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Biomedical subjects

K M Dhasmana

Publications and source records attributed to K M Dhasmana.

At least 37 records · Page 2Linked to original sources
PubMed1984

A study on the influence of ketamine on systemic and regional haemodynamics in conscious rabbits.

Effects of ketamine hydrochloride (2, 6 and 18 mg X kg-1, i.v.) were investigated on systemic and regional haemodynamics using a radioactive microsphere method in conscious rabbits. Ketamine decreased respiratory frequency in a dose-dependent manner for up to 5 min. A significant fall in the mean arterial blood pressure (with the two highest doses), together with a short lasting tachycardia, was observed with ketamine. The cardiac output and blood flow to many tissues were not changed by this anaesthetic agent. However, increased blood flow was noticed in discrete regions of the brain (cerebral hemispheres) and heart (left ventricular endocardium). Vasodilation in the cerebral hemispheres with this agent producing dissociative anaesthesia is in contrast to the generally observed decrease in cerebral blood flow with other anaesthetic agents.

Animals↗
PubMed1983

A comparison of systemic and regional hemodynamic effects of d-tubocurarine, pancuronium, and vecuronium.

This study was designed to compare the effects of three neuromuscular blocking agents, in a clinically relevant dose range, on the regional distribution of blood flow measured with 15-microns radioactive microspheres in anesthetized, optimally ventilated cats. d-Tubocurarine (400, 800, and 1,600 micrograms X kg-1) caused hypotension and a decrease in ascending aortic blood flow. Pancuronium (20, 40, and 80 micrograms X kg-1) only caused a moderate tachycardia, while vecuronium (40, 80, and 160 micrograms X kg-1) was devoid of any systemic hemodynamic effect. Neither pancuronium nor vecuronium caused major changes in regional blood flows. On the other hand, d-tubocurarine increased blood flow to the stomach but decreased that to the kidneys, liver, skin, spleen, intestine, and adrenal glands. These effects of d-tubocurarine show a striking resemblance to those elicited by the infusion of histamine. Blood flow to the nerve-stimulated tibialis anterior muscle, which was about six times that of the unstimulated muscle, was decreased significantly by all three neuromuscular blockers. In conclusion, the results clearly show that, while d-tubocurarine produces major cardiovascular disturbances, pancuronium and, in particular, vecuronium do not cause serious changes in systemic and regional hemodynamics in doses that are two to four times the ED90 for neuromuscular blocking action.

Animals↗
PubMed1982

Effects of fentanyl, and the antagonism by naloxone, on regional blood flow and biochemical variables in conscious rabbits.

Effects of fentanyl (cumulative doses: 25, 75 and 125 micrograms.kg-1, i.v.) on respiratory, systemic and regional haemodynamic and biochemical variables were studied in the conscious rabbit. The initial dose of fentanyl (25 micrograms.kg-1) produced a rise in blood pressure and a decrease in heart rate but, on subsequent doses, smaller effects were observed. The drug produced changes in arterial blood gases which were due to a severe decrease in respiratory frequency and an increase in muscular rigidity of chest and neck muscles. The blood flow to skin, stomach, mesentery plus pancreas, bones and fat was decreased by fentanyl. These changes resemble those obtained during alpha-adrenergic stimulation and, thus, may be related to a release of catecholamines during respiratory depression. On the contrary, however, hepatic arterial blood flow was increased and this effect may be responsible for the rapid metabolism and a short duration of action of fentanyl. Fentanyl also caused an increase in the concentration of glucose, lactate and inorganic phosphates in the arterial blood. These changes are probably due to hypoxia. Administration of naloxone not only reversed the residual effects of previous fentanyl administration but also antagonized the respiratory, haemodynamic and biochemical responses to the morphinomimetic drug.

Animals↗
PubMed1981

Cardiovascular effects of etomidate with emphasis on regional myocardial blood flow and performance.

The effects of 30-min infusions of etomidate 0.03, 0.12 and 0.24 mg kg-1 min-1 on systemic and regional haemodynamic variables and cardiac performance and metabolism were studied in pigs. The drug caused moderate, but dose-dependent, decreases in the cardiac output, arterial pressure and LVdP/dt max. Myocardial wall thickening, measured by echographic analysis, was decreased by the drug. However, heart rate, myocardial blood flow distribution and myocardial metabolism of lactate, glucose and free fatty acids remained unchanged. Cerebral blood flow was decreased substantially. However, renal blood flow changed only slightly.

Animals↗
PubMed1980

Haemodynamic and biochemical variables after induction of anaesthesia with fentanyl and nitrous oxide in patients undergoing coronary artery by-pass surgery.

The effects on the haemodynamic and biochemical parameters of three different anaesthetic induction regimes, namely fentanyl (4.1 micrograms.kg-1 or 15 micrograms.kg-1) plus 60 per cent nitrous oxide with oxygen and fentanyl 15 micrograms.kg-1 plus 60 per cent nitrogen with oxygen, were studied in patients undergoing coronary artery surgery. Fentanyl 15 micrograms.kg-1 with nitrous oxide and oxygen produced simultaneous reductions in oxygen uptake, cardiac index and left ventricular stroke work with an unaltered oxygen extraction. Diastolic blood pressure (an index of coronary artery perfusion) was only slightly reduced, and there were no changes in arterial lactate, glucose and free fatty acids. The lower dose of fentanyl (4.1 micrograms.kg-1) with nitrous oxide produced no haemodynamic changes but decreased the oxygen uptake and extraction. The patients receiving fentanyl 15 micrograms.kg-1 with nitrogen and oxygen showed increases in heart rate, blood pressure, cardiac index and left ventricular stroke work, together with a significant fall in oxygen extraction. Moreover, in the patients who received fentanyl 4.1 micrograms.kg-1 with nitrous oxide and oxygen and fentanyl 15 micrograms.kg-1 with nitrogen and oxygen there were significant increases in blood lactate, glucose and free fatty acids, indicating increased sympathetic activity. We conclude that fentanyl 15 micrograms.kg-1, together with 60 per cent nitrous oxide with oxygen provides a satisfactory haemodynamic and biochemical state during induction of anaesthesia in patients with myocardial function prejudiced by coronary artery insufficiency.

Adult↗
PubMed1973

On the mechanism of L-dopa-induced postural hypotension in the cat.

1. The effects of L-DOPA on postural hypotension and carotid occlusion pressor effect were studied, mainly in cats; the recovery of the blood pressure upon tilting was used as a measure of postural hypotension.2. L-DOPA (30 mg/kg) partially depressed the carotid occlusion pressor effect and caused some degree of postural hypotension, L-DOPA (100 mg/kg) had more marked effects; the responses returned to control after 90 to 150 minutes. L-DOPA itself caused a pressor response in all cats.3. The dopa decarboxylase inhibitor N(1)-(DL-seryl)-N(2)-(2,3,4-trihydroxybenzyl) hydrazine (RO4-4602, 50 and 10 mg/kg) had no effect itself on the tilt response but completely prevented the effects of L-DOPA on the carotid occlusion pressor effect and postural hypotension.4. After RO4-4602 (3 and 1 mg/kg), L-DOPA (100 mg/kg) caused a brief rise of blood pressure followed by a longer lasting fall in horizontally-orientated cats (i.e. ;supine' hypotension). No postural hypotension was observed after L-DOPA under these conditions.5. Noradrenaline elicited only small and transient effects on postural hypotension, but dopamine's effects were more marked and longer lasting. Pressor dose-response relationships for noradrenaline were the same before and after L-DOPA, as well as in cats pretreated with L-DOPA for 4 days.6. In cats with kidneys and intestines removed, the tilt reflex was still present. Dose-response curves to L-DOPA were the same as in normal animals. RO4-4602 (3 mg/kg) prevented postural hypotension and block of the carotid occlusion pressor effect; supine hypotension was also observed after L-DOPA.7. The recovery response to tilting in spinal cats was markedly depressed or absent unless the blood pressure was elevated by angiotensin, in which experiments L-DOPA depressed the recovery upon tilting (i.e. induced postural hypotension).8. Blood pressure responses to tyramine were increased after 10 mg/kg of L-DOPA, but depressed after 100 mg/kg. The response to tyramine was not depressed, however, when RO4-4602 was given to block the dopa-dopamine conversion.9. The response to sympathetic stimulation in pithed rats was depressed after L-DOPA and dopamine, but not after alpha-methyldopa.10. alpha-Methyldopa (300 mg/kg) given acutely caused a moderate degree of postural hypotension and a more marked postural hypotension if given for two days.11. It is concluded that it is possible to differentiate between the supine and postural hypotension caused by L-DOPA and that supine hypotension is due to a central effect and postural hypotension to an extracerebral effect. Postural hypotension is discussed in relation to six hypotheses presented to explain its effect. Postural hypotension after L-DOPA is probably not due to a-adrenoceptor blockade, a central effect or any effect on the kidney. The most likely hypothesis is that L-DOPA forms dopamine which acts as a false transmitter in the peripheral sympathetic nervous system.

Adrenergic alpha-Antagonists↗