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Biomedical subjects

K Prasad

Publications and source records attributed to K Prasad.

At least 253 records · Page 14Linked to original sources
PubMed1977

Frequency-dependent changes in the cardiac sarcolemmal ATPase.

1 Effects of various frequencies (0.25, 0.5, 1.0, 1.5 or 2.0 Hz) of stimulation for various durations (2, 5, 10 or 15 min) on the contractile force of trabecular or papillary muscles of dog myocardium were investigated. 2 Effects of various frequencies (0, 0.25, 0.5, 1.0, 2.0 Hz) of various stimulus strengths (0.5, 1, 10 V) for various durations (2,5,10 or 15 min) on the Mg2+/-dependent Na+/--K+/--adenosinetriphosinetriphosphatase (ATPase) of isolated sarcolemmal fraction of dog myocardium were determined. 3 There was a frequency-dependent increase in the contractility and inhibition of the Na+/--K+/--ATPase within 2 minutes. 4 Frequency-dependent increase in the contractility and inhibition of Na+/--K+/--ATPase decreased as the duration of stimulation was increased. 5 The diminution in the inhibition of ATPase was associated with a decrease in the contractility with prolonged stimulation. 6 These results suggest that the frequency-dependent increase in the myocardial contractility might be mediated through an inhibition of the sarcolemmal ATPase.

Adenosine Triphosphatases↗
PubMed1977

Possible mechanism for the frequency-dependent increases in the cardiac contraction in monkey.

The effects of various interventions on the frequency-dependent increases in the contractility of the papillary muscles of monkeys were investigated. Ouabain (10(-6)M) and KCl-free Krebs-Ringer solution, which are known to inhibit membrane Na+,K+-ATPase (EC 3.6.1.3), abolished the frequency-dependent increases in the contractility of the papillary muscles. Epinephrine (4.5 X 10(8)M) or quinidine (1.3 X 10(-5)M), which are known not to inhibit the membrane Na+,K-ATPase at these concentrations, did not alter the frequency-dependent increases in the contractility. These results indicate that the frequency-dependent increases in the contractility might be mediated through an inhibition of the sarcolemmal Na+,K+-ATPase.

Animals↗
PubMed1977

Influence of glucagon on the cardiovascular effects of procainamide.

Effects of glucagon on procainamide-induced cardiac toxicity were studied in anesthetized dogs. Procainamide in doses of 50 and 100 mg/kg produced dose-dependent decreases in the blood pressure, cardiac output, left ventricular work index, and left ventricular systolic pressure; and increases in the left ventricular end diastolic and right atrial pressure, and total systemic vascular resistance. Glucagon antagonized most of the effects of procainamide on the cardiovascular system. Glucagon may be effective in antagonizing procainamide-induced cardiac toxicity.

Animals↗
PubMed1977

The effects of glucose infusion on myocardial performance during acute hypoxia.

The effects of hypoxia with or without glucose infusion on the cardiac contractility, blood pressure, electrocardiogram, blood electrolytes (sodium and potassium), glucose, pH, Po2, and Pco2 in anesthetized dogs were studied. Hypoxia was induced by ventilating the dogs with reduced oxygen (10%) in the inspired air. Hypoxia produced a decrease in the cardiac contractility and blood pressure, and an increase in the heart rate and central venous pressure. It produced a decrease in the blood pH, Po2, and Pco2, and an increase in the blood glucose and potassium. Glucose infusion during hypoxia delayed the rate of decrease in the contractility and blood pressure significantly. The time for decrease in the contracility to 45 to 50% was increased by 67%. Glucose infusion prevented the loss of potassium from the cell. Glucose infusion however, was unable to correct acidosis. These results indicate that glucose infusion during hypoxia might prevent or delay the deterioration of myocardial function.

Acidosis↗
PubMed1977

Ultrastructure of failing myocardium due to induced chronic mitral insufficiency in dogs.

Left ventricular failure was produced in dogs by inducing mitral insufficiency and the cardiac muscle was examined for ultrastructural changes in thsese failing hearts after 5-10 months of mitral insufficiency. The left ventricular failure was established by haemodynamic measurements, chest X-ray and examination of the heart. In the failing heart, the increased number of mitochondria showed close approximation with the sarcolemmal membrane in the T-tubules as well as in the intercalated discs (ID); this is in contrast to what is seen in normal hearts, where T-tubules were mostly coupled with sarcoplasmic reticulum. It is possible that in the heart failing on account of mitral insufficiency mitochondria may be taking over the function of the sarcoplasmic reticulum. Although ID were jumbled up in the failing heart, the intercellular gap and specialized membrane junctions (gap and tight junctions, desmosomes) were quite comparable to normal, indicating that intercellular communication at ID in this type of heart failure is probably maintained. Nuclear chromatin in the failing heart was condensed and lined the inner nuclear membrane. Microbodies with a single limiting membrane were frequent and so were lipofuscin granules. The latter could be an end product of degenerative mitochondria. Golgi bodies in the failing heart were also present in locations away from the nucleus.

Animals↗
PubMed1976

Myocardial sarcolemmal ATPase in dogs with induced mitral insufficiency.

A study of the sarcolemmal Na+K+ATPase in the left failing heart due to induced mitral insufficiency was made in dogs. The sarcolemmal Na+K+ATPase markedly increased in the failing left ventricle. There was no change in the ATPase in the nonfailing right ventricle of the same dog. It was observed that during the early period of mitral incompetence, when there was an increase in the index of myocardial contractility, there was also a decrease in the sarcolemmal Na+K+-ATPase activity. There was no change in the MPG++-ATPase of the sarcolemmal fractions of either the failing or nonfailing ventricle. These results indicate that sarcolemmal Na+K+-ATPase appears to be involved in the reduction of the myocardial contractility during heart failure.

Adenosine Triphosphatases↗
PubMed1976

Potassium-induced changes in the electromechanical and ATPase activity of guinea pig heart.

The effects of various concentrations (0, 0.5, 1, 2, 4, and 8 mM) of potassium chloride on the simultaneously recorded action potential and contractility; and Mg++-dependent, Na++-K+-stimulated membrane ATPase of guinea pig's heart were studied. In KCl-free solution, the inhibition of the Na+-K+-ATPase was associated both with a shortening of the duration of action potential and an increase in the contractility. There was a decrease in the overshoot of action potential and an increase in the resting potential. Potassium chloride produced a concentration dependent lengthening of the action potential duration; decrease in the contraction and resting potential; and an increase in the overshoot of action potential and Na+-K+-ATPase activity. The changes in the action potential and contraction were associated with the changes in the Na+-K-ATPase activity. The changes in the ATPase activity preceded the changes in the action potential and contractility. The involvement of ATPase in the genesis of the resting potential; overshoot and duration of action potential; and contraction has been discussed.

Action Potentials↗
PubMed1976

Extracellular calcium and positive inotropy of ionophore (X537-A) in cardiac muscle.

The role of extracellular calcium in the positive inotropic effect of X537-A in dog's cardiac muscle was investigated. Ionophore (20 mug/ml) in the presence of external calcium increased the contractility by 67 +/- 12 percent within 2 min. In the absence of external calcium ionophore was ineffective in producing a positive inotropic effect in the muscle. Lanthanum, an inhibitor of calcium influx, in the concentrations of 2, 4, 6, and 8 mM produced a concentration dependent decrease in the contractility. Ionophore-induced increase in the contractility was inversely related to the concentration of lanthanum used. It is suggested that the release of calcium from intracellular stores under the effect of ionophore is not enough to maintain contractility. Also positive inotropic effect of ionophore appears to be mediated through the transportation of calcium across the sarcolemma. Such ionophore mediated transportation of calcium appears to be dependent upon surface binding of calcium.

Animals↗
PubMed1975

Electrophysiologic effects of glucagon on human cardiac muscle.

The effects of glucagon (5, 10, and 40 mug/ml) on the amplitude and dueation of action potential, effective refractory period, dv/dt of phase 0 of action potential, membrane responsiveness, and contraction in human papillary muscles obtained from patients undergoing corrective open heart surgery were investigated. Glucagon, in none of the concentrations, produced any significant change in the amplitude and dueation of action potential, or in force of contraction. Shortening of the effective refractory period was not significant. Glucagon enhanced the conduction and the membrane responsiveness by increasing the dv/dt of phase 0 of action potential and a shift of curve to the left. It is suggested that the latter properties of glucagon would abolish the "re-entrant" type of cardiac arrhythmias produced by cardiac glycosides or other drugs that initiate and perpetuate arrhythmias dur to altered conduction.

Action Potentials↗
PubMed1975

Glucagon-induced changes in the action potential, contraction, and Na+-K+-ATPase of cardiac muscle.

The effects of glucagon in concentrations of 0.294 times 10(-6) mol/l, 1.47 times 10(-6) mol/l; 2.94 times 10(-6) mol/l, 5.8 times 10(-6) mol/l, and 1.47 times 10(-5) mol/l on the simultaneously recorded action potentials and contractions; and microsomal and sarcolemmal Na+-tk+-atpase in the myocardium of the guinea pig, rabbit, dog, and pig were investigated. Glucagon in all the concentrations produced an inhibition of the Na+-K+-ATPase associated with an increase in the contractility and shortening of the duration of action potential in dog myocardium. The increase in contraction was concentration-dependent up to a certain concentration. Inhibition of sarcolemmal ATPase was more than that of microsomal ATPase. In none of the concentrations did glucagon produce any significant changes in the Na+-K+-ATPase. In none of the concentrations did glucagon produce any significant changes in the Na+-K+-ATPase, contractility, and action potential duration in the myocardium of guinea pig, rabbit, or pig. These results suggest that glucagon-induced positive inotropic effect might be due to an increase in the Ca++ influx as a result of inhibition of membrane Na+-K+-ATPase. Shortening of the action potential duration might also be due to an increased efflux of potassium as a result of an inhibition of Na+-K+-ATPase.

Action Potentials↗
PubMed1975

Cardiac metabolism and electromechanics of human heart.

The effects of substrates on the metabolic inhibitor-induced changes in the action potential and contraction of papillary muscles obtained from patients undergoing corrective open-heart surgery were studied. Anoxia produced a marked shortening of the action potential duration and a decrease in the resting potential, rate of rise of action potential, effective refractory period, and contractility. In anoxic muscle, although glucose completely restored the action potential duration, effective refractory period, and resting potential to control levels, it was unable to completely restore the contractility to the control level. Substrate depletion and metabolic inhibitors (iodoacetate, dinitrophenol) produced effects similar to that of anoxia, but at a faster rate. Glucose restored the action potential and, to a lesser extent, contractility to the control level in dinitrophenol-treated muscle but was ineffective in so doing the iodoacetate-treated muscle. Pyruvate, however, was effective in restoring the action potential and contracility in iodoacetate-treated muscle. Pretreatment of the muscle with glucose and, particularly, with glucose plus insulin prevented the combined effects of anoxia and lack of glucose on the action potential and contractility for a prolonged period. These results suggest that intravenous infusion of glucose and insulin before and during surgery might prevent or reduced the effect of anoxia on the electrical and mechanical activity of the heart during open-heart surgery.

Action Potentials↗