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Biomedical subjects

J Holtz

Publications and source records attributed to J Holtz.

At least 91 records · Page 5Linked to original sources
PubMed1990

Alpha-adrenoceptor subtypes in the coronary circulation.

The pathophysiological role of sympathetic coronary innervation in myocardial ischemia is not clear, probably due to the complexities of adrenergic vascular control. In the canine coronary bed in vivo under beta-adrenergic blockade, alpha 1- as well as alpha 2-adrenoceptor-mediated constrictions can be elicited with predominance of the former in the epicardial conductance arteries, and of the latter in coronary resistance vessels. However, this distribution of functional responsiveness cannot indicate distribution of receptor density and cannot remain unchanged under differing conditions. First, each of these two classes of alpha-adrenoceptors consists of a mixture of different, interacting subtypes; second, the smooth muscular responsiveness to these two classes of alpha-adrenoceptors is differently modulated by contractile preactivation, by beta 2-blockade, and by the influence of sympathetic cotransmitters; third, alpha-adrenoceptors on endothelial cells and on sympathetic nerve endings can substantially modulate sympathetic coronary constriction. Thus, this neurogenic coronary control possesses a great functional plasticity, which is not yet fully evaluated with the presently available pharmacological tools.

Animals↗
PubMed1990

Converting enzyme inhibition by enalapril in experimental heart failure.

We analyzed the effect of enalapril (0.1 mg/kg p.o. twice daily) on plasma electrolytes, urea, and creatinine in low cardiac output failure. In 14 male dogs implanted with chronic instrumentation, tachycardia was induced by ventricular pacing (265 impulses/min., 10-14 days). In 7 untreated dogs, pacing progressively lowered aortic flow by 44% and induced hyponatremia and elevations of plasma urea, creatinine, and potassium. Treatment with enalapril (n = 7) during pacing reduced the decrease in aortic flow by 33% and prevented changes in plasma urea, potassium, and sodium. We conclude that this is due to enalapril-induced retardation of heart failure progression.

Administration, Oral↗
PubMed1990

[Effect of atrial natriuretic factor on coronary vascular tone].

To test whether atrial natriuretic factor (ANF) may be involved in the modulation of coronary vasomotor tone, ANF was injected into angiographically normal left coronary arteries. Measurement of epicardial diameters of the circumflex (Cx) and left anterior descending artery (LAD) were made from biplane angiograms by an automatic contour-detection system. Bolus injection of ANF (0.07 micrograms/kg, diluted in 1 ml 0.9% NaCl, n = 7) increased diameter of proximal segments of LAD (11 +/- 4%) and Cx (10 +/- 4%) (p less than 0.02 each vs control) without altering heart rate and mean arterial pressure (MAP). Intracoronary nitroglycerin (NTG, 0.3 mg) increased diameters of identical LAD and Cx segments by 18 +/- 3% and 20 +/- 4%. Intracoronary ANF infusion (0.02 micrograms/kg/min over 5 min, followed by 0.1 micrograms/kg/min, n = 10) exerted dose-dependent increases in diameters of LAD and Cx (low dose: + 5 +/- 2%, p less than 0.05 vs control; high dose: + 13 +/- 3%, p less than 0.01 vs control). ANF-infusion increased arterial plasma ANF levels from 280 +/- 80 pg/ml during control to 894 +/- 82 pg/ml (low dose; + 614 pg/ml vs control) and to 2290 +/- 228 pg/ml (high dose). Severe ischemia in four patients undergoing angioplasty exerted substantial increase in arterial ANF levels (160 +/- 60 to 608 +/- 111 pg/ml; + 448 pg/ml vs control), similar to the increase elicited by low dose ANF infusion in man.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1990

[Waterhouse-Friderichsen syndrome in adults].

Only a minority of published cases of Waterhouse-Friderichsen-syndrome occurred in adults (Harms et al., 1973). At the autopsy of a 23 years old woman there were found sugillations of the eyelid, of the peri- and epicard, of the serosa of the small intestine and of the lung. In the region of the adrenal gland a brownish-red mass was detectable. Histologically an adrenal apoplexy with necrosis and in liver, spleen and lung a lot of neutrophils were seen. Streptococcus viridans was pointed out in the blood.

Adrenal Cortex↗
PubMed1990

[A case of amyloidosis of peripheral arteries of the heart and liver in an elderly patient].

Cases of isolated cardiac amyloidosis and amyloidosis of the liver are seldom mentioned in the literature (Pitkänen et al., 1984). At the autopsy of a 85 years old woman we found a severe common arteriosclerosis, especially of the brain and heart. A pacemaker was regularly implanted. By staining with Kongo red there was histologically shown an isolated amyloidosis of the peripheral heart and liver arteries.

Aged↗
PubMed1989

[Physical examination preceding entry into apprenticeship: preventive measure or administrative burden?].

The new Swiss federal legislation on vocational and trade training requires that all cantons organize a system of medical screening for young people entering an apprenticeship. This paper focuses on the principles and implementation of such an examination. It outlines the most frequent health problems young people may face upon leaving school and entering apprenticeship. It underlines the difficulties of this kind of examination, since absolute contra-indications to distinct professions are very rare. Indeed, the medical examination should not be a selection procedure but much more an occasion to facilitate the transition from school to workplace. With this objective, the canton of Vaud health authority has created an examination sheet that will be supplied each year to the physicians (private pediatricians, general practitioners and internists) examining about 5000 candidates. This instrument introduces a uniform history taking procedure oriented towards occupational medicine and focuses on a few important screening items. No laboratory tests are mandatory. The process does not use a contra-indication list, which most of the time appears fallacious. It insists on the importance of an assessment of each individual situation.

Adolescent↗
PubMed1989

Nitrate action on epicardial coronary arteries and tolerance: new aspects based on longterm glyceryl trinitrate infusions in dogs.

Continuous application of organic nitrates in patients causes a well-documented attenuation of their antianginal efficacy. N-acetylcysteine (NAC) is assumed to reverse this nitrate tolerance by replenishing depleted intracellular sulphydryl groups, but data on NAC application in patients are controversial. Therefore, we studied the effect of NAC on epicardial artery vasomotion under nitrate tolerance, and we examined under these conditions the epicardial artery dilations induced by glyceryl trinitrate (GTN) and those mediated by the endothelium, since the activation of soluble guanylate cyclase is a common mechanism of these two reactions. Tolerance was induced in chronically instrumented dogs by long-term GTN infusion (1.5 micrograms kg-1 min-1 i.v. for 5 to 6 days) and shifted the GTN dose response curve of epicardial arteries to 17- to 20-fold higher doses. However, there was no alteration of epicardial artery dilations induced by SIN-1, another activator of guanylate cyclase, or of endothelium-mediated dilations. Furthermore, NAC (100 mg kg-1 i.v.) did not alter the dose-response relation of GTN under tolerance. In vitro, however, NAC potentiated the activation of purified soluble guanylate cyclase by GTN, while NAC without GTN was ineffective. In non-tolerant dogs, NAC slightly (1.5- to 2-fold) augmentated dilations induced by 0.5-1.5 micrograms kg-1 min-1 GTN, and a similar small augmentation of GTN dilations by NAC is observed in patients, regardless whether they are tolerant to nitrates or not. We conclude: (1) a step prior to the guanylate cyclase activation is responsible for GTN-specific tolerance of epicardial arteries in vivo. (2) NAC does not reverse GTN-specific tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcysteine↗
PubMed1989

Nitrate tolerance in epicardial arteries or in the venous system is not reversed by N-acetylcysteine in vivo, but tolerance-independent interactions exist.

N-acetylcysteine is assumed to reverse nitrate tolerance by replenishing depleted intracellular sulfhydryl groups, but data on interactions of N-acetylcysteine and nitrates in patients with stable angina are controversial and disappointing. Therefore, we studied the effect of N-acetylcysteine on nitrate responsiveness of epicardial arteries and of the venous system (assessed as changes in effective vascular compliance) in dogs (n = 12) during long-term nitroglycerin treatment (1.5 micrograms/kg/min i.v. for 5-6 days). In dogs with nitroglycerin-specific tolerance (shift of venous or epicardial artery dilation to 15-17-fold higher dosages), N-acetylcysteine (100 mg/kg i.v.) had no dilator effect and did not alter the dose-response relations of nitroglycerin. Yet, in nontolerant dogs (n = 17), N-acetylcysteine augmented (1.5-2.0-fold) the dilation of epicardial arteries and the reduction of peripheral vascular resistance induced by 0.5-1.5 micrograms/kg/min nitroglycerin. In vitro, the augmentation of purified guanylate cyclase activity by nitroglycerin (10-100 microM) was potentiated by N-acetylcysteine (0.01-1.0 mM) in saline or in canine plasma, but N-acetylcysteine alone was ineffective. We conclude that 1) N-acetylcysteine does not restore nitroglycerin responsiveness in tolerant epicardial arteries or veins in vivo, 2) a small, tolerance-independent augmentation of nitroglycerin-induced dilation may result from N-acetylcysteine-induced extracellular formation of a stimulant of guanylate cyclase from nitroglycerin.

Acetylcysteine↗
PubMed1989

Sympathoadrenal inhibition by atrial natriuretic peptide is not attenuated during development of congestive heart failure in dogs.

The feedback control of neuroendocrine activity by cardiopulmonary blood volume is disturbed in congestive heart failure. By analyzing plasma catecholamine kinetics, we tested in 11 chronically instrumented conscious dogs whether attenuations in the sympathoadrenal inhibition induced by atrial natriuretic peptide (ANP) contributed to this disturbance. Low-output failure was brought about by continuous ventricular pacing at 265 beats/min for 2 weeks. This resulted in a decline in aortic flow by 37 +/- 5% (SEM), an increase in peripheral vascular resistance by 48 +/- 4%, a 13 +/- 3-fold elevation in plasma ANP, a 9 +/- 3-fold elevation in plasma renin activity, and an augmentation of the norepinephrine-release rate into plasma by 132 +/- 17%. During ANP infusion, the epinephrine-release rate declined by 26 +/- 5% per 10-fold elevation in plasma ANP before pacing and by 31 +/- 7% (not significantly different) after 2 weeks of pacing. Before pacing, ANP attenuated plasma renin activity and caused hypotension without a rise in norepinephrine-release rate. After 2 weeks of pacing, ANP lowered norepinephrine release (by 16 +/- 6%) without affecting blood pressure or plasma renin activity, and vascular nonresponsiveness to ANP was verified under autonomic blockade. These data indicate that, during the development of heart failure, an inhibitory action of ANP on norepinephrine release is unmasked by an ANP-specific vascular desensitization, whereas the inhibition of epinephrine release is observed throughout. It is concluded that ANP-induced sympathoadrenal inhibition is not attenuated and, therefore, does not contribute to the disturbed regulation observed early in the development of failure.

Adrenal Medulla↗
PubMed1989

[The effect of carbon dioxide baths on blood pressure of borderline hypertensive patients].

In 423 patients with borderline hypertension (at rest and/or during exercise) the potential blood pressure reducing effect of CO2-baths was studied. Using standardized blood pressure measurements at rest and during exercise, it was investigated to what extent a fourweek course of CO2-baths could induce a reduction of blood pressure in these patients. They were randomly assigned to a course of baths with either high or low CO2-concentration. A significant fall in blood pressure, both at rest and during exercise was observed in both groups during the course of treatment. Multiple regression analysis identified the loss in body weight during treatment as the main influence factor on reduction in blood pressure. By contrast, no (additional) specific therapeutic effect of CO2-baths on blood pressure reduction could be observed.

Adult↗
PubMed1989

Failure of the sulfhydryl donor N-acetylcysteine (NAC) to reverse nitrate tolerance in large epicardial arteries and the venous capacitance system of the dog.

NAC has been thought to reverse nitrate tolerance by replenishing depleted intracellular sulfhydryl groups, however data on interactions between N-acetylcysteine and nitrates in patients with stable angina are controversial and disappointing. Therefore, we studied the effect of NAC on nitrate responsiveness of epicardial arteries and of the venous system (assessed as changes in effective vascular compliance) in dogs (n = 12) during long-term nitroglycerine (GTN)-treatment (1.5 micrograms/kg/min for 5 to 6 days). In dogs with GTN-specific tolerance (shift of venous or epicardial artery dilation with 15- to 17-fold higher dosages), NAC (100 mg/kg i.v.) had no dilator effect and did not alter the dose response relations of nitroglycerin. However, in nontolerant dogs (n = 7) NAC augmented (1.5- to 2-fold) the reduction of peripheral vascular resistance induced by 0.5-1.5 microgram/kg/min GTN. In vitro, the augmentation of purified guanylate cyclase activity by GTN (100 microM) was potentiated by NAC (0.01-1.0 mM) in saline or in canine plasma, whereas NAC alone was ineffective. Therefore, NAC does not restore GTN-responsiveness in epicardial arteries or veins in vivo and a small, tolerance-independent augmentation of GTN-induced dilation may result from NAC-induced extracellular formation of a stimulant of guanylate cyclase from GTN.

Acetylcysteine↗
PubMed1988

Discrepancy between initial and steady-state resistance vessel responsiveness to short-term nitroglycerin exposure in the hindlimb of conscious dogs.

Since much of the antianginal efficacy of nitroglycerin can be ascribed to its ability to dilate large arteries and venous capacitance vessels at dosages that have little steady-state effect on vascular resistance, we re-examined the reasons for low responsiveness of resistance vessels to nitroglycerin in a peripheral vascular bed in vivo. In chronically instrumented conscious dogs, intra-iliac nitroglycerin (0.15, 0.5, and 1.5 micrograms/kg/min) resulted in substantial dose-dependent initial increases in iliac flow (35% +/- 7%, 60% +/- 11%, and 106% +/- 12%, respectively). However, unlike the responses of iliac large artery diameter, these dilations were not sustained during a 6-min infusion. In contrast, doses of nitroprusside, acetylcholine, and adenosine, which gave initial dilations comparable to nitroglycerin, resulted in considerably greater steady-state responses (p less than 0.001). Nitrate tolerance, autoregulatory escape, reflex vasoconstriction, and the influence of cyclooxygenase products were ruled out as potential explanations of this selective pattern of nitroglycerin response. It is proposed that the rapid attenuation of nitroglycerin-induced dilation in a representative peripheral vascular bed cannot be attributed to currently accepted hypotheses and contributes more to the unique and beneficial spectrum of nitrate vascular action than an a priori lack of sensitivity of resistance vessels.

Acetylcysteine↗
PubMed1988

Preferential venoconstriction by cyclooxygenase inhibition in vivo without attenuation of nitroglycerin venodilation.

Because prostacyclin is a rather potent venodilator in vivo, we analyzed the effect of cyclooxygenase inhibition on venous tone in 14 anesthetized dogs during ganglionic and beta-adrenergic blockade and atraumatic conditions. Effective vascular stiffness (a reciprocal of effective vascular compliance) as a variable of integrated venous tone was 0.30 +/- 0.01 mm Hg.kg/ml (n = 35) and was augmented up to twofold by diclofenac (1, 3, and 10 mg/kg i.v.), ibuprofen (6 and 60 mg/kg), or indomethacin (5 mg/kg) parallel to augmentations in central venous pressure, while the rise in arterial pressure was less than half of the increase induced by equivenoconstrictor dosages of norepinephrine. After preconstriction by indomethacin or diclofenac, nitroglycerin (1.5 micrograms/kg/min) lowered effective vascular stiffness (by 24 +/- 2% or 23 +/- 5%, respectively), similarly as during preconstriction by norepinephrine (by 24 +/- 4%). Long-term cyclooxygenase inhibition (diclofenac 2 x 1 mg/kg/day for 4 days) did not modify arterial pressure, heart rate, or hematocrit levels in conscious dogs at rest, but it lowered plasma volume to 52.5 +/- 1.9 ml/kg (sham treatment: 59.1 +/- 1.6 ml/kg, p less than 0.05, n = 4). In conclusion, venoconstriction by clinical dosages of cyclooxygenase inhibitors does not interfere with the venodilator action of nitroglycerin and is compensated chronically by adjustments of plasma volume.

Animals↗
PubMed1988

Sympathoadrenal activity and sympathoinhibitory hormones during acute and chronic nicotine application in dogs.

Though acute nicotine administration results in increased blood pressure and heart rate, previous work has shown that chronic nicotine treatment does not result in significant hypertension. In fact, surprisingly it has been shown to produce hypotension. We performed the present experiments to further analyze the effects of chronic nicotine treatment. In untreated dogs (n = 7) under pentobarbital anesthesia (with adrenal hormone release measured directly by cannulation of the adrenolumbar veins) cumulative nicotine infusions (1-24 micrograms/kg/min i.v.) caused dose-dependent release of epinephrine (from 3.0 +/- 0.7 to 111 +/- 30 micrograms/kg/min) and norepinephrine (from 0.4 +/- 0.1 to 11.2 +/- 3.1). However, significant release of leu-enkephalin and met-enkephalin immunoreactivity was observed only with the highest nicotine infusion (24 micrograms/kg/min). In untreated conscious dogs (n = 12), nicotine test infusions (3 and 10 micrograms/kg/min), 15 min, yielded smoking relevant plasma nicotine levels and augmented heart rate, mean arterial pressure, plasma catecholamine levels, and adrenal epinephrine release. Plasma-enkephalin immunoreactivities were only marginally elevated with the higher nicotine test infusion. Chronic nicotine treatment (1.5 micrograms/kg/min s.c. for 5 weeks, n = 7), only transiently (first 1-2 weeks) augmented mean arterial pressure, heart rate, and epinephrine release, but during the plateau phase of treatment, hemodynamics and catecholamine parameters were identical to the pretreatment period. Acute responses of hemodynamics and catecholamines to nicotine test infusions declined progressively during chronic treatment, but the time course of this attenuation seemed not related to the reversal of the transient hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Balance between endothelium-mediated dilating and direct constricting actions of serotonin on resistance vessels in the isolated rabbit heart.

To determine whether endothelium-derived relaxing factor (EDRF) contributes to the vasomotor action of serotonin (5-HT) in the coronary resistance bed, we used haemoglobin as an inhibitor of EDRF in isolated perfused rabbit hearts. The 5-HT-induced dilatation (14 +/- 2% change in vascular resistance) was converted to constriction (10 +/- 3% change) in the presence of haemoglobin, while the vasodilator responses to papaverine were not attenuated. This is consistent with a role for EDRF in the mediation of 5-HT-induced coronary resistance vessel dilatation.

Animals↗