (PG) biosynthesis was decreased in isolated kidneys and aorta but increased in the kidney medulla homogenate after a four-week linoleic acid free diet. 4.. Chemical sympathectomy by intracerebroventricular injections of 6-hydroxydopamine abolished the blood pressure increasing effect of linoleic acid free diet. We postulate that changes in the PG metabolism and in the activity of sympathetic nervous system are causes for the elevated blood pressure of linoleic acid free fed salt loaded rats and we conclude that the function of the cardiovascular system is influenced favourably by a linoleic acid rich diet.

Animals↗
PubMed1978

Influence of linoleic acid in the diet on arterial pressure of salt loaded rats. II. Effects on plasma catecholamine concentration, renin activity, and reactivity of isolated vessels.

1. A linoleic acid free diet and indomethacin treatment induce an increase in the epinephrine and norepinephrine concentrations in the plasma. 2. The renin activities in the kidney and plasma were increased by a linoleic acid free diet and decreased by indomethacin treatment. 3. The reactivity of isolated blood vessels to norepinephrine, angiotensin, PGE2 and PGA2 was intensified after linoleic acid free diet. Indomethacin treatment neutralized the differences between the different diet groups. We conclude that the increase in the sympathetic activity, in the renin activity and in the vasoreactivity after a linoleic acid free diet has promoted the elevation of blood pressure of salt loaded rats and that these prohypertensive changes have been caused by a diminished PG biosynthesis in kidneys and blood vessels.

Angiotensins↗