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Biomedical subjects

R K Saini

Publications and source records attributed to R K Saini.

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

A comparison of the cardiovascular, renal, and coronary effects of dopamine and monensin in endotoxic shock.

The present investigation was carried out in anesthetized dogs to compare the cardiovascular effects of dopamine and monensin, a carboxylic ionophore, in normal and E coli endotoxin-induced shock conditions. In control animals, monensin increased cardiac contractility, cardiac output, systemic blood pressure, and coronary blood flow in a dose-dependent manner, but had little or no effect on heart rate. However, unlike dopamine, which selectively increased renal blood flow, monensin did not affect renal blood flow in doses that produced a maximal increase in coronary blood flow or other hemodynamic effects. The duration of action of monensin was longer than 2 hr. Both dopamine and monensin reversed the cardiac depression and hypotension produced by E coli endotoxin, and in these experiments also, the duration of action of monensin was longer than 2 hr. Regional blood flow measurements with the radioactive microsphere (15 mu) technique demonstrated a marked decrease in organ blood flows at 60 min postendotoxin, but some recovery was observed at 90 min. In the left ventricle, reduction of flow to the endocardial region was greater than to the epicardium. In dogs with endotoxic shock, monensin produced a significant increase in organ blood flows towards or even above control values.

Animals↗
PubMed1980

The effect of monensin, a Na+-selective carboxylic ionophore, on coronary circulation.

Carboxylic ionophores are antibiotics that selectively complex with cations and facilitate their transport across biological membranes. Monensin is a monovalent ionophore that has been reported to exhibit a high degree of in vitro selectivity to transport Na+ ions. In anesthetized dogs, intravenous injections of 5-25 micrograms/kg of monensin produce a selective coronary vasodilator action. A maximal increase in coronary blood flow (CBF) with little or no effect on other cardiovascular parameters was produced. In the 50-200-micrograms/kg dose range, additional positive inotropic and systemic vasopressor effects were elicited. In dogs with normal coronary arteries, 25 micrograms/kg i.v. of monensin increased both subendocardial (ENDO) and subepicardial (EPI) blood flows, such that the ENDO/EPI ratio was changed from 1.10 +/- 0.03 before to 0.75 +/- 0.05 after monensin. The large dose (75 micrograms/kg i.v.) of monensin produced a maximum increase in ENDO flow but the EPI flow was less than that with the small dose; the ENDO/EPI ratio was increased to 1.19 +/- .14. In dogs with 80%-90% occlusion of the left anterior descending (LAD) coronary artery, both doses of monensin increased blood flow to normal and "border" zones but not the central ischemic zone. There was no evidence of "coronary steal" after monensin. This ionophore may be useful in increasing blood pressure and cardiac output after acute myocardial infarction.

Animals↗
PubMed1979

Streptozotocin-induced diabetes in the spontaneously hypertensive rat.

Spontaneously hypertensive rats (SHR) were more sensitive to the diabetogenic effects of streptozotocin than normotensive Wistar-Kyoto (WKY) rats. Thus, 10 days after intravenous administration of 25 mg/kg streptozotocin in SHR, mean pancreatic insulin content was decreased by 42% (p less than 0.05), and mean plasma glucose concentration was increased from 85 to 215 mg/dl (p less than 0.001), whereas between 37.5 and 50 mg/kg of streptozotocin was required to produce similar effects in normotensive WKY rats. Also, there was a progressive decrease in blood pressure in SHR injected with 25, 35.7, or 50 mg/kg of streptozotocin, whereas blood pressure was progressively increased after streptozotocin in normotensive WKY rats. The opposite effects of streptozotocin-induced diabetes on blood pressure in SHR and WKY rats could be observed at similar degrees of hyperglycemia and are presently unexplained.

Animals↗
PubMed1978

In vivo monitoring of the death rate of artificial murine pulmonary micrometastases.

A system is described for direct monitoring of the death rate of artificial murine pulmonary microscopic metastases in vivo. Metastatic fibrosarcoma cells or benign connective tissue cells labeled with [125I]iododeoxyuridine were injected i.v. Comparison of the long-term radioactive decay rate of these two cell types in the lung permitted identification of the portion of the decay curve reflecting the initial period of micrometastasis development and growth. About 5% of the injected tumor cells were retained in the lung in micrometastasis, and their average death rate could be monitored by loss of radioactivity from the lung. Systemic methotrexate (75.0 mg/kg) was administered as a single dose 80 hr after injection of tumor cells at a time when micrometastases had not yet become vascularized. This treatment killed about 60% of the micrometases and suppressed the appearance of gross metastases at 14 days.

Animals↗
PubMed1975

On the use of functional antagonism to estimate dissociation constants for beta adrenergic receptor agonists in isolated guinea-pig trachea.

In guinea-pig trachea, the maximum degree of relaxation that can be elicited by beta adrenergic receptor agonists depends upon the degree of contraction of the smooth muscle induced by cholinergic agonists. In these studies, it is shown that increasing concentrations of carbamylcholine (carbachol) result in a shift to the right of the dose-response curves to (-)-isoproterenol and (-)-soterenol and a reduction of the maximum degree of relaxation produced by these agonists relative to that produced by papaverine. Soterenol is demonstrated to be a partial agonist relative to isoproterenol since its maximum response is reduced to a greater extent by carbachol and it displaces the carbachol dose-response curves to the right less than does isoproterenol. The data were used to calculate, by three different theoretical models of drug-receptor interactions, a dissociation constant (KA) for soterenol. All values obtained were within 2-fold differences. The range of KA values for soterenol was from 5.4 to 9.6 times 10(-8) M. These values are about 100 times larger than the ED50 value for soterenol obtained in the absence of carbachol. The KA value estimated for (-)-isoproterenol (about 3 times 10(-8) M) by one of the models is also around 100 times larger than its ED50 value. This demonstrates further that ED50 values are unreliable indicators of the affinities of agonists for receptors.

Adrenergic beta-Agonists↗