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Biomedical subjects

K Prasad

Publications and source records attributed to K Prasad.

At least 37 records · Page 2Linked to original sources
PubMed1978

Acute effects of furosemide on blood electrolytes and hemodynamics in dogs.

The effects of furosemide on the hemodynamics, blood electrolytes, and urinary output in 5 anesthetized dogs were studied. There were no significant changes in blood Na+ or Ca++ levels, but K+ decreased significantly after 15 minutes of furosemide treatment. There were no significant changes in the blood pressure, heart rate, left ventricular systolic pressure, index of left ventricular contractility [(dp/dt)/IIP], or systemic vascular resistance. Left ventricular dp/dt decreased for 30 to 60 minutes. Later the dp/dt and (dp/dt)/IIP of left ventricular pressure exceeded control values, although increases were not significant. Left ventricular work index and stroke volume decreased significantly between 30 and 90 minutes. The cardiac output and cardiac index also decreased. Left ventricular end-diastolic pressure decreased significantly only at 30 minutes. Cardiac function remained unchanged and consistent with the electrolytes changes. Although there was a marked diuresis, which normally must have significantly decreased the effective blood volume and hence the myocardial contractility, the cardiac function remained unchanged. These results suggests that furosemide might have a direct effect on the myocardium. Clinical improvement in patients might be the result of a direct effect on the myocardium aside from its effect due to diuresis.

Animals↗
PubMed1978

Cardiovascular function in dogs with acute hypokalemia.

The effects of acute hypokalemia on plasma electrolytes, cardiovascular function, osmolality, and hematocrit were investigated in anesthetized dogs for 2 hours. There was progressive increase in the total systemic vascular resistance, but no change in the osmolality and blood hematocrit. All of the hemodynamic parameters decreased except the preferred index of myocardial contractility, [dp/dt]/IIP, which increased during hypokalemia. The changes in this index of myocardial contractility were associated with changes in the plasma potassium but not the plasma sodium. The results suggest that hypokalemia-induced increases in myocardial contractility might be associated with an increased influx of Ca++ as a result of hypokalemia-induced inhibition of sarcolemmal Mg++ -dependent, Na+-K+-ATPase.

Animals↗
PubMed1978

Electrophysiologic effects of propranolol on the human heart.

Effects of propranolol (10(-9) to 10(-4) Gm/ml) on various electrophysiologic properties of human papillary muscles obtained from patients undergoing corrective open heart surgery were studied to have an insight into the mechanism of its antiarrhythmic activity in man. Propranolol (10(-8) to 10(-6) Gm/ml) produced significant decreases in the action potential duration, effective refractory period and dv/dt of depolarization phase of action potential without significantly affecting the resting potential and amplitude of action potential. These effects were concentration dependent. High concentration (10(-4) Gm/ml) of propranolol not only produced greater decreases in the above parameters but also reduced the resting potential and amplitude of action potential. Although propranolol decreased both the action potential duration and effective refractory period, the shortening of the action potential duration was greater than the shortening of the effective refractory period. It shifted the membrane responsiveness curve to the right and down. It produced frequency dependent decreases in the dv/dt of phase 0 of action potential and the rate of repolarization. Propranolol also increased the threshold of stimulation. Propranolol produced electrophysiologic changes in the human myocardium qualitatively similar to those in canine myocardium. The probable mechanism of its antiarrhythmic activity in man has been discussed.

Action Potentials↗
PubMed1978

A preliminary study in the detection of cardiac disorders via phase-invariant signature algorithm of ECG.

The present paper presents a simple and unambiguous computer-assisted method for the detection of cardiac disorders by processing the electrocardiogram. A new technique "Phase Invariant Signature Algorithm (PISA)", has been described, which is useful in the detection of cardiac abnormalities by investigating certain statistical properties of the measured waveform of ECG in a "phase-locked" fashion. This method of detection of abnormalities in the heart was used in the changes in the hypoxic action potential and in the ECG due to ionic changes and ischemia in the heart of cats and dogs. The signature of the normal ECG or action potential was straight-line. Any change in the waveform of ECG or action potential was detected as spikes in the signature. This method of detection of cardiac abnormalities does not require a priori reference to any standard ECG. The results indicate that this new method is capable of detecting cardiac disorders at an early stage and hence a higher sensitivity than the presently available type of ECG analysis. This method is in the developmental stage and further studies are being carried out.

Animals↗
PubMed1978

Morphologic effects of dietary plant and animal lipids rich in docosenoic acids on heart and skeletal muscle of cynomolgus monkeys.

Cynomolgi (Macaca fascicularis) were fed diets containing 25% rapeseed oil (RSO), partially hydrogenated herring oil (PHHO), or a 3:1 mixture of lard and corn oil as control for 4 months. The RSO contained approximately 25% of the fatty acids as erucic acid; the PHHO contained a similar concentration of mainly cetoleic acid. The control diet did not include such fatty acids. At the time of necropsy, the RSO- and PHHO-fed monkeys showed myocardial and skeletal muscle lipidosis. Foci of mononuclear cell infiltration, although infrequent, occurred in all three groups and were thought to be nonspecific. The only significant intergroup difference in serum biochemical or hematologic parameters was an increase in serum glutamic-oxaloacetic transaminase activity in both RSO and PHHO groups. Ultrastructural studies confirmed the presence of lipidosis in cardiac and skeletal muscle and revealed mild mitochondrial degeneration, causing a depression of the P/O ratio of the RSO group and a State III respiratory rate depression of the PHHO group. The difference in the exposure/life span ratio represented by this experiment may account for the absence of clear intergroup differences such as are reported in rats used in similar studies, but a true species difference in regard to dietary oils containing docosenoic acids has to be considered as well.

Animals↗
PubMed1978

Cardiac intracellular and blood electrolytes in chronic mitral insufficiency.

A study of the alterations in the intracellular electrolytes in the left failing heart due to induced mitral insufficiency was made in dogs. The extracellular space increased significantly. There was no significant change in the plasma Na+ and Ca++. However, there was a significant decrease in the plasma K+. The ratio of wet weight to dry weight increased during mitral insufficiency, although not significantly. There were no significant changes in the tissue Na+, K+ and Ca++. However, there were significant decreases in the intracellular Na+ and Ca++, and tendency for an increase in the intracellular K+ during mitral insufficiency. These results suggest that the decrease in the myocardial contractility in chronic heart failure due to mitral insufficiency might be due to a decrease in the intracellular Ca++ and associated changes in Na+ and K+ as a result of increased sarcolemmal ATPase.

Animals↗
PubMed1977

Use of glucagon in the treatment of quinidine toxicity in the heart.

The effects of glucagon on quinidine-induced cardiac toxicity were studied in open-chest anaesthetised dogs. Glucagon along increased the heart rate and contractility; and decreased the blood pressure, duration of P-R and Q-T interval, and QRS complex. Quinidine produced dose-dependent decreases in the heart rate, blood pressure, and contractility, and lengthening of the duration of P-R and Q-T interval, and QRS complex. Glucagon abolished the changes produced by quinidine within two minutes, and appears to be a drug of choice in the treatment of quinidine toxicity in the heart.

Animals↗
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↗