European journal of clinical investigation
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Eur. J. Clin. Invest. · Aug 1983
Abnormal Na+,K+ cotransport function in a group of patients with essential hypertension.
In 50 normotensive controls, the increase in erythrocyte Na+ concentration up to 12.4 +/- 2.0 mmol/l cells (mean +/- SD) ensures half-maximal stimulation of outward Na+,K+ cotransport fluxes. Forty-six out of sixty-five patients with essential hypertension required more than 16 mmol/l cells of internal Na+ concentration to obtain a similar effect, strongly suggesting an abnormal cotransport function. ⋯ Conversely, countertransport fluxes were normal in fourteen hypertensives with abnormal cotransport function. The above results indicate that the total population of patients with essential hypertension is heterogeneous and includes one subgroup of subjects with abnormal Na+,K+ cotransport function, and another with increased Na+,Li+ countertransport fluxes.
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Eur. J. Clin. Invest. · Apr 1982
Human endothelial cell proliferation inhibiting activity in the sera of patients suffering from 'shock' or 'sepsis'.
The response of DNA-synthesis of human endothelial cells to sera derived from twenty-five patients suffering from 'sepsis' or 'shock' was measured by autoradiographic methods. In eight cases a constant decrease in proliferative response was found compared to that of sera from healthy donors. These proliferation values were shown to lie below the '60%-of-control-line'. ⋯ These results correlated well with the clinical state and outcome of patients but not with any of the over sixty clinical, therapeutic, laboratory and post-mortem parameters of investigation. Evidence is presented for a proliferation inhibiting activity in sera of patients in clinically poor states, and some physico-chemical properties of this 'factor' are described. Lethal injury to the cells or an impairment of cellular migration could not be observed within the observation periods used in this study.
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Eur. J. Clin. Invest. · Jun 1981
Effect of angiotensin-II blockade on systemic and hepatic haemodynamics and on the renin-angiotensin-aldosterone system in cirrhosis with ascites.
We have studied the effect of angiotensin-II blockade with saralasin on the cardiovascular and hepatic hemodynamics and on the renin-angiotensin-aldosterone system in fourteen patients with cirrhosis and ascites. Control measurements showed that most of the patients had a low mean arterial pressure, high plasma volume, normal or high cardiac index, low peripheral resistance and high plasma renin activity and aldosterone concentration. The wedged hepatic venous pressure was increased in each patient and the estimated hepatic blood flow was normal in most of them. ⋯ The decrease of the wedged hepatic venous pressure was directly related to the reduction of the mean arterial pressure and also to the control plasma renin activity. Our study indicates that in most patients with cirrhosis, ascites and high plasma renin activity, arterial pressure is maintained by the effect of endogenous angiotensin II on the peripheral vasculature, and we suggest that a pre-existing arterial hypotension secondary to an arteriolar vasodilatation is the cause of renin release in these patients. Our results also show that angiotensin-II blockade is accompanied by a reduction of the post-sinusoidal hepatic vascular resistance.
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Eur. J. Clin. Invest. · Feb 1981
Enhanced pulmonary and intestinal activation of procarcinogens and mutagens after chronic ethanol consumption in the rat.
Recent epidemiological surveys have indicated that alcoholics exhibit increased incidences of a variety of cancers. We have investigated, as a possible contributing factor to carcinogenesis in this population, the effect of chronic ethanol consumption on metabolic activation of procarcinogens by microsomes isolated from lungs and small intestine. These tissues are major sites through which procarcinogens enter the body and are also potential sites of procarcinogen metabolism. ⋯ In contrast, microsomes from the upper small intestine of ethanol-fed rats did exhibit both higher levels of BaP hydroxylase activity and enhanced activation of BaP to a mutagen. The ethanol feeding also enhanced the capacity of the intestinal microsomes to activate to mutagens both tryptophan pyrolyzate and 2-aminofluorene but did not influence the metabolic activation of these promutagens by pulmonary microsomes. Chronic ethanol consumption thus influences carcinogen metabolism in the intestine and lung in a manner which varies with respect to both carcinogen and tissue.