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Biomedical subjects

S Dai

Publications and source records attributed to S Dai.

At least 181 records · Page 10Linked to original sources

The effect of zinc on anaphylaxis in vivo in the guinea-pig.

The protective effects of pretreatment with zinc sulphate aerosols against bronchoconstriction induced by egg albumen or histamine aerosols were assessed in sensitized or non-sensitized guinea-pigs respectively. Pretreatment with an adequate concentration of zinc sulphate aerosol significantly prolonged the time of onset of bronchoconstriction in sensitized guinea-pigs challenged with egg albumen, but did not appreciably alter the onset time of histamine-induced bronchoconstriction in non-sensitized animals. These findings suggest that zinc aerosols may be of prophylactic value against bronchoconstriction of allergic origin.

Aerosols↗

The hemostatic effects of orally administered Yunnan Bai Yao in rats and rabbits.

The effects of orally administered Yunnan Bai Yao were studied on the bleeding time in rats and the blood clotting time in rabbits. Significant decreases were seen in both the bleeding and clotting times, observed over a 4 h period following administration. These effects were seen as early as 1/2 h and were still present at 4 h. Graded doses of Yunnan Bai Yao produced dose-related decreases in blood clotting times in the rabbits. The findings suggest that some active principle, able to affect the hemostatic mechanism, is absorbed after oral administration of the herbal preparation.

Administration, Oral↗

Intragastric NaHCO3 perfusion and vagal-induced ulcer formation in the rat stomach.

The effects of electrical vagal stimulation on gastric acid output and ulcer formation were studied in rats intragastrically perfused with saline or NaHCO3 solutions. Vagal stimulation produced a 100% incidence of glandular lesions and a significant increase in total acid output in saline-perfused stomachs. Antacid perfusion failed to prevent ulcer formation despite complete neutralization of the increased acid output. It is considered that vagal-induced gastric glandular lesions are not acid dependent.

Animals↗

Acute gastric ulcer formation in response to electrical vagal stimulation in rats.

Intermittent electrical stimulation of the left cervical vagus increased intragastric pressure and induced a 100% incidence of haemorrhagic ulcers in the glandular mucosa of rat stomachs. Atropine pretreatment of sub-diaphragmatic vagotomy prevented these effects. The findings substantiate the idea that stress-induced glandular ulcers result from vagal-mediated increased gastric contractions.

Animals↗

Effects of zinc chloride on gastric secretion and ulcer formation in pylorus-occluded rats.

The effects of 10-day pretreatment with i.p. injections of zinc chloride, 16 mg/kg, on gastric secretion and on gastric ulceration induced by stress or by acid accumulation were examined in pylorus-occluded rats. Zinc chloride pretreatment significantly reduced the volume of gastric secretion and the total acid output as well as the incidence of gastric ulcers induced either by stress or by acid accumulation. The findings support the idea zinc compounds may be useful in the treatment of gastric ulcers.

Animals↗

The haemostatic effects of the Chinese herbal drug Yunnan Bai Yao: a pilot study.

The effects of Yunnan Bai Yao on the bleeding time in rats and the blood clotting time in rabbits and man were studied. The medicinal preparation markedly shortened both the bleeding and clotting times; the decreases were significantly more intense than those inconsistently produced by starch or by starch with calcium. These preliminary findings suggest that the action of Yunnan Bai Yao appears not to be due to its pH (5.2) or to vasoconstriction, but other factors such as its calcium content or the physical effect of its particle size cannot yet be excluded.

Animals↗

Effects of stress and of autonomic blockers on gastric mucosal microcirculation in rats.

Changes in gastric mucosal microcirculation in rats were studied by using the method of intra-aortic injection of India ink, followed by microdissection of the mucosa. Acute stress, induced by restraint and exposure to cold for 2 hr, caused marked and significant vasodilatation in the gastric mucosa. This vasodilatation was prevented by pretreatment with atropine or chlorpromazine, but not by alpha- or theta-adrenoceptor blocking agents. Phentolamine caused significant vasoconstriction in the gastric mucosa of non-stressed rats, but when animals were stressed phentolamine induced a greater vasodilatation than was obtained with stress alone. These observations provide added support for the hypothesis that stress induces vagal overactivity, probably of central origin. The resulting strong contractions of the gastric wall, and compression of the intramural vessels, are probably responsible for degeneration of the mucosal cells leading to the formation of stress-induced ulcers in the rat.

Adrenergic alpha-Antagonists↗

Increased potency of vanadium using organic ligands.

The in vivo glucose lowering effect of orally administered inorganic vanadium compounds in diabetes was first reported in our laboratory in 1985. While both vanadate and vanadyl forms of vanadium are orally active, they are still not well absorbed. We have synthesized several organic vanadium compounds and one compound, bis(maltolato)oxovanadium(lV) or BMOV, has been extensively investigated. BMOV proved effective in lowering plasma glucose and lipids in STZ-diabetic rats when administered in drinking water over a 25 week period. The maintenance dose (0.18 mmol/kg/day) was approximately 50% of that required for vanadyl sulfate (VS). Secondary complications of diabetes were prevented by BMOV and no marked toxicity was noted. Oral gavage of STZ-diabetic rats with BMOV also reduced blood glucose levels. The ED50 for BMOV was 0.5 mmol/kg, while for VS the estimated ED50 was 0.9 mmol/kg. BMOV was also effective by the intraperitoneal route in STZ-diabetic rats. The ED50 was 0.08 mmol/kg compared to 0.22 mmol/kg for VS. Some animals treated p.o. or i.p. remained euglycemic for up to 14 weeks. An i.v. infusion of BMOV of 0.05 mmol/kg over a 30 min period reduced plasma glucose levels by 50% while VS was not effective.

Animals↗

The effects of metiamide on gastric secretion and stress ulceration in rats.

The effects of metiamide, a histamine H2 blocker, on gastric secretion and ulcer formation in stressed pylorus-occluded rats were investigated. Metiamide, like atropine, significantly reduced the volume of gastric secretion and total acid output in unrestrained pylorus-occluded rats. Both drugs produced greater decreases in the volumes of gastric secretion in stressed rats than in their corresponding unrestrained groups. Stress itself reduced both parameters. Metiamide, like atropine, significantly reduced the incidence of gastric stress ulcers. When given together these two drugs did not provide greater protection. The results obtained with metiamide indicate that histamine plays a role in basal gastric secretion and in the pathogenesis of stress ulcers. As no correlation between gastric acid secretion and ulcer formation was demonstrated in this study, it is suggested that H2 receptors may also be involved in gastric motility. However, the possibility that metiamide could exert its ulcer-protecting effects through other mechanisms cannot yet be excluded.

Animals↗

Morphine treatment and intravenous glucose tolerance tests in mice.

The effect of acute and chronic morphine treatment on i.v. glucose tolerance tests in mice was investigated. It was found that neither acute nor chronic morphine treatment affected the serum glucose disappearance with time after i.v. glucose loading, indicating that morphine has no significant effect on glucose tolerance. Analysis of hepatic glycogen and glucose levels in these mice revealed that morphine treatment might have some effects on glucose metabolism, but at the analgesic dose employed, did not impair the animal's physiological response to i.v. glucose loading.

Animals↗

A study of the actions of histamine on the isolated rat heart.

1. The effects of histamine on cardiac force, heart rate and coronary perfusion pressure were studied in the isolated rat heart, using the Langendorff perfused heart preparation. 2. Single injections of histamine induced dose-dependent decreases in contractile amplitude, heart rate and coronary perfusion pressure. 3. Perfusions of metiamide (above 1 x 10(-4) m) had a depressant effect on contractile force and heart rate, whereas diphenhydramine (4 x 10(-6) m) reduced only the heart rate. Both agents caused a fall in coronary perfusion pressure. 4. The negative inotropic and chronotropic effects of histamine on the isolated rat heart were not significantly influenced by either metiamide of diphenhydramine, or a combination of these drugs. However, the fall in coronary perfusion pressure induced by injections of histamine was significantly antagonized by metiamide or diphenhydramine. 5. These results suggest that the effects of histamine on the isolated rat heart may not be due entirely to stimulation of H1- or H2-receptors on the cardiac muscle cells. Evidence is presented for the existence of histamine H1- and H2-receptors in the coronary vessels.

Animals↗

The production of ventricular arrhythmias in the guinea-pigs isolated heart using hypoxic perfusion fluids containing adrenaline.

1. The effects of hypoxia, adrenaline perfusion, and their combination on cardiac rhythm were studied in the isolated perfused heart of the guinea-pig. 2. Hypoxia or adrenaline perfusion (5.5 mumol/l) produced a low incidence of ventricular arrhythmias (26% and 33%, respectively); however, the changes were not statistically significant. 3. A combination of hypoxia and adrenaline perfusion produced ventricular arrhythmias in each of twenty-three preparations: there were frequent ventricular premature contractions in eighteen preparations, and ventricular tachycardia or fibrillation in five preparations. The mean times of onset of these arrhythmias after hypoxia were 33.3 min (s.e.m. = 5.2) and 57.6 min (s.e.m. = 4.7), respectively. 4. The responsiveness of the frequent ventricular premature contractions to the antiarrhythmic effects of quinidine and lignocaine was tested in twelve preparations. Both drugs produced dose-dependent reductions in the percentage of ventricular ectopic beats. 5. These results suggest that a combination of hypoxia and adrenaline perfusion is a simple but reliable method of inducing ventricular arrhythmias in the isolated heart of the guinea-pig, and this provides a model that may be useful for the experimental evaluation of antiarrhythmic drugs.

Animals↗

Potentiation of depressor responses to arachidonic acid by angiotensin converting enzyme inhibitors in the rat.

In chloralose anaesthetized rats, intravenous administration of captopril, SQ 20881, SA 446 or MK 421 (0.5 mg/kg) potentiated the depressor responses to arachidonic acid 3 mg/kg given intravenously. Same doses of the above angiotensin converting enzyme inhibitors caused an approximately 100-fold decrease in sensitivity to the pressor effects of angiotensin I, with a concomitant similar increase in sensitivity to the depressor effects of bradykinin. Depressor responses to arachidonic acid, both before and after administering the converting enzyme inhibitors, were abolished by intravenous indomethacin (5 mg/kg). These results suggest that increased synthesis of prostaglandins in the circulation may contribute to the hypotensive effect of the angiotensin converting enzyme inhibitors, a group of newly developed antihypertensive agents.

Angiotensin I↗

Effects of acidosis or alkalosis on the actions of nifedipine on excitation-contraction coupling in the rat tail artery.

1. The clinical success of calcium channel blockers in the management of organ ischaemia is less than theoretically anticipated. Blood gas/pH changes are associated with organ ischaemia; therefore, we studied the possibility that pH changes could alter the pharmacological effects of the calcium channel blocker nifedipine on rat tail artery contracted by either noradrenaline (NA) or potassium. 2. Segments (2-2.5 cm) of the proximal third of the male Sprague-Dawley rat tail ventral artery were initially bathed and perfused with a physiological salt solution (PSS; pH 7.48) for 25-30 min, after which time bathing/perfusion was continued with a nominally calcium-free PSS made acidotic (pH 7.20), alkalotic (pH 7.67) or unaltered (control). After equilibration, the perfusion pressure (PP) responses to increasing concentrations of calcium in the presence of NA (3.0 mumol/L) or potassium (100 mmol/L) with nifedipine or its vehicle were recorded. 3. The calcium sensitivity of potassium- or NA-stimulated rat tail arteries was reduced during acidosis, as was the maximum PP in potassium- but not NA-stimulated tissues. Alkalosis reduced the calcium sensitivity in potassium- but not NA-stimulated contraction and had no effect on maximum PP. 4. The inhibitory effect of nifedipine (0.6 mumol/L) on contraction was enhanced during acidosis in either NA- or potassium-stimulated arteries and also during alkalosis in NA-treated arteries, although it had little effect during normal conditions. 5. The results indicate that changes in pH alter the vascular contractility profile in a manner dependent on the excitation-contraction coupling mode. The calcium antagonistic effect of nifedipine is pH dependent and it is suggested that pH changes associated with ischaemic conditions may alter the therapeutic profile of nifedipine.

Acidosis↗