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Biomedical subjects

S C Manchanda

Publications and source records attributed to S C Manchanda.

At least 91 records · Page 5Linked to original sources
PubMed1975

Effects of high altitude hypoxia on left ventricular systolic time intervals in man.

Effects of high altitude hypoxia on systolic time intervals were examined in 34 healthy men: 20 sea level residents studied at rest and at the end of 3 minutes steady isometric (handgrip) exercise at sea level and then serially for the first 5 days and on the tenth day, at an altitude of 3658 m, and I4 permanent residents at high altitude studied at high altitude. In the sea level residents there was a significant increase in the pre-ejection period (PEP), abbreviation of the left ventricular ejection time (LVET), both corrected for heart rate, and prolongation of the PEP/LVET ratio at high altitude. The maximum changes were seen on days 2 and 3; these parameters tended to approach sea level control values by the tenth day. The systolic time interval values of high altitude residents were similar to the control values of the sea level residents obtained at sea level but significantly different from the changes in the sea level values seen in the first 4 days at high altitude. It thus appears that while the high altitude residents do not show any left ventricular dysfunction as determined by systolic time intervals, healthy sea level residents when exposed to high altitude hypoxia show a significant depression of the left ventricular function for at least the first 4 days. This might be a contributing factor in the genesis of high altitude pulmonary oedema.

Adult↗
PubMed1975

Cardiovascular responsiveness to beta-adrenergic stimulation and blockade in chronic hypoxia.

Previous studies have shown that exposure to high altitude results in an initial increase in heart rate, followed by a return to sea-level values within several days; circulating catecholamines rise progressively during this time. Nine conscious dogs were studied in normoxia (N) and after 10 days' exposure to 445 torr (CH). The mean (plus or minus SE) hematocrit was higher in CH (50 plus or minus 2 vs. 42 plus or minus 1%) while Pa-o2 (53 plus or minus 1 vs. 97 plus or minus 2 torr) and PaCO2 (27 plus or minus 1 vs. 35 plus or minus 1 torr) were lower than in N. A 3.5-fold increase in plasma norepinephrine above the N value was found in CH. Arterial pH, heart rate (HR), and mean femoral arterial pressure (MAP) did not differ significantly in N and CH. Isoproterenol (ISO), 0.5 mug/kg iv, produced an average increase in HR of 92 plus or minus 9 beats/min in N, but only 66 plus or minus 8 beats/min in CH (P smaller than .02). Reduction in MAP after ISO were similar. Pretreatment with propranolol, 0.15 mg/kg iv, reduced HR equally in N and CH without affecting MAP, but diminished the HR response to ISO significantly more in CH than in N. The attenuated chronotropic response to beta-adrenoceptor stimulation following chronic hypobaric hypoxia suggests a relative cardiac refractoriness secondary to an increased level of sympathetic activity.

Adrenergic beta-Agonists↗
PubMed1974

Transthoracic electrical impedance in cases of high-altitude hypoxia.

Changes in transthoracic electrical impedance (T.E.I.) due to high-altitude hypoxia (3,658 m) have been measured in 20 young, healthy Indian soldiers. They were first studied at sea level (198 m) and then rapidly transported by air to 3,658 m, where they were studied daily from day 1 to day 5 and then on days 8 and 10. The mean (+/-S.D.) T.E.I. at sea level (34.6+/-0.6Omega) fell sharply to 29.6+/-0.8Omega, 30.3+/-0.9Omega, and 30.5+/-1.1Omega on days 1, 2, and 3 (P <0.001) and levelled off at 31.5+/-0.7Omega on day 10, which was comparable to the mean value obtained in 13 persons permanently resident at high altitude (32.2+/-0.7Omega). Five sea-level residents who had acute mountain sickness (A.M.S.) or high-altitude pulmonary oedema (H.A.P.O.) had a still lower mean value (22.5+/-1.1Omega). One normal healthy subject who at sea level had a T.E.I. of 34.7Omega developed H.A.P.O. when the T.E.I. fell to 21.1Omega. Ninety minutes after the administration of 80 mg of intravenous frusemide the value increased to 35.5Omega. In another subject with A.M.S. who received 40 mg of frusemide intravenously the T.E.I. rose from 21.9 to 33.2Omega.Since the study was non-invasive the changes in impedance could not be correlated objectively with alterations in either pulmonary blood volume or pulmonary extravascular water space. In the subject, however, with x-ray evidence of H.A.P.O. and a low T.E.I. intravenous frusemide produced a marked rise in T.E.I. together with clearing of the chest x-ray picture within 24 hours, indicating an inverse relationship between impedance and thoracic fluid volume. It is suggested that with further objective verification in man the measurement of T.E.I. may be a potentially promising technique for the early detection of increased pulmonary fluid volume.

Adult↗
PubMed1970

Haemodynamic studies with peruvoside in human congestive heart failure.

The immediate haemodynamic effects of peruvoside, a cardiac glycoside obtained from the Indian plant Thevetia neriifolia Juss, were studied in six patients with congestive heart failure. The drug was found to have an immediate and powerful positive inotropic and negative chronotropic effect, like ouabain, on the failing human heart. Oral peruvoside was also effective in the treatment of congestive heart failure when used on a short-term as well as a long-term basis. It therefore seems that peruvoside is a useful cardiac glycoside in the management of congestive heart failure in man as a quick-acting intravenous preparation. It is equally effective when used orally.

Administration, Oral↗
PubMed1969

Effect of frusemide on pulmonary blood volume.

Intracardiac frusemide given to seven patients recovering from high-altitude pulmonary oedema caused a significant reduction in the pulmonary blood volume before the onset of diuresis. This supports the suggestion that the mobilization of fluid from the pulmonary circuit is responsible for the relief of symptoms in some patients with pulmonary oedema even when a diuresis does not occur.

Adult↗
PubMedDate not supplied

Antiarrhythmic effects of prostaglandins E2 and I2 on ouabain-induced cardiac arrhythmias in cats: effect of vagotomy and adrenergic neuron blockade.

The effects of i.v. prostaglandins (PGs) E2 and I2 on ouabain-induced cardiac arrhythmias were investigated in chloralose-anaesthetized cats. Bilateral vagotomy and guanethidine-pretreatment interventions were employed to elucidate the involvement of vagal and sympathetic neural influences in these effects. PGE2 (1 micrograms/kg/min i.v. infusion for 5 min) and PGI2 (4-16 microgram/kg i.v. bolus injections) effectively suppressed the ouabain-induced arrhythmias in a control group of cats. The bilateral vagotomy or guanethidine-pretreatment interventions did not significantly alter the antiarrhythmic effects of PGE2 and PGI2. It is concluded that the presence of functionally intact sympathetic and vagal nerve supply to the heart is not a prerequisite for the antiarrhythmic effects of i.v. administered PGE2 and PGI2. The possible role of direct action of these PGs on the myocardium is discussed.

Anesthesia↗
PubMedDate not supplied

Effect of pre- and posttreatment of losartan in feline model of myocardial ischemic-reperfusion injury.

This study investigated the differential effect of losartan, an AT1 receptor blocker, when administered in pre- and postischemic phases, on the biochemical, hemodynamic and oxidative stress associated with regional ischemic-reperfusion injury in cat. Losartan (5 microg/kg/min) or normal saline was administered intravenously in open chest barbiturate anesthetized cats, 15 min before and 10 min after the occlusion of the left anterior descending (LAD) coronary artery. The LAD was occluded for 15 min followed by 60 min reperfusion. In the saline treated group, there was significant depression of hemodynamic functions, i.e., mean arterial pressure (MAP), heart rate (HR), left ventricular end diastolic pressure (LVEDP) and left ventricular (LV) peak (+/-) dP/dt, along with depletion of adenosine triphosphate (ATP) of the affected myocardium. Oxidative stress during reperfusion injury was evidenced by significant increase in plasma thiobarbituric acid reactive substances (TBARS) accompanied by significant reduction in myocardial superoxide dismutase (SOD) activities. In both treatment groups, losartan caused recovery of all the hemodynamic parameters and repletion of ATP along with no significant change in plasma TBARS and myocardial SOD activity. There was no effect on catalase activity. Results from the study suggest that the effects of pre- and posttreatment of losartan are comparable in functional recovery of the heart from ischemic-reperfusion injury.

Adenosine Triphosphate↗