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R D Patil

Publications and source records attributed to R D Patil.

6 recordsLinked to original sources
PubMed1995

Local modulation of adrenergic responses in the hindlimb vasculature of the intact conscious rat.

1. Local modulation of adrenergic responses was examined in the hindlimb vasculature of chronically instrumented intact conscious rats. Sprague-Dawley rats (n = 22) were instrumented with a Doppler flow probe around the right common iliac artery, a polyethylene catheter inserted just distal to the flow probe and a left carotid arterial catheter. 2. The effects of various concentrations of the alpha 1-adrenergic receptor agonist phenylephrine (0.005-0.075 microgram kg-1), the alpha 2-adrenergic receptor agonist clonidine (0.1-0.7 microgram kg-1), and the endogenous adrenergic receptor agonist adrenaline (0.02-0.08 microgram kg-1), were investigated under control conditions, and in the presence of the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine methyl ester hydrochoride (L-NAME) (NO-X, 0.2 mg kg-1) and the cyclo-oxygenase inhibitor indomethacin (CO-X, 10 mg kg-1). Results were presented as dose-response curves. 3. Heart rate and arterial pressure were not altered by any of the agents because all were locally injected into the hindlimb vasculature and the selected doses were lower than those which elicited systemic responses. 4. Maximal vasoconstrictor responses to phenylephrine were enhanced in the presence of NO-X (50 +/- 6%) and CO-X (70 +/- 9%). Maximal vasoconstrictor responses to clonidine were also enhanced in the presence of NO-X (75.3 +/- 4.8%) and CO-X (50.6 +/- 5.7%). 5. The responses to adrenaline were biphasic; NO-X significantly attenuated the vasodilator response (87 +/- 6%), and enhanced the vasoconstrictor response (51 +/- 7%). CO-X attenuated the vasoconstrictor response (71 +/- 6%). 6. These results demonstrate local modulation of responses to alpha 1- and beta-adrenergic receptor agonists by receptor-mediated dose-dependent release of NO and prostaglandins.

Adrenergic Agonists↗
PubMed1993

Integrated cardiovascular physiology: a laboratory exercise.

Examining the hemodynamic responses to exercise provides a unique opportunity to analyze and integrate cardiovascular physiology because more is learned about how a system operates when it is forced to perform than when it is idle. We designed a laboratory exercise that examines the cardiovascular responses to exercise in a sedentary individual, an athlete, an individual with quadriplegia, and an individual with heart transplantation. The special populations were chosen because of their unique limitations and adaptations, which directly influence cardiovascular function. Basic anatomic and physiological data about the special populations are provided, and the students are challenged to analyze and assimilate information from figures, answer questions, make calculations, and plot graphs. The answers to the questions are provided in the APPENDIX. This laboratory exercise should be attempted in a group to foster discussions and interactions. The laboratory does not require any equipment or software. This exercise should be attempted after the cardiovascular section of the physiology course so that the students can integrate and apply the information presented during the course.

Adult↗
PubMed1993

Acute exercise enhances nitric oxide modulation of vascular response to phenylephrine.

The influence of the release of endothelium-derived nitric oxide (NO) on the vasoconstrictor response to phenylephrine (PE) was evaluated before and after a single bout of dynamic exercise. Each rat ran on a motor-driven treadmill at 12-18 m/min, 10-18% grade until exhaustion (avg time 45 min). Sprague-Dawley rats (n = 6) were instrumented with a Doppler ultrasonic flow probe around the right common iliac artery. Just distal to the flow probe, a catheter was placed into the right iliac artery for local infusions. A Teflon catheter was placed in the descending aorta to measure mean arterial blood pressure (MAP) and heart rate (HR). PE (0.005-0.075 microgram/kg) and NO inhibitor N omega-nitro-L-arginine methyl ester hydrochloride (L-NAME, 0.2-0.25 mg/kg) were injected into the functionally isolated hindlimb. HR and MAP were not altered by any of the injections because we selected doses below those which elicited systemic responses. Dose-response curves to PE were generated in the control and postexercise condition, with and without the NO synthase inhibitor L-NAME. Exercise significantly attenuated the maximal vasoconstrictor response to PE (45.6 +/- 1.6%). L-NAME enhanced the maximal vasoconstrictor response to PE 49.8 +/- 4.5% in the control condition and 121.4 +/- 5.9% in the postexercise conditions. Thus, although NO inhibition enhanced the vasoconstrictor response to PE in the control and postexercise conditions, the enhanced vasoconstrictor response to PE after L-NAME was significantly greater in the postexercise condition. Results suggest that NO contributes to the exercise induced attenuation of alpha 1-adrenergic receptor stimulation.

Animals↗
PubMed1991

Rhabdomyolysis and acute renal failure following a single dose of succinylcholine.

A 30-year old with rhabdomyolysis and acute renal failure is presented. The attack followed a minor operation under general anaesthesia during which succinylcholine was administered as muscle relaxant. The fasciculations which occurred immediately after injection of succinylcholine may possibly have precipitated rhabdomyolysis.

Acute Kidney Injury↗
PubMed1991

Rhinocerebral mucormycosis associated with diabetic ketoacidosis.

Rhinocerebral mucormycosis with hemiparesis occurred in a young woman who was not a known diabetic. Rhyzopus species grew from the initial nasal biopsy. The patient was treated with amphotericin B, in addition to control of diabetic ketoacidosis. Surgical intervention was not done. The patient died on the fourth day of hospitalisation.

Adult↗