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Biomedical subjects

S Dai

Publications and source records attributed to S Dai.

At least 163 records · Page 9Linked to original sources
PubMed1986

Effects of hypoxaemia and hyperoxaemia on some cardiovascular responses of rats to adrenaline.

Systemic blood pressure and pulse rate responses to intravenously administered adrenaline during hypoxaemia or hyperoxaemia were studied in urethane-anaesthetized rats. Hypoxaemia or hyperoxaemia was induced by ventilating the animals with 15% O2/85% N2 or with 100% O2, respectively. Hypoxaemia significantly decreased the diastolic blood pressure and elevated the pulse rate; the reflex falls in pulse rate in response to adrenaline were significantly reduced. Hyperoxaemia, on the other hand, did not cause remarkable changes in blood pressure or pulse rate, but significantly depressed diastolic blood pressure to adrenaline. It is suggested that the compensatory cardiovascular reflexes may be impaired by hypoxaemia, and that hyperoxaemia reduces vasoconstrictor response to catecholamine possibly by lessening or enhancing the sensitivities of the vascular alpha 1- or beta 2-adrenoceptors, respectively.

Animals↗
PubMed1985

Sulphasalazine and experimental stress ulcers.

The effects of sulphasalazine on gastric ulceration induced by restraint at 4 degrees C (stress) for 2 h were studied in rats. Doses of 63 or 125 mg/kg s.c., which had no effect on stomach wall prostaglandin E2 (PGE2) levels, prevented stress ulceration but not the lesions produced by indomethacin. Stress significantly increased gastric glandular mucosal PGE2 levels. Indomethacin pretreatment (20 mg/kg, p.o.) markedly reduced PGE2 levels in the same region of the stomachs, and worsened stress-induced lesion formation. Pretreatment with sulphasalazine of animals given indomethacin and then subjected to stress did not appear to affect the indomethacin component of indomethacin-stress ulceration. Oral administration of PGE2 200 micrograms/kg significantly elevated gastric PGE2 levels, but had no effect on stress ulceration. It appears that neither the antiulcer activity of sulphasalazine nor stress-induced ulceration is associated with gastric tissue PGE2 increase or decrease, respectively. The protective mechanism may result from the ability of sulphasalazine to inhibit lipoxygenase activity.

Administration, Oral↗
PubMed1985

The influence of morphine on acid secretion by the isolated rat gastric mucosa.

The influence of morphine on acid secretion by the isolated gastric mucosa was studied in adult rats. A wide range of morphine concentrations (1 X 10(-4) to 1.6 X 10(-3) M) was found to have no effect on basal acid output, or on acid secretion maximally stimulated by bethanechol or histamine. It is suggested that the opiate receptors in the rat gastric mucosa, if there are any, are not involved in modulating acid secretion.

Animals↗
PubMed1985

A study on the aetiology of reserpine ulceration and the antiulcer action of solcoseryl in rat stomach.

The aetiology of reserpine-induced gastric ulcer formation and the antiulcer effects of solcoseryl were studied in rats. Intraperitoneal injection of reserpine produced severe ulceration, as well as mast cell and histamine depletion, in the gastric glandular mucosa. Mepyramine and cimetidine markedly antagonized the gastric lesions, but did not influence the reduced mast cell count; atropine pretreatment significantly inhibited both parameters. Intramuscular injection of solcoseryl lessened ulcer severity and prevented the decreased mast cell counts and histamine levels in reserpine-treated rats. However, the same dose of solcoseryl injected intraperitoneally was ineffective. Solcoseryl, irrespective of the route of administration, did not influence the gastric secretory activities of reserpine. It is concluded that reserpine ulceration is both cholinergic- and histamine-mediated, and that the antiulcer effects of solcoseryl appear to be due to prevention of histamine depletion in the gastric mucosa.

Actihaemyl↗
PubMed1985

Gastric secretion and mucosal lesions in morphine-dependent rats.

The gastric mucosa and basal gastric secretion of morphine-dependent rats with pyloric occlusion were examined. Morphine tolerance and dependence were induced by administering increasing concentrations of morphine sulphate in the drinking water for 3 weeks, and were confirmed by a decreased analgesic response to morphine in the tail-immersion test and by occurrence of a naloxone-precipitated withdrawal syndrome, respectively. It was found that although the basal gastric secretion of morphine-dependent rats was not significantly different from that of naive animals, the former group showed a significantly higher gastric glandular mucosal ulcer index. Intraperitoneal injection of naloxone induced significant withdrawal effects but did not produce significant changes in gastric secretion or in ulcer index.

Animals↗
PubMed1985

Effects of hypoventilation on the cardiovascular responses of rats to adrenaline and acetylcholine.

Blood pressure and pulse rate in response to administered adrenaline and acetylcholine during hypoventilation were studied in urethane-anaesthetized rats. Hypoventilation was induced by decreasing the stroke volume of artificial ventilation from 1 ml/100 g to 0.3 ml/100 g. There was a significant rise in pulse rate accompanied by minimal changes in blood pressure during hypoventilation. The blood pressure and pulse rate in response to adrenaline were significantly reduced. The depressant effect of acetylcholine on pulse rate was intensified, but that on blood pressure was not significantly affected. These findings suggest that the compensatory cardiovascular reflexes may be impaired during hypoventilation.

Acetylcholine↗
PubMed1985

Human milk-derived growth factor prevents duodenal ulcer formation.

Human milk was fractionated to obtain a partially purified growth factor preparation. The growth factor in this fraction, designated as human milk growth factor III, exhibits chromatographic and biological characteristics similar to epidermal growth factor-urogastrone. Pretreatment of mice with human milk growth factor III significantly reduces the incidence, number, total length, and severity score of cysteamine-induced duodenal ulcers.

Animals↗
PubMed1984

Decreased acid secretion and gastric lesion production by morphine in rats.

The effects of graded doses of morphine on gastric secretion were studied in conscious rats with pyloric occlusion. It was found that, at doses which significantly prolonged the reaction time in the tail-immersion test, morphine significantly decreased both the volume and total acid output of gastric secretion. It was also observed that morphine produced gastric mucosal lesions in a dose-dependent manner. Pretreatment with naloxone 4 mg/kg significantly alleviated the gastric effects of morphine 32 mg/kg. It is suggested that the depressant effects of morphine on gastric secretion and the ulcerogenicity of the narcotic result from its stimulant activity on opiate receptors.

Analgesics↗
PubMed1984

Effects of SK&F 93479 on experimentally induced ventricular arrhythmias in dogs, rats and mice.

The effects of SK&F 93479, a potent histamine H2-receptor antagonist, on ventricular arrhythmias induced by coronary artery ligation in dogs and rats, and by aconitine infusion in mice were investigated. It was found that SK&F 93479 in large doses, significantly prevented the occurrence of spontaneous ventricular fibrillation and the changes in ventricular fibrillation threshold following coronary artery ligation in dogs. In rats subjected to ligation of the main left coronary artery, it significantly reduced the incidence of ventricular fibrillation, and significantly prolonged the time of onset of ventricular tachycardia and ventricular fibrillation. On the contrary, SK&F 93479 did not significantly alter the incidence or the time of onset of cardiac dysrhythmias caused by aconitine infusion in mice. These findings suggest that SK&F 93479 lacks non-specific antiarrhythmic activity and that its protective effects against coronary artery ligation may be mediated by its histamine H2-receptor antagonizing action. They also support the hypothesis that histamine may contribute to the genesis of ventricular arrhythmias resulting from acute myocardial ischaemia.

Aconitine↗
PubMed1984

Morphine preference in rats previously morphine dependent.

Morphine preference and tendency to relapse to morphine tolerance and dependence were studied in rats which were previously made morphine dependent. Tolerance to, and physical dependence on, morphine were initially produced by administration of increasing concentrations of morphine sulphate in 5% sucrose solution for 3 weeks. A test for drinking preference was performed 4 days after the rats had been successfully detoxified and showed no significant signs of morphine dependence. It was found that, while control animals drank only negligible amounts of morphine solution, previously morphine-dependent rats consumed significantly larger volumes of morphine solution and had recurrence of morphine tolerance and dependence. The present findings show that chronic administration of morphine in drinking fluid produces tolerance and physical dependence as well as addiction in rats; the latter definition is exemplified by these animals having a high tendency to relapse after successful drug withdrawal.

Animals↗
PubMed1984

Protection by SK&F 93479 against the haemodynamic effects of coronary artery ligation in dogs.

The effects of SK&F 93479, a potent histamine H2-receptor antagonist, on the changes in haemodynamics induced by coronary artery ligation were investigated in anaesthetized dogs. Intravenous bolus injection of SK&F 93479 1 mg/kg followed by 1 mg/kg/h infusion caused transient decreases in systemic blood pressure, left ventricular pressure, and dLVP/dtmax, but did not significantly alter heart rate. Coronary artery ligation produced haemodynamic depression, and this was significantly prevented by pretreatment of the animals with SK&F 93479. These findings suggest that histamine may contribute to the haemodynamic changes arising from acute myocardial ischaemia.

Animals↗
PubMed1983

Effects of naloxone on serum corticosterone and gastric lesions in stressed rats.

In rats subjected to restraint and exposure to cold, naloxone did not significantly influence the increased serum concentrations of corticosterone or the incidence of stress ulceration, but it significantly reduced the severity of gastric lesions. These findings suggest that endogenous opioids released during stress may contribute to the pathogenesis of stress ulceration. They also support the theory that the adrenocorticosteroids are unimportant aetiological factors in stress ulcer formation.

Animals↗
PubMed1983

Antagonism of pentobarbitone-induced respiratory depression by naloxone in rats.

The effects of naloxone, pentobarbitone, or their combination, on arterial blood gases were studied in urethane-anaesthetised rats. Naloxone itself did not significantly alter the blood gases. Pentobarbitone significantly decreased PO2 and elevated PCO2, and these effects were prevented by pretreatment with naloxone. Arterial blood pH was unaffected by any of the drugs. The findings suggest that naloxone lacks a specific analeptic effect, but can antagonise respiratory depression induced by pentobarbitone.

Animals↗
PubMed1982

The lack of effect of histamine on spontaneous activity in the isolated human myometrium.

The effects of histamine on the spontaneous activity of the isolated human myometrium were studied. Both the frequency and force of contractions of the muscle strips were not significantly altered by histamine. The presence of either a histamine H1- or H2-receptor antagonist in the organ bath did not significantly change the responses of the uterine muscle to histamine. These findings suggest that histamine has negligible effects on the human myometrium, possibly due to the absence, or paucity, of histamine receptors.

Adult↗
PubMed1978

Some observations on the gastric effects of phentolamine in rats.

The effects of graded doses of phentolamine on gastric secretion, gastric emptying rate, gastric mucosal mucus content and gastric mucosal lesion incidence were studied in conscious rats 2 h after intramuscular administration. In pylorus-occluded rats, phentolamine (5, 10 or 20 mg/kg) produced dose-dependent decreases in the gastric secretory volume and total acid output. Similar doses of the drug also produced dose-dependent decreases in the gastric emptying rate in animals without pylorus occlusion (intact rats), but did not affect the gastric mucosal mucus content. The incidence of gastric mucosal lesions in pylorus-occluded or intact animals rose with increasing doses. The findings are discussed in the light of the possibility that phentolamine, in the dose range examined, possesses a sympathomimetic action which would underlie the gastric lesions observed.

Animals↗
PubMed1978

Effects of zinc sulphate pretreatment on gastric acid secretion and lesion formation in rats infused intravenously with graded doses of methacholine.

The effects of intraperitoneal pretreatment with zinc sulphate (22, 44 or 88 mg/kg) were studied on gastric acid secretion and lesion formation induced by methacholine (125, 250 or 500 microgram/kg/h) infused intravenously in rats with stomachs perfused in situ. Graded infusions of methacholine produced dose-dependent increases in gastric acid secretion and lesion incidence in saline-pretreated control rats. These effects were progressively reduced by increasing pretreatment doses of zinc sulphate. The relationship between these findings and the action of zinc on gastric mast cells is discussed.

Animals↗