Search PubMed⌕ Search

Biomedical subjects

S D Seth

Publications and source records attributed to S D Seth.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1988

Comparison between serum isonicotinic acid hydrazide (INH) levels and urinary sulfadimidine (sulfamethazine) acetylation as predictors of INH acetylator status.

The acetylator status of 40 children with pulmonary tuberculosis was investigated by (1) sulfadimidine (SDM; sulfamethazine) acetylation test in urine and (2) estimation of isonicotinic acid hydrazide (INH) levels. The antimode was at 70% based on the frequency distribution of SDM acetylation. Children acetylating less than 70% of administered SDM were taken as slow acetylators while those with more than 70% as rapid acetylators. The serum INH antimode was at 0.85 micrograms/ml. Thus serum values less than 0.85 micrograms/ml categorised a child as rapid and those with more than 0.85 micrograms/ml as slow acetylators. The sensitivity of these two methods was similar with a correlation coefficient r = 0.64. Thus the determination of the type of acetylator by SDM acetylation test is equally reliable and technically simpler and is recommended instead of INH serum concentration.

Acetylation↗
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↗
PubMed1985

Alterations in isoproterenol-induced cardiac metabolic changes by a quaternary analog of propranolol, UM-272.

Effect of UM-272, a dimethyl propranolol has been studied in experimental myocardial necrosis induced by isoproterenol (ISP, 85 mg/kg, SC X 2 days) in rats. Administration of ISP caused increased serum creatine phosphokinase (CPK), lactate dehydrogenase (LDH) and decreased myocardial glycogen, adenosine triphosphate (ATP) creatine phosphate (CP) and glycolysis through phosphofructokinase (PFK). Myocardial tissue lactate was markedly increased. All these changes resulted in development of myocardial necrosis as calculated from the CPK depletion from the injured myocardium. Rats given UM-272 (10 mg/kg or 20 mg/kg i.p.) 5 days before and 2 days during ISP administration showed significant improvement in all the parameters studied. Furthermore, UM-272 (20 mg/kg X 7 days) in control rats caused a significant (P less than .001) increase in ATP and CP content of the myocardium while other parameters remained unaltered. It would appear from the present study that the cardioprotective effect in ISP induced injury is not related to beta blockade as UM-272 is devoid of beta-blocking properties.

Animals↗
PubMed1984

Oxyfedrine and propranolol. A comparative experimental approach to protect myocardium against isoprenaline-induced myocardial necrosis.

Myocardial necrosis was produced in rats by isoprenaline (ISP) administration (85 mg X kg-1 s.c.) for two consecutive days. Rats sacrificed at 12, 24, 30, 36 and 48 h, respectively, after the last injection of ISP showed a marked increase in serum enzymes, viz. creatine phosphokinase (CPK), lactic dehydrogenase (LDH) and aspartate transaminase (AST) and tissue content of lactate. In addition, there was a significant reduction in the glycogen content of myocardium and the activity of enzyme phosphofructokinase (PFK) was changed in biphasic fashion, i.e. initial enhancement of activity was followed by a persistent fall. All these changes were present along with typical infarct-like necrosis as seen microscopically. Both oxyfedrine (OXF, 2, 4 and 8 mg X kg-1 i.m.) and propranolol (PROP, 1, 2 and 4 mg X kg-1 i.m.) administered for 5 days before and two days during ISP administration were effective in providing protection. However, with 8 mg X kg-1 dose of PROP sporadic high mortality was observed. Serum AST and CPK levels in OXF (4 and 8 mg X kg-1) and PROP (2 and 4 mg X kg-1) pretreated animals returned back to the range of controls. Unlike OXF, the LDH level in PROP pretreated rats, though reduced significantly, remained always higher than the control values. The beneficial effect of OXF on myocardial glycolytic flux was dose-dependent. 8 mg X kg-1 of OXF increased (31%) the glycogen content significantly (p less than 0.01) and the activity of enzyme PFK and tissue lactate content were brought back to normal. PROP did not exhibit dose-dependent reduction in the lactate content of the myocardium and it was never restored back to the range of control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Interaction of ouabain and propranolol in the central nervous system. Neurally-mediated effects on the cardiovascular system.

The effect of intracerebroventricular (i.c.v.) ouabain alone and after pretreatment with i.c.v. (+/-)-propranolol, (+)-propranolol, UM-272 (a quaternary analogue of propranolol) and lignocaine, on arterial blood pressure (BP), heart rate (HR) and cardiac rhythm was investigated in chloralose anesthetized, vagotomized cats. Ouabain elicited an increase in BP and HR followed by cardiac arrhythmias of ventricular origin. Pretreatment with (+/-)-propranolol, (+)-propranolol or UM-272 attenuated/prevented the cardiovascular effects of ouabain whereas lignocaine did not modify the response appreciably. Since UM-272, which lacks local anesthetic activity and beta-blocking activity also shared the antagonism with (+/-)-and (+)-propranolol, it is deduced that neither beta-blocking nor local anesthetic activity of propranolol could be responsible for this antagonism. This is supported by the fact that lignocaine which has a comparable local anesthetic effect of propranolol failed to modify significantly the cardiovascular response to ouabain. The antagonism appears to be a direct neural depressant effect independent of local anesthetic action. The neural depressant effect may be due to an interference in depolarization process and/or a neurone-blocking effect.

Animals↗