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Biomedical subjects

S C Manchanda

Publications and source records attributed to S C Manchanda.

At least 55 records · Page 3Linked to original sources
PubMed1997

Protective actions of a thromboxane receptor antagonist, SQ 29548 on the ischemic myocardium: morphologic and hemodynamic effects.

The effects of thromboxane A2 (TXA2)/prostaglandin endoperoxide receptor blockade on myocardial infarct size and cardiac dynamics were determined in a canine model of 24 h acute myocardial infarction. Anesthetized open-chest dogs were subjected to left anterior descending (LAD) coronary artery occlusion. Twenty minutes post-occlusion the dogs were given i.v. saline (0.9% NaCl solution) (n = 12) or the TXA2 receptor antagonist SQ 29548 (0.2 mg/kg i.v. loading dose +0.2 mg/kg/h i.v. for 4 h) (n = 10). SQ 29548 treatment resulted in a significant (P < 0.01) reduction in infarct size. Heart rate (HR) and systolic blood pressure (SAP) were not markedly affected by the drug. The sharp rise in the left ventricular end diastolic pressure (LVEDP) in the saline-treated animals was significantly lowered by SQ 29548 treatment and the correction of this variable was maintained till 24 h post-occlusion. The lowered maximal rate of rise of left ventricular pressure (LVdP/dt max) in the saline-treated animals was corrected albeit non-significantly by the drug treatment. Thus, SQ 29548 treatment resulted in a significant salvage of myocardial tissue and marked alterations in left ventricular dynamics. The study suggests a deleterious role for thromboxane A2 in ischemia; indicating that TXA2 blockade may have potential as a mode of therapy for ischemic heart disease.

Animals↗
PubMed1997

Combination treatment with trimetazidine and diltiazem in stable angina pectoris.

OBJECTIVE: To assess antianginal efficacy and possible adverse haemodynamic effects of combination treatment with trimetazidine and diltiazem in patients with stable angina. DESIGN: Double blind, randomised, placebo controlled trial of four weeks duration. SETTING: Outpatient department of two Indian hospitals. SUBJECTS: 64 male patients with stable angina, uncontrolled on diltiazem alone. INTERVENTIONS: Diltiazem 180 mg and trimetazidine 60 mg, or diltiazem 180 mg and placebo daily. MAIN OUTCOME MEASURE: Change in exercise time to 1 mm ST segment depression. RESULTS: 33 patients (55%) had no exercise induced angina at 3 mm ST segment depression at inclusion in the study (silent ischaemia). Intention to treat analysis showed that of 32 patients in each treatment group, the number (%) of patients responding to trimetazidine compared to placebo was: for anginal attacks, 28 (87.5) v 15 (46.9), p < 0.001; for exercise time to 1 mm ST segment depression, 21 (65.6) v 9 (28.1), p < 0.003; for exercise time to angina, 12 (37.5) v 5 (15.6), p < 0.05; and for maximum work at peak exercise, 17 (53.1) v 8 (25), p < 0.02. Compared to placebo, there was net improvement with trimetazidine in mean anginal attacks of 4.8/ week (95% confidence interval (CI) 7.5 to 2.1; p < 0.002); in mean exercise times at 1 mm ST segment depression of 94.2 seconds (95% CI 182.8 to 5.6; p < 0.05), and at onset of angina of 113.1 seconds (95% CI 181.6 to 44.6; p < 0.02); and in mean maximum work at peak exercise of 1.4 metabolic equivalents (95% CI 2.4 to 0.3; p < 0.05). CONCLUSIONS: Patients with stable angina uncontrolled with diltiazem had a clinically important improvement after combination treatment with trimetazidine, without adverse haemodynamic events or increased side effects.

Angina Pectoris↗
PubMed1997

Hypertensive crisis.

Explore the source record for details and available documents.

Antihypertensive Agents↗
PubMed1997

Oxyfedrine in myocardial stunning.

Effect of oxyfedrine (OXF)(1 mg/kg) administered just before reperfusion (post-treatment) was investigated in a canine model of myocardial stunning. In the saline-treated animals, myocardial stunning was evidenced by fall in MAP, decrease in LV peak (+) dP/dt, rise in LVEDP and incomplete regeneration of myocardial ATP, after reperfusion. OXF was found to be effective in preventing the haemodynamic and metabolic changes associated with myocardial stunning.

Animals↗
PubMed1996

Effect of pressure on transmural fluid flow in different de-endothelialised arteries.

The effect of pressure on filtration across different de-endothelialised arteries has been studied experimentally, and the existing theoretical model is validated. Segments of different arteries are excised, de-endothelialised and cannulated. Bovine serum albumin Krebs solution is used as perfusate. Transmural water flux is measured by following the movement of an air bubble in a calibrated capillary, which connects the artery to a pressure reservoir; the pressure of which is varied. The hydraulic conductivity Lp is calculated from the flux values. Using available experimental parameters in the case of the thoracic and abdominal aorta, a theoretical model is validated using the experimental results. As the elastic constant for the carotid artery is not available, the theoretical model is used to calculate the elastic constant at different transmural pressures. The values calculated are in the range -4.9 x 10(-8) to -5.7 x 10(-9) cm2 dyne-1 between 50 and 135 mm Hg. Both theoretical and experimental results show a decrease in Lp values with an increase in transmural pressure for the thoracic and abdominal aorta, whereas a different trend is observed in the case of the carotid artery. The Lp values increase at 90 mm Hg, as compared with 50 mm Hg, and with a further increase in transmural pressure the values decrease.

Animals↗
PubMed1994

Role of aspirin in modulating myocardial ischemic reperfusion injury.

The role of low-dose aspirin (3 mg/kg, i.v.) in attenuating ischemic reperfusion injury was studied in a canine model. Regional ischemia for 40 min was produced by temporary occlusion of the left anterior descending coronary artery and thereafter reperfusion instituted for 3 h. Mean arterial pressure (MAP), heart rate (HR), left ventricular end diastolic pressure (LVEDP), positive (+) LV dP/dtmax and negative (-) LV dP/dtmax were monitored along with myocardial adenosine triphosphate (ATP), creatine phosphate (CP), glycogen and lactate. Following reperfusion, there was a significant fall in (i) MAP, (ii) (+) LV dP/dtmax and (iii) (-) LV dP/dtmax. LVEDP was corrected after about 2 h of reperfusion. Replenishment of only myocardial CP occurred, without any change in ATP and glycogen, although lactate accumulation was corrected. Aspirin administered 15 min before reperfusion (post-treatment) caused normalisation of LVEDP within 15 min and prevented any deterioration in (-) LV dP/dtmax, although it had no effect on MAP and (+) LV dP/dtmax. After 3 h of reperfusion (post-treatment), myocardial ATP, CP, glycogen and lactate contents became normal. The number of premature ventricular complexes was significantly reduced after aspirin treatment. The present study indicates that low-dose aspirin post-treatment can ameliorate at least some of the deleterious consequences of reperfusion injury of the myocardium.

Adenosine Triphosphate↗
PubMed1994

Influence of subvalvular fibrosis on results and complications of percutaneous mitral commissurotomy with use of the Inoue balloon.

In 136 consecutive patients who underwent percutaneous transvenous mitral commissurotomy (PTMC) with use of the single rubber-nylon (Inoue) balloon Inoue balloon angiographically analyzed subvalvular fibrosis was assessed retrospectively with regard to results and complications. There were 53 males and 83 females, with a mean age of 22 +/- 11 years (range 10 to 48 years). For the entire group, mitral valve area increased from 0.7 +/- 0.3 to 2.1 +/- 0.6 cm2 (p < 0.001). Valve area increased from 0.7 +/- 0.12 to 1.8 +/- 0.14 cm2 in patients with severe subvalvular fibrosis (n = 55) and from 0.8 +/- 0.11 to 1.9 +/- 0.12 cm2 in cases with mild to moderate subvalvular fibrosis (n = 80; p = NS). The number of patients with 2+ or greater increase in mitral regurgitation was not different between the two groups (6% vs 5.5%, p = NS). None of the patients required mitral valve replacement immediately after PTMC. We conclude that, with use of the Inoue balloon, PTMC can be successfully performed in patients with severe subvalvular fibrosis.

Adolescent↗
PubMed1993

Recovery from reperfusion injury in intact canine heart by nifedipine.

Effect of nifedipine post-treatment (100 micrograms/kg slow bolus followed by 3 micrograms/kg/min infusion) on the functional and metabolic changes of the heart after a brief regional ischemia (I) (20 min.) followed by 1 hr of reperfusion (R) was studied in pentobarbitone-anaesthetized open-chest coronary ligated dogs. In the control group, 1 hr of reperfusion failed to cause any significant recovery of the depressed LVdP/dtmax and that of the elevated LVEDP (LVdP/dtmax, pre-ischemic: 2720 +/- 90 mm Hg/sec., 20 min. of I: 2410 +/- 120 mm Hg/sec and 60 min. of R: 2210 +/- 130 mm Hg/sec. LVEDP, pre-ischemic: 5.25 +/- 0.2 mm Hg, 20 min. of I: 10.5 +/- 0.9 mm Hg and 60 min. of R: 7.5 +/- 0.5 mm Hg). However, 1 hr of reperfusion caused a significant recovery of ischemia-induced depletion of myocardial creatine phosphate (CP) content only, but not that of ATP. On post-treatment with nifedipine (i.e., infusion started just before reperfusion), there was a significant recovery in LVEDP (8.25 +/- 0.6 mm Hg after 20 min. of ischemia to 5.0 +/- 0.4 mm Hg after 1 hr of reperfusion) and there was no further deterioration in LVdP/dtmax, as observed in untreated dogs. More significantly, nifedipine caused a near normal recovery of both ATP and CP contents of the affected myocardium. Therefore, the present study shows that post-ischemic administration of nifedipine prevented reperfusion injury of the ischemic myocardium, as evidenced by both functional and metabolic recovery.

Adenosine Triphosphate↗
PubMed1993

Effect of verapamil post-treatment in myocardial reperfusion injury.

Effect of verapamil post-treatment (0.2 mg/kg bolus, followed by 0.01 mg/kg/min infusion) on the functional and metabolic changes of the heart after a brief regional ischemia (20 min) followed by 1 hr of reperfusion was studied in open-chest pentobarbitone anaesthetized dogs. In control dogs 1 hr of reperfusion failed to cause any improvement of depressed myocardial contractility (LVdP/dtmax and LVEDP) caused by 20 min of ischemia, which confirmed the earlier reported phenomenon of 'Stunned Myocardium'. Myocardial ischemia caused a significant loss of high-energy phosphate (HEP) content of the affected myocardium (ATP decreased by 60% and CP decreased by 75% of non-ischemic level). Following 1 hr of reperfusion, myocardial ATP was not replenished, though creatine phosphate became near normal. When verapamil was administered just before reperfusion, it showed a profound beneficial effect on the incidence of fatal reperfusion arrhythmias. At the end of 1 hr of reperfusion in this group, the recovery of the myocardial contractility was incomplete, but a significant replenishment of the myocardial HEP content was observed. Thus verapamil post-treatment can prevent reperfusion-induced myocardial injury but functional recovery may be delayed due to the drug's inherent direct myocardial depressant effect.

Adenosine Triphosphate↗
PubMed1991

Silent myocardial ischemia after percutaneous transluminal coronary angioplasty and its prognostic significance.

A cohort of 175 patients who underwent successful percutaneous transluminal coronary angioplasty (PTCA) were subjected to a treadmill exercise test to determine the prognostic significance of silent and symptomatic myocardial ischemia during the follow-up (average 11.7 months). The cardiac events during the follow-up were defined as cardiac death, nonfatal myocardial infarction, class III angina, and need for repeat angioplasty or coronary artery bypass surgery. During exercise, 39 patients (22%) had abnormal exercise-induced ST depression without chest pain (Group I). A group of 22 patients (13%) had both exercise-induced chest pain and ST-segment depression (Group II), and 114 patients (65%) had normal exercise test and no chest pain (Group III). The groups were similar in sex distribution, history of previous myocardial infarction, distribution of vessel disease, and presence of left ventricular dysfunction. Group III included more patients with complete revascularization. Follow-up data revealed that cardiac event rates in Groups I and II were significantly higher than in Group III (41%, 41%, vs. 16%) (p less than 0.01). The event rates in Groups I and II with multivessel angioplasty also were significantly higher than in Group III (58%, 61%, vs. 21%) (p less than 0.01). Exercise-induced silent myocardial ischemia is frequently seen early after successful PTCA and is more prevalent in patients undergoing multivessel angioplasty and incomplete revascularization. Both silent and symptomatic ischemia early after PTCA are predictors of an unfavorable prognosis.

Angioplasty, Balloon, Coronary↗
PubMed1991

Isoproterenol fails to produce myocardial necrosis in streptozotocin-induced diabetic rats.

Biochemical alterations in the hearts of non-diabetic and 5 weeks of streptozotocin-induced diabetic rats following isoproterenol (ISO) administration were compared. Serum lactate dehydrogenase (LDH) and myocardial adenosine triphosphate (ATP), creatine phosphate (CP), lactate and glycogen were used as indices of myocardial injury. Hearts from diabetic rats (blood glucose greater than 350 mg/dl), before ISO administration, had normal lactate levels but significantly low high-energy phosphate (HEP) levels and high glycogen levels in comparison to non-diabetic rats. No difference was observed in serum LDH levels between these two groups. ISO administration to non-diabetic rats caused myocardial necrosis as evidenced by a significant depletion of myocardial glycogen and HEPs along with significant myocardial lactate accumulation and an increase in serum LDH. However, the hearts from diabetic rats failed to show any significant HEP depletion, accumulation of lactate and leakage of LDH into serum following ISO-administration, though myocardial glycogen level was significantly lowered. These observations, in conjunction with earlier reports, point to the hypothesis that, in diabetes, there are certain alterations in the sarcolemma which hamper the process by which ISO causes myocardial necrosis.

Animals↗
PubMed1988

Modified method for the production of cardiac arrhythmias by ouabain in anesthetized cats.

A modified method of producing ouabain-induced cardiac arrhythmias in chloralose-anesthetized cats has been developed, whereby prolonged arrhythmias with low incidence of mortality (12%) are observed. Furthermore, the employment of a modified arrhythmia scale in the present model allowed a quantitative estimation of antiarrhythmic efficacy of test drugs and also made it possible to unravel the arrhythmogenic nature of these substances. This improved method could be conveniently used for the quantitative screening of both the antiarrhythmic or the arrhythmogenic nature of test drugs.

Anesthesia↗
PubMed1987

The involvement of the sympathetic nervous system in the centrogenic pressor and tachycardiac effects of prostaglandins E2 and F2 alpha in anaesthetised cats.

The intracerebroventricular (i.c.v.) administration of prostaglandin E2 (PGE2, 1 micrograms) and prostaglandin F2 alpha (PGF2 alpha, 10 micrograms) produced prolonged pressor and tachycardiac responses in chloralose-anaesthetised cats. Phenoxybenzamine-pretreatment completely prevented the pressor response without altering the tachycardiac response, whereas propranolol intervention completely inhibited the tachycardiac response and also attenuated the pressor response. The pretreatment with pentolinium completely antagonised both the pressor and tachycardiac responses to i.c.v. PGE2 and PGF2 alpha. The results suggest that the centrally administered PGE2 and PGF2 alpha augment sympathetic outflow to the heart and vascular system and thereby cause excitatory cardiovascular responses in anaesthetised cats.

Animals↗
PubMed1987

The vagal involvement in the antiarrhythmic and arrhythmogenic effects of prostaglandin F2 alpha on ouabain-induced cardiac arrhythmias in cats.

The effects of prostaglandin F2 alpha (PGF2 alpha) on ouabain-induced cardiac arrhythmias were investigated in chloralose-anaesthetized cats. Bilateral vagotomy and atropine intervention were employed to elucidate the involvement of vagal neural influences. PGF2 alpha (2-16 micrograms/kg i.v. bolus) predominantly suppressed the ouabain-induced ventricular and supraventricular arrhythmias and less commonly aggravated them in vagi-intact cats. The antiarrhythmic effect of PGF2 alpha was considerably, but not statistically significantly, decreased while its arrhythmogenic effect was significantly (p less than 0.05) increased in atropine-pretreated group. In vagotomised group PGF2 alpha failed to abolish the arrhythmias but it aggravated them to a degree comparable to that observed in vagi-intact group. It is concluded that the PGF2 alpha exhibits both antiarrhythmic and arrhythmogenic properties and these are largely due to elicitation of two opposing neural reflexes - one being protective and another being deleterious to ouabain-induced arrhythmias.

Animals↗
PubMed1987

The lack of involvement of central nervous system in the antiarrhythmic effects of prostaglandins E2, F2 alpha, and I2 in cat.

The role of the central nervous system (CNS) in the antiarrhythmic effects of prostaglandins (PGs) E2, F2 alpha, and I2 was studied by administering each agent into the left lateral cerebral ventricle (i.c.v. administration) of chloralose-anaesthetized cats. The cardiac arrhythmias were produced by intravenous (i.v.) infusion of ouabain (1 microgram/kg/min). The PGs E2, F2 alpha and I2 on i.c.v. administration in the dose range of 1 ng to 10 micrograms failed to inhibit ouabain-induced cardiac arrhythmias. However, when infused i.v., PGE2 (1 microgram/kg/min), PGF2 alpha (5 micrograms/kg/min), and PGI2 (2 micrograms/kg/min) effectively suppressed these arrhythmias. The standard antiarrhythmic drug propranolol (0.5-8.0 mg) on i.c.v. administration also significantly reduced the ouabain-induced cardiac arrhythmias. It is suggested that the CNS is not the site of action of PGs E2, F2 alpha, and I2 in antagonising the ouabain-induced cardiotoxicity in cats.

Animals↗
PubMed1986

Myocardial infarction in young Indian patients: risk factors and coronary arteriographic profile.

One hundred four patients (101 men, three women), under 40 years of age, with myocardial infarction (MI), underwent coronary arteriography. Eighty patients had significant obstructive coronary artery disease (CAD) (group 1), 23 had normal coronary arteries (group 2), and one patient had coronary ostial stenosis as a result of nonspecific aortoarteritis (group 3). Coronary risk factors in group 1 included smoking (76.2%), hypercholesterolemia (36.3%), hypertension (32.5%), positive family history (28.7%), and diabetes mellitus (5%). Multiple risk factors were frequent (56.2%). Smoking was common (p less than 0.01) and diabetes mellitus less frequent (p less than 0.05) as compared to older (greater than 40 years) patients with MI and arteriographically proved CAD. The frequency of one-, two-, and three-vessel disease was 33.7%, 26.2%, and 40%, respectively, in group 1. Group 2 patients were almost devoid of coronary risk factors. The only group 3 patient had left coronary ostial stenosis with no risk factors. Similar to their counterparts in developed countries, young Indian patients with MI and obstructive CAD have a high frequency of coronary risk factors, especially smoking and severe multiple-vessel disease. Since normal coronary arteriograms are also frequent in this setting, a detailed evaluation is recommended for purposes of prognosis and management.

Adolescent↗