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Biomedical subjects

K Kar

Publications and source records attributed to K Kar.

At least 37 records · Page 2Linked to original sources
PubMed1983

Effect of antiarrhythmic drugs on serum free fatty acid levels during experimental cardiac arrhythmias in the cat.

The level of free fatty acid (FFA) in serum has been estimated before and after ventricular fibrillation (VF) induced by electrical stimulation, intravenous administration of ouabain, aconitine or ligation of the left anterior descending branch of coronary artery. FFA contents were found to be significantly increased after VF. Quinidine, disopyramide, lidocaine and phenoxybenzamine, when administered intravenously 30 min before electrical stimulation (E.S.), have no effect on serum FFA contents by themselves. All the antiarrhythmic drugs except phenoxybenzamine prevent the rise in FFA contents normally observed after VF. These drugs in appropriate doses also protect the animals against VF upto 100 volts. Propranolol did not provide protection against VF but prevented increase in FFA levels. Verapamil neither showed any protection against VF nor blocked the elevation of FFA after E.S. These results indicate that most of the antiarrhythmic drugs which are effective against the precipitation of VF by E.S. block the increase in serum FFA levels.

Animals↗
PubMed1983

Ultrastructural changes in the neural lobe of the rat pituitary following nicotine pretreatment.

The effect of nicotine on the ultrastructural changes and hormone contents of the neural lobe of the pituitary were studied in the rat. Nicotine caused a significant release of both vasopressin and oxytocin from the neural lobe. The examination of the neural lobe with electron microscope reveals the nerve terminals depleted of neurosecretory granules. These results suggest that a definite correlation exists between hormone contents and ultrastructural morphology.

Animals↗
PubMed1982

Supra spinal influence on ventricular fibrillation threshold and cardiac stores of norepinephrine in the cat.

The relationship between ventricular fibrillation threshold (VFT) as measured by voltage required to evoke ventricular fibrillation and the concentration of norepinephrine (NE) in different parts of the myocardium under experimental interventions has been studied in anaesthetized cats. A selective increase in VFT and a marked reduction in NE content have been observed after spinal transection, removal of spinal cord from cervical 6 to thoracic 6 or carotid sinus denervation. Reserpine pretreatment significantly reduces NE content of myocardium but fails to affect VFT. The fibrillating left ventricle shows a marked decline in NE content from the control level of 1.55 +/- 0.32 to 0.82 +/- 0.09 micrograms/g and there is also a similar concomitant reduction in NE content of the entire heart. Defibrillation brings back normal rhythm, but does not restore the NE content immediately. The results suggest that a marked reduction in cardiac stores of norepinephrine significantly affect VFT and that the central nervous system plays an important role in the genesis of sustained ventricular arrhythmia.

Animals↗
PubMed1978

UDP-glucose 4-epimerase from Saccharomyces fragilis. Involvement of sulfhydryl group(s) at the active site.

UDPglucose-4-epimerase (EC 5.1.3.2) from Saccharomyces fragilis is inactivated by 0.1 mM 5,5'-dithiobis-(2-nitrobenzoate) in 6 min. Unlike p-chloromercuribenzoate-inactivated or heat-inactivated enzymes, the dithiobisnitrobenzoate-inactivated enzyme retains the dimeric structure and NAD is not dissociated from the protein moiety. Inactivation of the enzyme by dithiobisnitrobenzoate can not therefore be attributed to any subsequent loss of structural integrity or to the detachment of the cofactor from the apoenzyme. The inactivated enzyme can be almost fully reactivated in the presence of mercaptoethanol and characteristic properties of native enzyme are regained. The inactivation by dithiobisnitrobenzoate can be substantially protected by UDPglucose or UDPgalactose indicating a possible critical involvement of one or more sulfhydryl groups at the active site.

Binding Sites↗
PubMed1975

Spasmolytic constituents of Cedrus deodara (Roxb.) Loud: pharmacological evaluation of himachalol.

Himachalol has been identified as the major antispasmodic constituent in the wood of Cedrus deodara. The pharmacological studies of himachalol on various isolated smooth muscles (guinea pig ileum, rabbit jejunum, rat uterus, and guinea pig seminal vesicle) and against different agonists (acetylcholine, histamine, serotonin, nicotine, and barium chloride) indicated spasmolytic activity similar to that of papaverine. It was a more potent antagonist of barium chloride-induced spasm of guinea pig ileum than papaverine but less effective in reverting a similar spasm of rabbit jejunum and had no relaxing effect alone. In the conscious immobilized cat, intragastric administration of himachalol or papaverine (100 mg/kg) produced equal inhibition of carbachol-induced spasm of the intestine, lasting about 2 hr, but himachalol had a faster onset of action. Himachalol was devoid of spasmolytic effect on the bronchial musculature of guinea pig but was 3.3 times more potent than papaverine in antagonizing epinephrine-induced contraction of the guinea pig seminal vesicle. Intravenous injection of himachalol (3-10 mg/kg) in the cat produced a dose-dependent fall in blood pressure and an increased femoral blood flow.

Animals↗