Search PubMed⌕ Search

Biomedical subjects

K Prasad

Publications and source records attributed to K Prasad.

At least 217 records · Page 12Linked to original sources
PubMed1985

Coat formation in coated vesicles.

The proteins of Mr 100 000-110 000 present in the protein coat of coated vesicles have been shown to facilitate formation of a homogeneous small-size basket (coat) when added to clathrin [Zaremba, S., & Keen, J.H. (1983) J. Cell Biol. 97, 1339]. We have prepared this protein of coat proteins by two different methods and shown that they are very important for the binding of clathrin to uncoated vesicles to form coated vesicles. By labeling the three components (clathrin, 100 000-110 000 proteins, and uncoated vesicles) with different fluorescent markers and analyzing their distribution on sucrose gradients, we have been able to determine the composition of the products formed. In the presence of the 100 000-100 000 fraction of coat proteins, not only does the size distribution of the clathrin basket become uniform but also the rate of polymerization is strongly increased.

Animals↗
PubMed1985

Effect of prazosin treatment on the cardiac sarcolemmal ATPase in failing heart due to mitral insufficiency in dogs.

Prazosin has been used in the treatment of congestive heart failure. It is, however, not known whether prazosin gives only haemodynamic benefit or if it also produces a decrease in the cardiac sarcolemmal Na+-K+-ATPase which has been reported to be increased in the failing heart. The present investigation deals with the effect of 3 months of prazosin treatment in dogs with 3 months of induced mitral insufficiency (MI) on the sarcolemmal Na+-K+-ATPase activity. The dogs were divided into four groups each comprising of five dogs. A--normal; B--3 months of MI; C--6 months of MI; D--3 months of prazosin treatment after 3 months of MI. Three months of MI produced a decrease in the dp/dt and an increase in the end-diastolic pressure of left ventricle but no change in the index of left ventricular contractility and cardiac index. Also there was no change in the sarcolemmal Na+-K+-ATPase. There was a significant decrease in the index of left ventricular contractility and cardiac index and an increase in the LVEDP associated with a significant increase in the left ventricular sarcolemmal Na+-K+-ATPase at 6 months of MI. Sarcolemmal Mg2+-ATPase of both ventricles increased after 6 months of MI the significance of which is not known as yet. There was no change in the sarcolemmal Na+-K+-ATPase of the nonfailing right ventricle. Prazosin treatment prevented the deterioration of the left ventricular contractility and function and also prevented the increase in the sarcolemmal Na+-K+-ATPase observed in failing heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1985

PISA--a new noninvasive method for early detection and quantification of ischemia in hypertensive patients.

Hypertension if untreated, is known to produce cardiac damage. Cardiac complications result from the effects of hypertension on the myocardium and/or to accelerated atherosclerotic changes in the coronary arteries. Presently available diagnostic tools are able to detect cardiac complications only when they are relatively at an advanced stage. Early detection of cardiac complications would have the advantage of early treatment, with potential for reversal. PISA (Phase-Invariant Signature Algorithm) - a new noninvasive method has been shown by us to have high sensitivity and specificity for diagnosis of ischemic heart disease. This method was therefore used in 25 healthy individuals, 20 patients with documented ischemic heart disease and 50 hypertensive patients (duration 1-6 years) with no end-organ disease in order to determine if these patients have myocardial ischemia and/or infarction. These patients were on antihypertensive medication. Healthy individuals as expected, had phase-invariant PISA signature and low PISA index. All 20 patients with documented ischemic heart disease had phase variant signature and had high PISA index in two or more leads. The sensitivity of this method for detection of ischemic heart disease was found to be 100%. Twenty-nine of the 50 hypertensive patients were found to have phase-variant (abnormal) PISA signatures and their PISA index was beyond the upper limit of normal PISA range (mean + 3S.D. of healthy individual). This study suggests that these 29 hypertensive patients possibly have ischemic heart disease. This PISA study indicates that 8 patients have anterior wall, 10 inferior wall, and 11 both anterior and inferior wall ischemia and/or infarction. These twenty-nine patients have varying degree of ischemia and/or infarction.

Adult↗
PubMed1985

Effect of chronic prazosin treatment on the cardiac function and electrolytes in failing heart due to chronic mitral insufficiency.

The effect of three months of prazosin treatment on the hemodynamics, cardiac extracellular space; plasma, tissue and intra-cellular Na+, K+, and Ca++ were investigated in dogs with left ventricular failure due to chronic mitral insufficiency. Mitral insufficiency of 6 months duration significantly decreased the LV systolic pressure, LV dp/dt, LV (dp/dt)/IIP, LVWI, CI, and increased the LVEDP, mean right atrial pressure, heart rate and systemic vascular resistance. Associated with these hemodynamic changes were an increase in the extra-cellular space, tissue and intracellular K+; and a decrease in the tissue and intracellular Ca++. Prazosin treatment produced an improvement in the hemodynamics which was associated with a decreased in the extracellular space, and intracellular K+, and an increase in the intracellular Ca++. Plasma Na+ and Ca++ increased with 6 months of M.I. Prazosin treatment brought back the plasma Na+ and K+ to control level. However, plasma Ca+ decreased significantly with prazosin treatment. The changes in right ventricular hemodynamics and electrolytes were not consistent with the right ventricular failure. These results indicate that decrease in the myocardial contractility in chronic heart failure due to mitral insufficiency might be due to a decrease in the intracellular Ca++. Prazosin treatment was able to reverse the hemodynamic and electrolyte changes induced by failing heart due to mitral insufficiency.

Animals↗
PubMed1984

Stability and structure of clathrin.

The effects of urea on the dissociation and structural transitions of clathrin (8 S) have been evaluated by various techniques. The dissociation of the light chains in 3 M urea has been shown by light scattering, ultracentrifugation, and column chromatography. The dissociated components still retain the capacity to form the characteristic polygonal structure of the coat after removal of the urea. At higher concentrations of urea, the secondary and tertiary structures are eliminated, as documented by various spectroscopic techniques, i.e., tryptophan polarization and emission maxima, circular dichroism, and difference spectra. Two distinct transitions are observed by all techniques, one between 3 and 6 M urea and a second one which starts at 7 M but is still incomplete by 9.6 M urea. A concentration-dependent aggregation of clathrin chains occurs in 4 and 5 M urea solutions, as observed by light scattering and sedimentation. The results indicate that there are two large, independent domains in clathrin heavy chains and that each domain may have a single, highly cooperative transition.

Animals↗
PubMed1984

Organization and dynamics of lipids in bovine brain coated and uncoated vesicles.

Three characteristics have been demonstrated by the chemical analysis of bovine brain coated vesicles following removal of the coat proteins: a high protein content, a high cholesterol/lipid ratio and a high percentage of phosphatidylethanolamine amongst the phospholipids. The study of lipid bilayer organization and dynamics has been performed using the fluorescent probes pyrene and parinaric acid (cis and trans). This has allowed the study of both lateral mobility and rotational motion in the lipid bilayer of the coated and uncoated vesicles. Lateral mobility in the fluid phase of the lipid is slightly reduced by the presence of the clathrin coat, as indicated by the lower diffusion coefficient of pyrene in coated compared with uncoated vesicles. At all temperatures from 6 degrees to 30 degrees C, solid-phase domains, probed by trans parinaric acid, coexist with fluid-phase domains in the lipid bilayer. The temperature dependence of the parinaric acid lifetimes and of their amplitudes strongly suggests that the solid phase domains decrease in size with temperature, both in coated and uncoated vesicles. However, the difference in the value of the anisotropy at long times (r infinity), between coated and uncoated vesicles (a difference which is more pronounced for cis than for trans parinaric acid), indicates that the presence of the clathrin coat introduces disorder in the surrounding lipids, thus suggesting a possible role of the clathrin in the formation of the pits on the plasma membrane.

Animals↗
PubMed1984

Effects of chronic digoxin treatment on cardiac function, electrolytes, and sarcolemmal ATPase in the canine failing heart due to chronic mitral regurgitation.

This study was designed to determine whether digoxin therapy in the canine heart failing because of mitral regurgitation (MR) provides only hemodynamic benefit and accompanying subjective improvement or if it also reverses the changes in intracellular Ca++ and sarcolemmal Na+-K+-ATPase. The dogs were divided into four groups: control, MR of 3 months' duration, MR of 6 months', and digoxin treatment for 3 months after 3 months of MR. Six months of MR produced a marked decrease in the index of myocardial contractility and function associated with a decrease in intracellular Ca++ and Na+, and an increase in intracellular K+, extracellular space, sarcolemmal Na+-K+-ATPase, and Mg++-ATPase. Digoxin treatment tended to return the changes in the index of myocardial contractility and cardiac function, intracellular Ca++, Na+, K+, extracellular space, and sarcolemmal Na+-K+-ATPase of the failing heart toward control levels. Digoxin treatment did not affect Mg++-ATPase. The right ventricle, which did not fail, also did not show any significant changes in the parameters measured. The results showed that digoxin treatment not only improved the index of myocardial contractility and cardiac function of the failing heart but also tended to return the electrolytes and sarcolemmal Na+-K+-ATPase toward control levels.

Animals↗
PubMed1984

Structural characterization of labeled clathrin and coated vesicles.

Clathrin (8 S) and coated vesicles have been covalently labeled by using the sulfhydryl-labeling fluorescent probe N-(1-anilinonaphthalene)maleimide. A large increase in energy transfer from Trp to anilinonaphthalene (AN) residues was observed in clathrin in the pH range approximately 6.5-6.0, where the rate of clathrin self-association increased rapidly. The change in energy transfer was indicative of a conformational rearrangement, which could be responsible for the initiation of the clathrin self-association reaction to form coat structure. The AN label was found in both the coat and membrane proteins after dissociation of coated vesicles at pH 8.5. The labeled coat and membrane proteins readily recombined to form coated vesicles after reducing the pH to 6.5, indicating that the labeling did not interfere with the ability of clathrin to self-associate and interact with uncoated vesicles to form coat structure. A comparison of the AN fluorescence with the Coomassie blue pattern after electrophoresis in sodium dodecyl sulfate-gels revealed that a 180,000-Da protein (clathrin) was mainly labeled in coated vesicles, while a 110,000-Da protein was also strongly labeled in uncoated vesicles. AN-labeled baskets and coated vesicles have been prepared. Trypsin digestion reduced the sedimentation rate of baskets from 150 S to 120 S and of coated vesicles from 200 S to 150 S. Gel electrophoresis of baskets and coated vesicles showed extensive conversion of clathrin (Mr 180,000) to a product of Mr approximately equal to 110,000, suggesting equivalent structural organization of the coat in coated vesicles as in baskets. In both cases, the peptide(s) released from the vesicles by digestion were essentially free of fluorescent label. In the case of the uncoated vesicles, tryptic digestion released most of the proteins remaining after coat removal.

Centrifugation, Density Gradient↗
PubMed1984

Effect of chronic digoxin treatment on cardiac function, electrolytes and ATPase in failing heart due to pressure overload.

A decrease in the cardiac function and intracellular calcium, and an increase in the cardiac sarcolemmal ATPase have been reported in aortic stenosis of 6 to 9 months duration in dogs. The present investigation deals with the effect of 3 months of digoxin treatment on cardiac function, electrolytes and ATPase in dogs with 3 months of aortic stenosis in order to determine whether digoxin treatment gives only haemodynamic improvement or if it also improves the condition of the myocardium in terms of contractility and biochemical changes. There were no significant changes in any of the haemodynamic parameters of left and right ventricles except the left ventricular end-diastolic pressure which increased significantly at 3 months of aortic stenosis. All the hearts developed left ventricular hypertrophy. Concomitant with these changes, there was a tendency for a decrease in the total tissue Ca2+, intracellular Ca2+ and K+, and a tendency for an increase in the sarcolemmal ATPase. There were no significant differences in any of the haemodynamic parameters between the aortic stenotic and digoxin treated aortic stenotic dogs indicating that digoxin was at least maintaining the haemodynamics close to the pretreatment level. Although digoxin treatment prevented the changes in the sarcolemmal ATPase and extracellular space, it did not prevent the further decrease in the total or intracellular Ca2+. The total and intracellular Ca2+ was still significantly higher than previously observed after 6 to 9 months of aortic stenosis. These results suggest that digoxin treatment not only tended to prevent further deterioration of cardiac function but also tended to prevent further changes in the sarcolemmal ATPase and electrolytes.

Adenosine Triphosphatases↗
PubMed1984

Effect of prolonged prazosin treatment on hemodynamic and biochemical changes in the dog heart due to chronic pressure overload.

A decrease in cardiac function and intracellular calcium, and an increase in cardiac sarcolemmal ATPase have been reported in experimentally induced aortic stenosis of 6 to 9 months duration. Prazosin has been used in the treatment of heart failure due to mechanical ventricular overload. It is, however, not known whether prazosin treatment gives only hemodynamic benefit with accompanying subjective improvement or if it also improves the condition of the myocardium in terms of contractility and biochemical changes. The present investigation deals with the effects of 3 months of prazosin treatment on cardiac function, electrolytes, and ATPase in dogs with aortic stenosis of 3 months duration. Although there were no significant changes in most of the left and right ventricular hemodynamic parameters, the left ventricular end-diastolic pressure increased significantly after 3 months of aortic stenosis. Prazosin prevented further deterioration of cardiac function. All the dogs developed left ventricular hypertrophy and all chest X-rays showed cardiomegaly. Concomitant with these changes, there was a tendency towards a decrease in total tissue Ca++ and intracellular Ca++ and K+ and a tendency towards an increase in sarcolemmal Na+-K+-ATPase. Prazosin treatment, although it markedly reduced left ventricular end-diastolic pressure, did not reduce the cardiomegaly. There were no significant changes in any of the other hemodynamic parameters. Prazosin treatment decreased sarcolemmal ATPase and tended to increase intracellular Ca++. It appears therefore that prazosin not only tends to bring the cardiac function towards control values but also tends to correct the ATPase and intracellular Ca++ levels of the failing heart.

Animals↗
PubMed1983

Synthesis and beta-lactamase inhibitory activities of some clavulanic acid analogues.

Clavulanic acid analogs lacking the C-3 carboxyl group are potent inhibitors of both plasmid and chromosomally mediated beta-lactamases. They exhibit only low intrinsic anti-bacterial activity, but potentiate the activity of ampicillin and cephaloridine against beta-lactamase producing Escherichia coli and Enterobacter cloacae in vitro. No synergism was observed in beta-lactamase negative strains. The E. coli TEM 1 and the E. cloacae P99 enzymes are inhibited in a progressive and irreversible manner by these compounds.

Anti-Bacterial Agents↗
PubMed1983

Haemodynamic effects of ionophore (X-537A) in cats.

The effects of ionophore X-537A in the doses of 0.5, 1, 2 and 3 mg/kg were studied on the blood pressure, heart rate, left ventricular contractility, cardiac output, cardiac index, left ventricular work index and systemic vascular resistance in open-chest anaesthetized cats. This compound increased the contractility significantly for 15, 60, 120 and 30 min in the doses of 0.5, 1, 2 and 3 mg/kg respectively. A dose of 0.5 mg/kg was ineffective in raising the blood pressure. Doses of 1, 2 and 3 mg/kg, however, raised the blood pressure significantly for 60, 60 and 15 min respectively. There was an increase in the heart rate, but significant only with doses of 1 and 2 mg/kg. Cardiac output, cardiac index, left ventricular work index and systemic vascular resistance did not change significantly with 0.5 mg/kg of X-537A. Doses of 1 and 2 mg/kg increased the cardiac output, cardiac index, left ventricular work index and total systemic vascular resistance for a variable period of time. A dose of 3 mg/kg of ionophore produced a decrease in the cardiac output, cardiac index, and left ventricular work index, and an increase in the total systemic vascular resistance and cardiac contractility for variable periods. Most of the cardiac effects did not last for more than 1 hr, and repeated administration had no effect on cardiovascular function.

Animals↗
PubMed1982

Reversibility of coated vesicle dissociation.

The dissociation of the coated vesicles to clathrin and uncoated vesicles and their reassociation have been studied under various conditions. The extent of reassociation is pH dependent and increases slightly with increasing concentrations of the components. Unlike the self-association of clathrin which is strongly salt dependent, the reassociation of clathrin and uncoated vesicles is practically independent of salt concentration. The coated vesicle gradually loses its coat with increasing pH, and the dissociation process is not an all or none reaction. Ca2+ inhibits dissociation of the coated vesicles and enhances the reassociation of clathrin and uncoated vesicles. Our results show that, although many conditions result in reassociation of protein and lipid vesicle, few conditions result in vesicles of both the same size and composition as native coated vesicles.

Animals↗
PubMed1980

Effects of enflurane on cardiovascular function in dogs with induced chronic mitral valve disease.

The effect of enflurane on cardiovascular function was investigated in normal dogs and in dogs with chronic heart failure because of induced mitral valve disease (MVD). No significant changes were observed in heart rate (HR), right atrial pressure (RAP) and total systemic vascular resistance (TSVR) in normal dogs. However, significant decreases in HR and increases in RAP and TSVR were observed in dogs with MVD. There were no changes in pulmonary arterial pressure and left ventricular end-diastolic pressure in either group. Cardiac output, cardiac index, arterial pressure, left ventricular work index and left ventricular dp/dt and dp/dtIIP showed a concentration-dependent decrease in both groups but the changes were greater in dogs with MVD.

Anesthesia, Inhalation↗
PubMed1980

Studies on the effects of glucagon on ouabain-induced cardiac disorders using the PISA method.

This paper presents the application of a newly developed noninvasive system (PISA; Phase-Invariant Signature Algorithm) in the early detection and quantification of the effects of glucagon on the ouaban-induced electrophysiological disturbances in the heart of the dog. Three doses (20, 30, and 40 migrograms/kg) of ouabain were administered intravenously to each of six anesthetized dogs and broadband ECGs were recorded on FM tape for 100 min. The records were analyzed for PISA signatures and indexes at 20, 40, 60, 80, and 100 min after ouabain administration. There were dose-dependent increases in the PISA indexes. Ouabain (20 micrograms/kg) did not produce any observable changes in the conventional ECG, although it produced significant increases in the PISA indexes. In a second group sox dogs, glucagon (50 micrograms/kg) was administered intravenously 20 min after ouabain (40 micrograms/kg) administration and the ECGs, both conventional and for PISA analysis, were recorded for a further period of 80 min. Glucagon reversed the effects of ouabain on the PISA indexes. These indicate that the PISA method has the capability of early detection and quantitication of drug-induced cardiac disorder.

Action Potentials↗