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Biomedical subjects

A Korn

Publications and source records attributed to A Korn.

126 records · Page 7Linked to original sources
PubMedDate not supplied

The role of adrenergic mechanisms in the blood pressure regulation of leg-amputees.

An increased occurrence of hypertension has been reported among leg-amputees. In order to investigate whether leg amputation is followed by an elevation of sympathetic tone, possibly enhanced by continuous mechanical irritation of the amputation stump by wearing a prosthesis, blood pressure (BP), pulse-rate (PR) and plasma catecholamines (norepinephrine, NE, and epinephrine, E) were measured in six hypertensive leg-amputees during prosthesis walking as well as during irritation of the amputation stump by vacuum suction in the supine position. Six patients suffering from essential hypertension and six normotensive subjects served as control groups. Basal levels of plasma NE and E did not differ in the three investigated groups. Mechanical stump(limb) irritation as well as walking induced a rise of NE but not of E, accompanied by a rise of BP and PR in amputees as well as in the control subjects. Elevation of NE and BP was most accentuated in hypertensive amputees when walking with prosthesis. Within each investigated group there was a positive correlation between NE and mean arterial blood pressure (MAP), (p less than 0.001 in hypertensive amputees and non-amputees, p less than 0.05 in normotensives). We conclude that mechanical limb irritation induces a rise of BP by sympathetic nervous stimulation. Thus wearing of a vacuum-prosthesis may support a consistent rise in BP.

Adult↗
PubMedDate not supplied

Action of ethanol and some alcoholic beverages on gastric acid secretion in anaesthetized rats.

The action of intragastric ethanol in various concentrations equivalent to those found in alcoholic beverages (1.5-40 v/v), ethanol 96% (v/v) and of some commonly ingested alcoholic beverages produced by alcoholic fermentation (beer, wine, champagne, martini and sherry) or by fermentation plus distillation (e.g. whisky, cognac, calvados, armagnac and rum) on gastric acid output (GAO) was studied in anaesthetized Wistar rats. Ethanol concentrations of 1.5%, 4% and 10% v/v did not significantly alter basal GAO, whereas all higher concentrations of ethanol (20%, 40% and 96% v/v) significantly (P < 0.05) and dose-dependently decreased the GAO. All alcoholic beverages produced by fermentation significantly increased GAO by 30-35% of maximal acid output (MAO; 48 micrograms/kg pentagastrin intramuscularly), whereas alcoholic beverages produced by fermentation plus distillation significantly decreased GAO as compared to control (isotonic glucose and distilled water). Glucose solutions to which yeast was added, resulting in fermentation, were as potent stimuli of GAO as beer. Lyophilized fermented glucose at different concentrations (dilution of 1:20 to 1:1) dose-dependently stimulated GAO: the highest dilution (1:20) had no effect, the 1:5 dilution significantly increased gastric acid secretion similarly to that of beer and fermented glucose. The highest concentration of lyophilized fermented glucose (1:1) was as potent as the MAO after pentagastrin (90% of MAO). In conclusion, the present investigation shows for the first time that, in rats: (1) ethanol in a concentration > 10% v/v inhibits GAO; (2) lower ethanol concentrations (< 10% v/v) do not alter GAO; (3) alcoholic beverages produced by fermentation but not those produced by alcoholic fermentation plus distillation are powerful stimulants of GAO; (4) the stimulatory non-alcoholic ingredients of these alcoholic beverages are most likely produced during the process of fermentation of carbohydrates and removed during the following process of distillation.

Alcoholic Beverages↗
PubMedDate not supplied

Effect of ketanserin on phenylephrine-dependent changes in splanchnic hemodynamics and systemic blood pressure in healthy subjects.

We studied the effect of ketanserin on basal status and phenylephrine-dependent changes in arterial blood pressure and splanchnic hemodynamics in seven healthy subjects. The drug was administered as an intravenous bolus of 10 mg followed by infusion of 4 mg/h. After a basal period of saline or ketanserin infusion, phenylephrine was infused at a constant rate in a fixed dose sequence of 1, 2, and 3 micrograms/kg/min. Blood pressure was measured intraarterially. Splanchnic blood flow, mean wedged hepatic blood pressure, and splanchnic vascular resistance were assessed by means of the hepatic venous catheter technique using indocyanine green dye. At steady-state plasma concentrations, basal arterial pressure and heart rate were not altered in this small group of normal subjects, whereas mean wedged hepatic venous pressure was lowered by ketanserin. During saline infusion, phenylephrine provoked a dose-dependent rise in arterial and wedged hepatic blood pressure; these effects were attenuated by ketanserin. Phenylephrine induced a significant, but not dose-dependent, decrease in estimated splanchnic blood flow. Ketanserin did not relevantly influence basal or phenylephrine-dependent splanchnic blood flow. We suggest that the hypotensive action of ketanserin is in part related to an interaction at alpha 1-adrenoceptors. Moreover, a dissociation of effects on vascular alpha-receptors seems to exist in the splanchnic and systemic circulations.

Adult↗
PubMedDate not supplied

Release and vasoactive actions of catecholamines during inhibition of prostaglandin synthesis in normal man.

To assess the effect of prostaglandin inhibition upon the vasoactive actions of endogenous and exogenous catecholamines in healthy man, indomethacin (150 mg/day for 3 days) was administered to six healthy men in the sodium-repleted state. Pretreatment with indomethacin did not interfere with the response of blood pressure and pulse rate to orthostasis (10 minutes), a cold pressor test (2 minutes), and the intravenous (i.v.) administration of norepinephrine (NE) (50, 100, and 200 ng kg-1 min-1). Basal plasma concentrations of epinephrine (E) and NE as well as the concentrations of E during orthostasis and cold pressor test remained uninfluenced by pretreatment with indomethacin. While the release of NE during orthostasis appeared to be suppressed in the indomethacin-treated state, it was unchanged during the cold pressor test. These results indicate that inhibition of endogenous prostaglandin synthesis may suppress the release of NE, but does not have a major impact on the vasoactive actions of endogenous and exogenous catecholamines in normal men.

Adult↗
PubMedDate not supplied

Rioprostil, a new prostaglandin E1 analogue does not affect glucose homeostasis in healthy volunteers.

Rioprostil is a synthetic prostaglandin E1 analogue currently under study for peptic ulcer healing. Rioprostil, like prostaglandin E, caused an impairment of glucose tolerance in animal studies. We have studied the effects of single therapeutic doses of rioprostil (300 micrograms and 600 micrograms) on glucose homeostasis after oral glucose tolerance tests in 12 healthy volunteers. Plasma glucose, insulin, and C-peptide concentrations were not significantly different after rioprostil and placebo. These results indicate that a clinically significant interference of rioprostil with glucose tolerance is unlikely.

Adult↗