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Biomedical subjects

J J Leonard

Publications and source records attributed to J J Leonard.

At least 37 records · Page 2Linked to original sources
PubMed1981

Changes in regional myocardial blood flow and variable development of hypertrophy after aortic banding in puppies.

Supravalvar aortic banding was performed in 6 to 12 week puppies. Sixteen animals were studied 7.3 (3.5 to 10) months later, closed-chested under morphine-chloralose, catheters being positioned in the great vessels and heart, including the left atrium for microsphere injection. Compared with 11 controls, eight dogs developed biventricular hypertrophy, four isolated left ventricular hypertrophy and four had no hypertrophy. The left ventricular systolic pressure was similar (P greater than 0.05) in these 3 banded groups (mean, 30 +/- 2 [SEM] kPa, [222 +/- 16 mmHg], n = 16). The left ventricle was divided into three coronal slices with approximately 59 samples being taken from subendocardial, midwall, and subepicardial layers and additional samples from the atria and right ventricle for regional myocardial flow measurement. As left ventricular hypertrophy increased, the subendocardial/subepicardial flow ratio decreased (r = -0.8). Heterogeneity of left ventricular regional myocardial flow, including a base-to-apex decrease in flow, present in controls, was markedly reduced in the banded dogs. Analysis of variance was found to be the most sensitive test for detecting left ventricular perfusion abnormalities since in banded dogs without hypertrophy, total and regional subendocardial/subepicardial flow ratios were not significantly different from control values, whereas the subendocardial circumferential flow pattern determined by analysis of variance was significantly different from control in these dogs (P less than 0.05).

Animals↗
PubMed1981

Immediate coronary artery bypass for acute evolving myocardial infarction.

Two hundred twenty-seven consecutive patients had chest pain and electrocardiographic, coronary angiographic, ventriculographic, and retrospective enzyme changes consistent with acute evolving myocardial infarction (AEMI). These patients underwent coronary artery bypass grafting an average of less than 6 hours after the start of chest pain. The mean age was 55.8 years (range 28 to 79 years). Sex, coronary artery involvement, and preoperative and postoperative enzymes and electrocardiograms are presented. Follow-up angiocardiograms done an average of 12.7 months postoperatively revealed 99 patent primary grafts in 102 patients (94.3%). Ejection fractions were normal, unchanged, or improved in 86.3% of the patients. Two ventricular aneurysms measuring less than 2.5 cm in diameter were noted. Surgical in-hospital mortality was 1.76% and first-year mortality was 1.44%. Conventional therapy in 200 AEMI patients treated at the same hospitals resulted in an in-hospital mortality of 11.5%. Follow-up of 213 patients having coronary artery bypass grafting revealed that 14% had mild angina. AEMI interrupted by coronary artery bypass grafting early in the syndrome yields results which are superior to conventional management.

Acute Disease↗
PubMed1981

Left atrial transport function.

These studies show that the left atrial booster pump action serves as a supercharger which can increase left ventricular stroke volume in the range of 25 percent; and in patients with aortic stenosis, stroke work in the range of 50 percent (4). These changes can occur in the face of increased resistance to left ventricular filling in clinical conditions such as aortic stenosis where there is diminished left ventricular compliance and in mitral stenosis where there is stenotic resistance to left ventricular filling from the atrium. In spite of this fact, assessment of left atrial function by measurement of cardiac output changes occurring after return from atrial fibrillation to normal sinus rhythm yields erratic and confusing results. The reason for this is that atrial function, per se, is not a primary determinant of steady state cardiac output. Sequential A-V pacing may temporarily increase stroke volume in an acute setting like myocardial infarction. Nevertheless, one cannot infer from such observations that the use of permanent transvenous A-V sequential pacing will augment steady state cardiac output over a period of time. This is an important point to remember when considering the use of sequential A-V pacing, since it requires insertion of more complicated pacing and sensing wires as well as a more complex circuitry. All of these features lead to an increased risk of pacemaker malfunction. This increased risk of malfunction is not justified unless there is good evidence that atrial contribution is important in a given patient.

Aortic Valve Stenosis↗
PubMed1979

The Bezold reflex: a special case of the left ventricular mechanoreceptor reflex.

Our previous finding that increasing myocardial contractility caused reflex systemic hypotension, the left ventricular (LV) mechanoreceptor reflex, suggested that the classical Bezold reflex (systemic hypotension and bradycardia after intracoronary administration of veratrum alkaloids) may be initiated by these same LV mechanoreceptors. In our working LV preparation with the coronary and systemic circulations isolated and perfused separately, intracoronary injection of veratrum alkaloids, like that of catecholamines or ouabain, had a positive inotropic effect which produced the hypotensive response typical of the LV mechanoreceptor reflex. To test directly if veratridine's positive inotropic effect initiates the Bezold reflex, verapamil, which blocks the slow Ca(2+) channels of myocardial cells but leaves intracardiac nerves unaffected, was injected by the intracoronary route to prevent the increased contractility from intracoronary injection of veratridine which also abolished the reflex hypotension, demonstrating conclusively that increasing myocardial contractility and thereby activating LV mechanoreceptors but not chemoreceptors initiates the Bezold reflex. Contrariwise, decreasing contractility or cardiac asystole by administration of tetrodotoxin, verapamil, or EDTA resulted in an increase in the systemic resistance, indicating that changes in the magnitude of the stimulus initiating the LV mechanoreceptor reflex (i.e., changes in myocardial contractility) lead to directionally opposite changes in peripheral resistance, as in the sino-aortic mechanoreflexes. Thus, it is concluded that the Bezold reflex is a special case of the LV mechanoreceptor reflex. The latter, by means of feedback mechanisms, functions normally by continuously matching the peripheral resistance to the LV contractile state so as to maintain the arterial pressure constant, thereby playing an important role in blood pressure regulation.

Animals↗
PubMed1977

Left ventricular mechanoreceptors: a haemodynamic study.

1. To study the function of the left ventricular mechanoreceptors, a working left ventricle preparation was devised in dogs which permitted control of pressure and flow of the isolated perfused coronary circulation and of the flow of the isolated, separately perfused systemic circulation. The systemic circulation was perfused at a constant rate so that changes in systemic pressure reflected changes in systemic resistance.2. Increases in myocardial contractility produced by injection of catecholamines into the isolated, perfused coronary circulation produced a fall in the pressure (resistance) of the isolated, separately perfused (at a constant rate) systemic circulation.3. Completeness of isolation of the coronary and systemic circulations was shown by the marked difference in appearance times between the reflex hypotensive responses from catecholamine injections into the isolated coronary circulation and the direct hypertensive response from a similar injection when the circulations were connected as well as by the marked difference between the pressure pulses recorded simultaneously on both sides of the aortic balloon separating the two circulations.4. Myocardial beta receptor blockade produced by injection of propranolol into the isolated coronary circulation abolished or attenuated the changes in left ventricular myocardial contractility as well as the subsequent hypotensive responses following the similar injection of catecholamines.5. Electrical stimulation of a sympathetic nerve innervating the heart resulted in increases in left ventricular myocardial contractility and subsequent systemic hypotensive responses indistinguishable from those following injection of catecholamines.6. That distortion of the mechano- or stretch receptors in the left ventricular myocardium was the cause of the hypotensive responses was demonstrated by increasing left ventricular myocardial contractility by mechanically obstructing the left ventricular outflow which produced hypotensive responses similar to those following the injection of catecholamines or nerve stimulation.7. Bilateral high cervical vagotomy abolished the hypotensive responses following injection of catecholamines into the isolated coronary circulation or following left ventricular outflow obstruction in all but one instance, indicating the importance of vagal fibres to the afferent arm of the reflex.8. It is suggested that the left ventricular mechanoreceptors function normally to reduce the peripheral resistance in order to prepare the systemic circulation to receive the left ventricular output and, especially during exercise, to prepare the systemic circulation to receive the augmented cardiac output with a minimum alteration in the systemic blood pressure and to distribute this augmented output preferentially to the skeletal muscles.

Animals↗
PubMed1977

Simultaneous regional myocardial blood flows by tritiated water and microspheres.

Regional myocardial blood flow (RMF) was measured simultaneously by use of labeled 8-mum microspheres and the constant-rate infusion of 3H2O in 22 open-chest dogs (Na pentobarbital anesthesia) under markedly different hemodynamic conditions. Following cardiac excision, three adjacent 80-mg tissue samples were taken from the subendocardial, mid-wall, and subepicardial layers of quadrantal left ventricular (LV) segments of the basal and midventricular cardiac slices, and from one segment of the apical slice, totaling 81 samples per LV. RMF was calculated by the microsphere reference-flow technique and by two 3H2O tissue-uptake models. Good agreement between techniques (r=0.9-0.96) was found in comparing flows to the myocardial layers. Using Kety's "single-mixer" model of 3H2O tissue uptake, fairly good agreement was found between techniques in the 80-mg tissue samples; the cofficient of variation from regression was 18.5% which improved markedly to 12.3% when the flow values for each technique were averaged in the three adjacent samples. Analysis of variance showed that flow to the various LV subdivisions (layer, segment, slice) of control animals was heterogeneous.

Animals↗
PubMed1974

Autonomic mechanisms in hemodynamic responses to isometric exercise.

Selective autonomic blockade with intravenous propranolol, practolol, atropine, and combined atropine-propranolol was utilized to elucidate the role of the autonomic nervous system in the hemodynamic responses in young adult male volunteers to handgrip sustained at 30% of maximal voluntary contraction for 3 min. The initial 30 s of the tachycardia response was found to be mediated by withdrawal of vagal dominance, as evidenced by blockade of this response by prior atropinization. The mid and late portion of the heart rate response curve was demonstrated to be sympathetic in origin, since it was unaffected by atropine, but was suppressed by combined atropine-propranolol blockade. Sympathetic stimulation appears to be a secondary mechanism for increasing the heart rate, however, as it becomes operative only after the first mechanism of vagal withdrawal has been utilized. This was confirmed by the finding that beta adrenergic receptor blockade alone had little effect on the heart rate response curve. The pressor response to handgrip was accompanied by increased cardiac output and no change in calculated systemic vascular resistance. After propranolol, handgrip resulted in increased peripheral resistance and an equivalent rise in arterial pressure, but no increase in cardiac output. It was concluded that the increase in resistance was the result of sympathetically induced vasoconstriction. This response was shown to be independent of peripheral beta adrenergic receptor blockade by the use of practolol, a cardio-selective beta adrenergic receptor-blocking drug which caused identical hemodynamic responses to those observed after propranolol. Left ventricular ejection time (corrected for heart rate) was prolonged by handgrip. The increased afterload imposed on the left ventricle by sustained handgrip may explain the prolongation of ejection time index. Preejection period was prolonged by SHG after propranolol and shortened after atropine. In addition to confirming the previously defined role of the parasympathetic nervous system, this study delineates the role of the sympathetic nervous system in the heart rate and pressor responses to sustained handgrip.

Adult↗