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Biomedical subjects

F Schwarz

Publications and source records attributed to F Schwarz.

At least 217 records · Page 12Linked to original sources
PubMed1976

Coronary and contractile reserve in the dog heart with chronic multiple coronary occlusions before and after aortocoronary bypass.

Peak isovolumetric left ventricular pressure and dp/dtmax before and after norepinephrine (N.E.) infusion and cross-clamping of the aorta was identical in normal dogs and in dogs with chronic coronary artery occlusion (C.C.O.) before and after aortocoronary bypass. In normal dogs, coronary reserve was 7.9 and 7.4 times control for the subendocardium and the subepicardium. After C.C.O., coronary reserve was 7.0 and 5.7 times control in the normal area and 2.4 and 3.5 times control in the collateral dependent area (endo vs. epi). After N.E. myocardial blood flow increased to 57% of the coronary reserve in normal dogs, and to 100% in dogs with C.C.O. After bypass, myocardial blood flow normalized. In dogs with C.C.O., N.E. stimulated the contractile reserve maximally and the coronary reserve is completely expended.

Animals↗
PubMed1976

Vascular and cardiac contractile reserve in the dog heart with chronic multiple coronary occlusions.

Nineteen mongrel dogs survived chronic occlusion of the left circumflex and of the right coronary artery without infarction due to the timely development of a collateral circulation. Only 38 per cent of the conductance of the arteries before occlusion was restored by collateral vessels. In these animals and in 15 control dogs with normal coronary arteries myocardial contractility, contractility reserve, and myocardial blood flow were studied. The same was done in dogs with chronic coronary artery occlusion after aortocoronary bypass. Myocardial blood flow was determined woth the tracer microsphere technique. Contractility reserve was tested and defined as isovolumetric left ventricular pressure and dp/dt max with norepinephrine infusion and cross-clamping of the aorta. Contractile reserve was not significantly different between normal dogs and dogs with chronic coronary artery occlusion before and after aortocoronary bypass. Myocardial blood flow during control conditions was homogenously distributed in all three groups studied. The ratio of blood flow to the endocardium and the epicardium was not significantly different from inity. Coronary reserve was determined at peak reactive hyperemia following a 20 second period of coronary artery occlusion, with ongoing norepinephrine infusion. Under these conditions subendocardial fow in normal dogs rose by a factor of 7.9 while subepicardial flow increased 7.4 times. In dogs with chronic occlusion of two coronary arteries the increase of myocardial flow was nonnomogenous; subendocardial flow to areas supplied by a normal coronary artery rose by a factor of 7.0 while subepicardial flow increased 5.7 times control. Subendocardial collateral flow rose by a factor of 2.4 and subepicardial collateral flow increased 3.5 times control. In normal dogs norepinephrine alone did not result in maximal coronary flow but only 57 per cent thereof. Dogs with chronic coronary occlusion, however, required the entire coronary reserve in areas that were supplied by a normal coronary artery, whereas areas supplied by collaterals became ischemic. Opening of an aortocoronary bypass restored normal flow to previously ischemic areas, and reduced the flow to areas supplied by a normal artery. With the bypass open no differences existed between normal dogs and those with two occluded coronary arteries. We conclude that the norepinephrine-stimulated contractile reserve of hearts with chronic coronary occlusion was comparable to that of normal hearts; however, norepinephrine forced these hearts to spend the entire flow reserve of the remaining normal artery while producing ischemia in collateral-dependent areas. The same dose of norepinephrine did not require the entire flow reserve of normal dogs.

Animals↗
PubMed1976

Spontaneous hypercortisolism without Cushing's syndrome.

A very high cortisol production rate (CPR) with elevated plasma ACTH was found in a hypertensive, hypokalemic, but otherwise healthy male patient. There were no symptoms or signs of Cushing's syndrome. The hypercortisolism appeared to be of the pituitary dependent type. During the follow-up of 36 months, no changes in outward appearance occurred, notwithstanding persistent hypercortisolism. The possibility of either Conn's syndrome or of an enzymatic defect in steroidogenesis could be ruled out. One of the three children (a healthy boy of 20 years) also showed hypertension and hypercortisolism. A possibly genetically determined hyposensitivity to the glucocorticoid action of cortisol is postulated.

Adrenocorticotropic Hormone↗
PubMed1976

Long-term observations of cardiac arrhythmias during and after cardiac surgery. I. Acquired heart disease.

Twelve arrhythmias that occurred during and following surgery for acquired heart disease were studied in a group of 52 randomly selected patients. In cases of aortic and mitral valve replacement, Björk-Shiley prosthetic valves were used, and procain-magnesium-aspartate solution was applied for cardiac arrest. Registration and analysis of rhythm disturbances were carried out at 10 different time intervals, spaced narrowly in the intra-and early postoperative phases, then more widely up to the 96th hour of observation. Arrhythmic incidence and occurrence per case and phase are given, thereby allowing an account of transient arrhythmias as well. The peak occurrence of serious rhythm disturbance was found, intraoperatively, at about the time of aortic cross-clamping and release (ischaemic effect) with the exception of the mitral-commissurotomy group. The 1st-6th postbypass hours showed an arrhythmia trough, followed by a 2nd peak (9th-96th postoperative hour) made up of less serious arrhythmias (electrolyte- and acid-base disturbances; digitalis effects). All 12 arrhythmia types, as well as the five separately considered ventricular arrhythmias of the "first arrhythmia peak", did not reveal any significant relation to: patients' age, N.Y.H.A. criteria, pre-operative PAm or the duration of anaesthesia, surgery and bypass time.

Adult↗
PubMed1976

Long-term observation of cardiac arrhythmias during and after cardiac surgery. II. Congenital heart disease.

Twelve arrhythmias that occurred in conjunction with surgery for congenital heart disease were studied in a group of 38 randomly selected patients. Halothane was used for anaesthesia and procaine-magnesium-aspartate solution for cardiac arrest. Registration and analysis of rhythm disturbances were carried out at 10 different time points, spaced narrowly in the intra- and early postoperative phases, then more widely up to the 96th hour of observation. Arrhythmic incidence per case and occurrence per case and phase are given, thereby also allowing an account of transient arrhythmias. The peak occurrence of intra-operative rhythm disturbances was found at about the time of aortic cross-clamping and release (ischaemia and halothane effect). A decline in arrhythmic incidence in the 1st-6th post-bypass hours was followed by a 2nd peak in the 6th-23rd postoperative hours (electrolyte and acid-base disturbances and/or a digitalis effect). All 12 arrhythmia types of the cardiopulmonary bypass group, as well as the separately considered ventricular arrhythmias of the first "arrhythmia peak", did not reveal any significant relation to: patients' age, total anaesthesia time, total surgery time and total bypass time. It is recognized that any comparative evaluation of operative arrhythmias, and especially a study of the causes and development of "surgically induced" A-V block, is problematic.

Adolescent↗
PubMed1976

[Function and reserve of the hypertrophic left ventricle in aortic valve disease].

Left ventricular function was analyzed by angiography in 31 patients with aortic valve disease and in 12 patients without heart disease (control group). Ejection fraction, percentage shortening of minor equator, mean velocity of fiber shortening and men left atrial pressure were considered as parameters of left ventricular function. Contractile reserve was tested by a single postextrasystolic beat. Patients with pure aortic stenosis and an increase of left ventricular muscle mass to 220% of the normal value showed no impairment of left ventricular function. Patients with pure aortic regurgitation and a left ventricular muscle mass of 260% of normal showed no significantly impaired function. Both groups increased ejection fraction and percentage shortening of the minor equator after premature beat comparable to the control group. Patients with combined lesions of the aortic valve had a left ventricular muscle mass of 360% of normal. This group showed decreased ejection fraction, percentage shortening of minor equator and mean velocity of fiber shortening as compared to the control group while mean left atrial pressure was significantly elevated. After premature beat all parameters remained depressed as compared to control group. We conclude that the degree of hypertrophy determinates cardiac function in aortic valve disease. Moderate hypertrophy shows normal function at rest, while severe hypertrophy shows impaired function.

Adult↗
PubMed1975

[Intra-atrial cardioversion in supraventricular tachycardial arrhythmia].

Cardioversion by rapid atrial stimulation has been carried out in 29 patients with supraventricular tachycarida and 12 patients with "coarse" atrial fibrillation. Atrial stimulation rates of 60-1200/min and electrical impulses of 6-25 mA were used. Intracardial conversion was successful in 86% of the cases presenting supraventricular tachycardia. Cardioversion was not achieved with atrial fibrillation but atrial flutter and atrial tachycardia were both found to be easily converted. Transformation of an arrhythmia into sinus rhythm or into stable atrial fibrillation with a slowed ventricular rate was the criterion for a successful conversion. Transient arrhythmias prior to an eventual stable rhythm was observed in 28% of the cases. Two mechanisms to explain the induced change in supraventricular tachycardias are discussed: (1) interruption of atrial or junctional foci (overdrive suppression) and (2) interruption of a re-entry circle by single premature beats. Cardioversion using atrial stimulation is indicated in atrial flutter, atrial tachycardias and junctional tachycardias. The method is of advantage in that it does not require anesthesia or interruption of digitalis therapy and its use involves no complications. Cardioversion using DC-shock is to be preferred in all cases of atrial fibrillation.

Adult↗
PubMed1975

[Vagal effect on sino-atrial node frequency and A-V overdrive in hypersensitive carotid sinus reflex and sick sinus syndrome].

Two syndromes, hypersensitive carotid sinus reflex (HCSR) and "sick sinus syndrome" (SSS) were studied in 28 patients, 6 of whom served as controls. Carotid sinus pressure was performed during sinus rhythm (CSP 1) and atrial stimulation just above the sinus rate (CSP 2). Overdrive suppression was also tested. Vagal stimulation provoked different effects in HCSR and in SSS. The vagal reaction to CSP 1 was more manifest in HCSR than in both SSS and the controls. After CSP 2 A-V conduction was delayed longer in HCSR than in SSS and the controls. Following atropine, the vagal effect on HCSR was more pronounced than on SSS and the controls. With HCSR, the duration of vagal influence on R-R intervals (A-V conduction) was significantly shorter than on P-P intervals (sinus rate). After atropine, there was less vagal effect on A-V conduction than on the sinus rate in HCSR, meaning that A-V conduction was shorter and less affected than the sinus rate by carotid sinus pressure. Prolonged suppression following overdrive established the diagnosis of SSS. This suppression was found not to be affected by atropine. A dependency of suppression on the rate and duration of overdrive could not be ascertained for SSS. The newly formulated "postdrive P-P interval recovery time" subdivided SSS in such a way that two different degrees of severity could be illustrated. The conclusion was that HCSR was caused by an excessive reaction to vagal stimulation rather than by a dysfunction of the sinus node or A-V conduction system. SSS might be based on tissue damage in the sinus nodal region but it did not show increased sensitivity to vagal influence.

Adult↗
PubMed1975

[Contraction disorders of the left ventricle in ischemic heart disease. Studies using atrial stimulation].

Sixty-one patients with suspected ischemic heart disease (IHD) have been investigated by atrial stimulation (AST). Group A patients had normal coronarograms and served as controls. Group B patients had pathological conronarograms (at least 50% stenosis in one of the 3 vessels) and normal ventriculograms. Group C patients had pathological coronarograms and ventricular aneurysms. During AST, group C patients exhibited lower dp/dt max and dp/dt min as well as higher left ventricular end-diastolic pressure (LVEDP) and/or mean pulmonary artery pressure (MPAP) than groups A and B. Group B differed from group A only by increased MPAP during AST. When compared to controls, contractility in group C was reduced even at rest. AST offers an excellent means of diagnosing IHD if heart rates of 140/min and above are used. An abnormal increase in MPAP serves as the simplest parameter for IHD. Elevated MPAP at rest prompts suspicion of ventricular aneurysm. It is possible to deduce a quanitative estimate of contracitility by correlating dp/dt max to LVEDP. A hyperbolic relation results.

Adult↗
PubMed1975

The excretion of metabolites of testosterone and of estradiol in male patients with chronic renal failure.

Intravenous infusions of 14C-testosterone (Te) either alone or in combination with 3H-estradiol (E2) were given to five normal male subjects, twelve male patients on haemodialysis (HD) treatment and to one patient with a very restricted renal function. The elimination of radioactivity was measured in urine, HD fluid and faeces. Urinary excretion diminished with renal function. It was negligible at a creatinine clearance of less than one ml per minute. A quarter of both isotopes was eliminated by six HD treatments within three weeks. No difference was found in this respect between nephrectomized patients and those who were still in possession of their kidneys. The main excretion occurred in the stools. E2 metabolites, and to a lesser extent Te metabolites, appeared in the faeces within 24 hours, which might be explained by biliary excretion only. More 3H (E2 metabolites) than 14C (Te metabolites) was found in the faeces; more 14C than 3H found in HD fluid.

Adult↗
PubMed1975

Frequency potentiation and postextrasystolic potentiation in patients with and without coronary arterial disease.

Frequency potentiation and postextrasystolic potentiation of myocardial contractility were induced in 17 patients found not to have cardiac disease (group 1) and in 10 patients with coronary arterial disease (group 2). Atrial stimulation was performed starting at a rate of 110/min and going up to 200/min (frequency potentiation). Single, premature ventricular beats with decreasing coupling intervals were induced every fifteenth beat during basal atrial stimulation at 125/min, after which compensatory pauses were provided (posts used an an index of contractility. With increasing heart rate dp/dt max was augmented equally, in both groups of patients, by frequency increases and premature beats (the coupling interval of the extrasystole being expressed as heart rate). dp/dt min and left ventricular systolic pressure remained unchanged while left ventricular end-diastolic pressure decreased in both groups of patients with the two forms of potentiation It was concluded that both these forms of potentiation have the same augmenting effect on myocardial contractility. Shortening the coupling intervals of premature beats caused a decreased in left ventricular end-diastolic pressure, suggesting that the Frank-Starling mechanism was not involved in postextrasystolic potentiation. Patients with coronary arterial disease had lower values of dp/dt max, dp/dt min, and higher values of left ventricular end-diastolic pressure during rest and stimulation procedures, while the systolic pressures equalled those in the control group. Though individual case values from the healthy and diseased hearts might be similar, it was only under the stress of potentiation that the true state of contractility was made apparent. Impairment of dp/dt min was not found without an impairment of dp/dt max in the presence of myocardial ischaemia.

Adolescent↗