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Biomedical subjects

M M Laks

Publications and source records attributed to M M Laks.

At least 73 records · Page 4Linked to original sources
PubMed1984

Exercise subcostal two-dimensional echocardiography: a new method of segmental wall motion analysis.

This study determines the effectiveness of the subcostal view 2-dimensional (2-D) echocardiogram in providing images of left ventricular wall motion at rest and during symptom-limited upright bicycle exercise, and compares 2-D echocardiographic regional wall motion analysis with first-pass radionuclide angiography. Diagnostic-quality subcostal 2-D echocardiograms at rest were obtained in 95% of unselected persons studied (16 of 17 normal subjects and 23 of 24 patients who had had myocardial infarction [MI] ). All who had adequate studies at rest had diagnostic-quality maximal exercise studies. Segmental wall motion at rest and exercise determined by 2-D echocardiography correlated well with radionuclide angiography in both the normal and post-MI groups. The chi-squared values for the 3 segments analyzed were: anterior 52 (p less than 0.001), apical 56 (p less than 0.001) and inferior 37 (p less than 0.001). It is concluded that subcostal view 2-D echocardiography at rest and at the peak of symptom-limited upright bicycle exercise is a feasible and accurate noninvasive method for the analysis of segmental left ventricular function.

Adult↗
PubMed1984

Noninvasive measurement of the rest and exercise peak systolic pressure/end-systolic volume ratio: a sensitive two-dimensional echocardiographic indicator of left ventricular function.

Thirty-five patients with previous myocardial infarction and 25 normal subjects underwent subcostal view two-dimensional echocardiography at rest and at peak up-right bicycle exercise. The purpose was to assess changes in left ventricular volume with maximal upright bicycle exercise and to compare the utility of the peak systolic pressure/end-systolic volume index ratio and ejection fraction as indicators of left ventricular function. With exercise, normal subjects had a decrease in end-systolic volume index (22 +/- 8 to 11 +/- 3 ml/m2) (p less than 0.001); the normal ejection fraction (59 +/- 9 to 72 +/- 8%, p less than 0.001) and the pressure/volume ratio (6 +/- 3 to 18 +/- 6, p less than 0.001) increased. In patients with prior myocardial infarction there was no change in end-systolic volume index, ejection fraction or pressure/volume ratio with exercise. Although at peak exercise significant differences between normal subjects and patients with prior infarction were demonstrated in end-systolic volume index (p less than 0.001), ejection fraction (p less than 0.001) and pressure/volume ratio (p less than 0.001), the pressure/volume ratio provided sharper delineation between the two groups than did ejection fraction. The exponential relation of the pressure/volume ratio and ejection fraction at peak exercise demonstrates that the pressure/volume ratio is more sensitive as an indicator of normal or borderline left ventricular function and that ejection fraction is more sensitive in quantifying the degree of left ventricular dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Chronic norepinephrine infusion and insulin and glucagon secretion in the dog.

The effect of epinephrine on glucose homeostasis has been studied extensively in many species, but there is little data on the effects of another catecholamine, norepinephrine. This study was designed to examine the alterations that occur in insulin and glucagon secretion during a chronic low-dose infusion of norepinephrine in free-roaming dogs. A total of four intravenous glucose tolerance tests and insulin-induced hypoglycemia tests were performed on each of five dogs infused with norepinephrine (1.4 g/min) for 3 mo and on each of eight control dogs. The infusion resulted in a threefold increase in plasma norepinephrine without a significant effect on blood pressure. Fasting serum glucose was elevated significantly in the norepinephrine-infused dogs [102.4 +/- 2.1 vs. 92.8 +/- 1.7 (SE) mg/100 ml]. Fasting plasma glucagon was elevated by the norepinephrine infusion (58.4 +/- 7.6 vs. 31.3 +/- 3.1 pg/ml), whereas fasting serum insulin was inhibited (12.3 +/- 1.3 vs 16.8 +/- 1.7 U/ml). Glucagon secretion in response to hypoglycemia was markedly enhanced in the infused dogs compared with controls. It has been reported that the infusion of norepinephrine in humans will inhibit insulin secretion and increase serum glucose concentrations but have no effect on serum glucagon concentrations. The stimulation of glucagon by norepinephrine has been demonstrated in the isolated, perfused canine pancreas but has not been reported previously in the free-roaming dog.

Adrenal Glands↗
PubMed1984

Norepinephrine increases beta-receptors and adenylate cyclase in canine myocardium.

Norepinephrine, a known inducer of myocardial hypertrophy, was found to have marked effects on the myocardial adrenergic system, which occurred prior to the development of a significant increase in heart weight. The chronic subhypertensive infusion (1.4 microgram/min) in free-roaming dogs produced a threefold increase in plasma norepinephrine (determined by radioimmunoassay). After 3 mo of infusion, right and left ventricular norepinephrine content (ng/mg protein) decreased significantly by twofold (right, 2.50 +/- 0.24; left, 2.08 +/- 0.36) compared with controls (right, 4.76 +/- 1.48; left, 4.65 +/- 1.49), and beta-receptor density (125I-pindolol) increased (right, 0.122 +/- 0.029; left, 0.153 +/- 0.021) over the controls (right, 0.082 +/- 0.015; left, 0.069 +/- 0.008 pmol/mg protein). Accompanying the beta-receptor changes, isoproterenol-stimulated adenylate cyclase activity also increased significantly [right, 29.2 +/- 2.1; left, 29.5 +/- 1.0 vs. controls, right, 13.8 +/- 1.1; left, 20.2 +/- 2.2 pmol adenosine 3',5'-cyclic monophosphate (cAMP) generated X min-1 X mg protein-1]. Because the above changes occurred in the absence of cardiac hypertrophy, it suggests that alterations in the myocardial adrenergic system are dependent on the stimulus (in this case norepinephrine) invoking the change and not the degree of hypertrophy. It also suggests that changes in the adrenergic system may not directly reflect the mechanism involved in the development of hypertrophy.

Adenylyl Cyclases↗
PubMed1984

The neurologic complications of cardiovascular disease.

Many cardiac disorders masquerade as neurologic problems. Differential diagnosis is discussed, as well as common neurologic presentations of cardiovascular disease, particularly stroke syndromes arising from emboli, the multitude of disorders that results in loss of consciousness, and neurologic symptoms and signs caused by cardiac drugs.

Arrhythmias, Cardiac↗
PubMed1983

Beta-adrenergic receptor and cyclic AMP alterations in the canine ventricular septum during long-term norepinephrine infusion: implications for hypertrophic cardiomyopathy.

Norepinephrine infusion in dogs has been shown to cause ventricular septal hypertrophy that mimics the syndrome of hypertrophic cardiomyopathy in humans. To characterize the mechanisms involved in septal hypertrophy, the adrenergic system of the right and left ventricles and the septum were analyzed before and after norepinephrine infusion. In the normal unperturbed state, the septum was found to be more sensitive to beta-adrenergic stimulation than either the right or left ventricles. That is, more cyclic AMP could be generated with a smaller dose of beta-agonist (isoproterenol) in septal tissue homogenate than in homogenates of the right or left ventricles. With infusions of norepinephrine (1.4 micrograms/min) to subhypertensive levels over 3 months, beta-receptor number increased twofold to threefold in the ventricles and septum. Adenylate cyclase activity also increased in the ventricles, but not in the septum. The sensitivity of adenylate cyclase to beta-agonist stimulation increased in the septum but remained unchanged in the right and left ventricles. We conclude that the alterations in the myocardial adrenergic system occur in response to the norepinephrine infusion and are not a consequence of hypertrophy. We formulated a hypothesis suggesting that depleted tissue stores of cyclic AMP and/or adenosine triphosphate may be one of the mechanisms involved in the development of hypertrophic cardiomyopathy.

Adenylyl Cyclases↗
PubMed1982

Ejection fraction derived using dye dilution and angiographic methods.

Ventriculographically derived ejection fraction (EF-V) is the most frequently used method to measure left ventricular (LV) function, However, significant error may result in the measurement of end-systolic volume (ESV), which is used to calculate EF-V. This error is ascribed to the variable, irregular, nonellipsoidal geometry of the end-systolic ventricular chamber. Since stroke volume (SV) is determined more accurately by dilution methods than by ventriculography, an improved measure of ESV can be calculated by subtracting green dye determined SV from the ventriculographic determined end-diastolic volume (EDV). The purpose of this study was to measure a correlated ejection fraction (EF-C) using EDV by ventriculography and SV derived using green dye. In eight anesthesized dogs cardiac outputs (COs) were calculated by green dye and left ventriculography. CO determined by ventriculography was greater than that measured by green dye (p less than 0.005). EF-V (55 +/- 15%) was always greater than EF-C (32 +/- 12%) (p less than 0.005). These studies (1) may partially explain the discrepancy in CO calculated from the use of dilution methods and ventriculography and (2) present a method to improve the calculation of LV ejection fraction.

Animals↗
PubMed1982

Ventilatory control during experimental maldistribution of VA/Q in the dog.

To determine the role of the peripheral chemoreceptors in mediating the hyperpnea associated with acute, nonocclusive inflation of a balloon in the main pulmonary artery of the conscious dog, we performed balloon inflations in awake and lightly anesthetized (chloralose-urethan) dogs before and after a) bilateral carotid body resection (CBR), b) cervical vagotomy (V), and c) after both CBR and V. In the intact awake state, balloon inflation increased VE from a mean of 4.91 to 7.16 1/min, usually within 1.5-2.0 min. Mean arterial PO2 decreased from 82 to 71 Torr and end-tidal PCO2 was reduced by 6 Torr. Arterial PCO2 and pH were unchanged in the steady state (as evidenced by discrete blood samples), even in those dogs in which VE increased up to 7.5 1/min. However, an indwelling PCO2 electrode in the femoral artery demonstrated a consistent transient elevation of arterial PCO2 prior to the steady state regulation. Vagotomy alone did not impair the ability to regulate PCO2 during balloon inflation. In some cases with CBR alone, arterial PCO2 was regulated at control levels in the steady state, but the transient increase during the early phase of balloon inflation was more marked (mean increase, 2 Torr). We conclude that the peripheral chemoreceptors are responsible for a significant component of the dynamic ventilatory behavior during this early phase (1.5-2.0 min) of acute maldistribution of VA/Q.

Anesthesia, General↗
PubMed1982

The differential diagnosis of acute pericarditis from the normal variant: new electrocardiographic criteria.

We examined the quantitative electrocardiographic differentiation of acute pericarditis from normal variant ST-T changes. The ECGs of 19 patients with acute pericarditis were compared with those of 20 subjects with typical normal variant changes. Patients were excluded if their ECGs demonstrated conditions that markedly altered repolarization. The positive predictive values (PPV) and negative predictive values (NPV) of previously reported criteria were not high (PPV = 0.54-0.83, NPV = 0.56-0.58). In contrast, in the present study, a T-wave amplitude in lead V6 of less than or equal to 0.3 mV diagnosed acute pericarditis (p less than 0.005, PPV = 0.85, NPV = 0.85), but there was overlap of patients between the groups. The ratio of the amplitude of the onset of the ST segment to the amplitude of the T wave in that lead (ST/T ratio in V6) proved to be the most reliable discriminator. An ST/T ratio greater than or equal to 0.25 diagnosed all patients with acute pericarditis (p less than or equal to 0.005, PPV = 1.0, NPV = 1.0). The ST/T ratio greater than 0.25 in V4, V5 (both p less than 0.005, PPV = 0.87, NPV = 1.0) and I (p less than or equal to 0.005, PPV = 0.80, NPV = 0.81) were also significant discriminators. Thus, if V6 is unavailable, an ST/T ratio greater than or equal to 0.24 in V5, V4 or I is highly suggestive of acute pericarditis. An ST/T ratio greater than or equal to 0.25 in V6 discriminated the ECGs of all patients with acute pericarditis from normal variants in this study.

Acute Disease↗
PubMed1981

Cardiac conduction and rhythm disturbances following suicidal ingestion of mesoridazine.

The phenothiazine derivatives, particularly chlorpromazine and thioridazine, are known to produce significant electrocardiographic abnormalities. Until now, documented life-threatening arrhythmias have not been reported following large doses of mesoridazine, the besylate salt of a metabolite of thioridazine and a relatively recent addition to the phenothiazine group. We describe such a case in which alterations in both impulse conduction (first-degree atrioventricular block, prolonged QRS duration, and right axis deviation) and impulse formation (supraventricular and ventricular tachycardia) were noted following a suicidal ingestion of mesoridazine. The electrophysiologic mechanisms underlying phenothiazine-induced arrhythmogenesis are reviewed.

Adult↗
PubMed1980

Improved echocardiographic evaluation of the closed-chest canine: methods and anatomic observations.

This report describes an improved and convenient method of obtaining echocardiograms from the precordial surface of the closed-chest conscious dog. All major cardiac structures were identified using contrast echocardiography. Anatomic relations and the orientation of cardiac structures to the ultrasound transducer in the position of study were established by postmortem examinations. Good quality echocardiograms were obtained from nine of 11 conscious dogs. Highly significant correlations were found when comparing left ventricular systolic time intervals measured from simultaneous echo and pressure recordings. This method has advantages over other echo techniques; namely, elimination of surgical intervention, displacement of interfering lung tissue, and wider field available for study with a minimum of reverberation artifact. The ability to obtain echocardiograms from the chronic experimental dog under physiologic conditioins might provide new and improved applications of echocardiography for the evaluation of human cardiac disorders.

Animals↗
PubMed1980

The electrophysiologic effects of intravenous lidocaine in the Wolff-Parkinson-White syndrome.

Twelve patients with the Wolff-Parkinson-White syndrome underwent electrophysiologic study, before and after the bolus intravenous administration of lidocaine, 1 mg./kg. There was no significant increase in the effective refractory period of the anterograde AV node pathway, the anterograde or retrograde accessory pathway, or the atrial or ventricular muscle; intravenous bolus administration of lidocaine is unlikely to terminate the re-entry tachycardias, or decrease the rate of the ventricular response in atrial fibrillation, in the WPW syndrome. There was no significant increase in the anterograde or retrograde AV conduction times; bolus administration of lidocaine is unlikely to decrease the rates of the re-entry tachycardias. In addition, lidocaine failed to alter significantly features related to tachycardia initiation. Except in isolated, unpredictable cases, intravenous bolus administration of lidocaine is not likely to be of benefit in the supraventricular tachyarrhythmias of the WPW syndrome.

Adolescent↗
PubMed1980

Time course of changes in the mechanical properties of the canine right and left ventricles during hypertrophy caused by pressure overload.

We developed a mathematical model of the right and left ventricles to determine whether there is a change in the mechanical properties of muscle during the hypertrophy process resulting from pulmonary arterial banding. Pressure-volume data were obtained from 10 normal dog hearts and 8 dog hearts in which the pulmonary artery was banded for periods of 2--40 weeks. These data were applied to the model, and the time course of wall stress and muscle stiffness was quantified for both ventricles. The results demonstrate that (1) myocardial stiffness is increased in pressure-overload hypertrophy (2) normal right and left ventricular muscle exhibits similar mechanical properties and (3) the relationships between wall stresses and the volume/mass ratios to the period of banding are biphasic. We concluded that (1) increase in muscle stiffness is due to several factors. In the early stages of hypertrophy, it may be predominantly due to fibrosis and, in the later stages, to substantial increases in muscle mass. (2) The progressive increase in muscle stiffness concomitant with the increase in muscle mass may be due to the presence of myocardial cellular projections and fibrosis. (3) The appropriate timing for surgical/medical intervention should take place before low volume:mass ratios and, hence, low wall stresses are attained.

Animals↗
PubMed1980

Pulmonary arterial hypertension induced by distention of the main pulmonary artery in conscious newborn, young, and adult sheep.

Distention of the main pulmonary artery by balloon inflation in sheep results in presumably reflex elevation of pulmonary arterial pressure and resistance distal to the balloon. This response to main pulmonary artery distention is significantly greater in newborn lambs than in older lambs or adult sheep. In several of the newborn lambs, pulmonary artery pressure was raised to suprasystemic levels. Further, in some of the newborn animals, these increases in pulmonary artery pressure and resistance were sustained after deflation of teh balloon for periods up to 2 hr. The functional significance of this pulmonary hypertension reflex was not elucidated. However, the data strongly suggest that this reflex may contribute to the maintenance of high pulmonary vascular resistance during fetal and early neonatal life.

Age Factors↗
PubMed1980

Experimental pulmonary hypertension produced by surgical and chemical denervation of the pulmonary vasculature.

The purpose of this study was to investigate the hypothesis that balloon distention of the main pulmonary artery (MPA) induces pulmonary hypertension that is produced by a neural reflex and to investigate the possible efferent components of its reflex arc. Using a specially designed triple-lumen balloon catheter, positioned under fluoroscopy in the MPA, the hemodynamic responses to MPA distention were studied before and after the following: surgical denervation of the bifurcation of the MPA, chemical sympathectomy (6-hydroxydopamine), 100 percent oxygen breathing, and vagotomy. Our findings suggest that the experimental pulmonary hypertension caused by distention of the MPA is produced by excitation of stretch receptors in or near the bifurcation of the MPA and that the efferent limb of this reflex is predominantly mediated via the adrenergic nervous system.

Adrenergic Fibers↗