Browsing by Author "K.S. Rao"

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Action of vinblastine on myenteric neurones of guinea-pig ileum
(1982) K.S. Rao; S.B. Deshpande; R. Rani
Motor activity of guinea-pig ileum in vitro was monitored by recording isometric tension. Superfusion of the serosal surface with vinblastine (22μM) increased the motility of ileum but failed to do so in the presence of local anaesthetics and also in preparations depolarised with K+-Tyrode. Atropine (6μM) or pentolinium (186 μM) reduced the motor response of vinblastine but higher concentration of atropine (60 μM) or pentolinium (930 μM) did not further attenuate the response. Strychnine (58 μM) reversibly blocked the atropine-resistant motor response elicited by vinblastine. It is concluded that vinblastine produces its motor effects by stimulating the non-cholinergic and to some extent cholinergic excitatory neurones of myenteric plexuses.
Blood coagulation profile in patients with acute diffuse peritonitis
(1978) B. Dube; B.N.S. Bhatnagar; K.S. Rao
Coagulation studies conducted on 42 patients with acute peritonitis of varying etiology revealed statistically significant prolongation of kaolin cephalin clotting time, decrease of platelets and elevation of plasma fibrinogen and serum fibrinogen degradation products. The relationship of the coagulopathy to bacterial invasion of peritoneal cavity was indicated by the absence of significant change in KCCT, prothrombin time, and bleeding time in patients with sterile peritoneal fluid. The results suggest a process of insidious defibrination intricately superimposed on the hypercoagulable state in these patients.
Changes in monogalactosyl diglyceride & other glyco & phospholipids in developing & aging chick cerebrum & cerebellum
(1979) K.N. Singh; K.S. Rao
Changes in the concentrations of monogalactosyl diglyceride as well as other glycolipids, cholesterol and different species of phospholipids have been studied in cerebral and cerebellar regions of developing and aging chick brain. Very low levels of glycolipids are noticed in embryonic brain while nearly reaching adult levels by the 5th day after hatching, with only a slight increase occurring beyond this stage of life. The deposition of monogalactosyl diglyceride in cerebrum was found to be unique in that all the accretion of this liquid occurs between the 16th day of embryonic life and the 5th day after hatching: that is during a period characterised by a high rate of myelination. Beyond 5 days there was little increase in the concentration of this galactolipid. Significant amounts of both choline and ethanolamine phosphoglycerides are observed in the embryonic brain with a continued increase in the levels up to 120 days after hatching. Two-fold increases in the concentrations of sphingomyelin, phosphatidylserine and phosphatidylinositol are found between embryonic life and the 5th day post-hatching, with only a slight further enhancement of the levels throughout the rest of the life span studied. These results indicate that deposition of monogalactosyl diglyceride could be used as a sensitive and specific biochemical parameter to follow myelination.
Effect of indomethacin (a prostaglandin synthetase inhibitor) on the permeability of blood-brain and blood-CSF barriers in rat
(1980) P.K. Dey; H.S. Sharma; K.S. Rao
[No abstract available]
Enhanced contractility of the rat stomach during suppression of angiotensin converting enzyme by captopril in vitro
(1991) R. Rani; K.S. Rao
Intragastric pressure (IGP) was used as an index, of the effect of serosal application of captopril (SQ 14,225; d‐3‐mercapto‐2‐methylpropanoyl‐l‐proline) on the contractility of rat stomach in vitro. Captopril, at concentrations > 0.3 μm, enhanced the spontaneous gastric motility (GM) in a concentration‐dependent manner whereas concentrations < 0.3 μm selectively potentiated 4 nm bradykinin (BK)‐evoked gastric contractions without significantly affecting the spontaneous GM. The kallikrein inhibitor, aprotinin (100 u ml−1), markedly antagonized the enhanced GM to 1.4 μm captopril and BK (4 nm)‐evoked contractions, without affecting the contractions evoked by angiotensin 1 (10 nm) and acetylcholine (0.4 μm). The angiotensin II antagonist, saralasin (50 μm) failed to mimic aprotinin. The enhanced GM to captopril was markedly inhibited by tetrodotoxin (1 μm), and partially inhibited by atropine (1 μm). These results indicate that in vitro, captopril (> 0.3 μm) enhances gastric contractility through kininase/ACE inhibitory action, presumably by increasing the concentration of undegraded tissue kinins and substance P. This motor response seems to be predominantly due to activation of the cholinergic neurones but non‐cholinergic excitatory neurones are also involved. 1991 British Pharmacological Society
Gastric relaxation evoked by captopril (SQ 14,225) in anaesthetized rats
(1988) R. Rani; K.S. Rao
Captopril-induced gastric motor response, reflected as change in intragastric pressure (IGP) in rats under urethane anaesthesia, was investigated. Single injection (i.v.) of captopril decreased the gastric motor tone in 2 distinct phases: a transient (6-10 min) short-latency relaxation (SLR) was followed by a long-lasting (1 hr) delayed relaxation (DGR). The SLR coincided with the time course of simultaneously evoked changes in the cardiorespiratory parameters by captopril. Neither phase of the gastric relaxation exhibited dose-dependency. The kallikrein inhibitor, aprotinin markedly attenuated both phases of the relaxation, the angiotensin II antagonist saralasin was without significant effect. The DGR was sensitive to subdiaphragmatic vagotomy, bilateral adrenalectomy, propranolol (3 mg/kg) and indomethacin (10 mg/kg), but resistant to guanethidine (5 mg/kg). The SLR was only partially blocked by vagotomy, guanethidine and indomethacin. It was almost abolished by adrenalectomy, though insensitive to propranolol. It is argued that the captopril-induced gastric relaxation, especially the DGR, is predominantly due to the enhanced endogenous kinin activity which reflexly releases adrenal medullary catecholamines by exciting chemosensitive vagal afferents of abdominal origin. This kinin-induced activation of vagal afferents seems to be mediated by prostaglandins.
Metabolic adaptation in nutritionally small-for-date rat brain flow of glucose carbons in vitro into glyco- and phospholipids
(1978) K.S. Rao; B.K. Tiwari; K.N. Singh
[No abstract available]
Motor reflexes of stomach elicited by phenyldiguanide in the rat
(1980) K.S. Rao
Intragastric pressure (IGP) as an index of gastric motor activity was used to investigate gastric motor responses elicited by phenyldiguanide (PDG) in rats under pentobarbitone anesthesia. PGD injected into the atrium produced an inhibitory gastric motor response whereas an aortic injection resulted in an increase in IGP. Intracarotid injections were without effect. Atropine reduced the response to atrial PDG but not to aortic PDG. Cervical vagotomy abolished the response to both atrial and aortic PDG. Guanethidine and spinal transection abolished the response to atrial PDG only. It is concluded that PDG acts by stimulation of nonmedullated vagal afferents. The efferent pathway for PDG-evoked gastric relaxation is through sympathetic nerves and the efferent system for gastric contraction involves a noncholinergic, nonadrenergic excitatory mechanism.
Protein energy ratio as a critical factor in determining growth and glycogen content of muscles in rats
(1989) S.B. Deshpande; K.S. Rao; M.B. Mandal; I.D. Saxena
[No abstract available]
Visceral reflex responses following right intra-atrial injection of phenyldiguanide in rats
(1978) P.K. Dey; K.S. Rao
[No abstract available]