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Biomedical subjects

S C Hui

Publications and source records attributed to S C Hui.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1982

Captopril inhibits pressor responses to peripheral sympathetic nerve activation in cats and rats.

1. In cats, under chloralose anaesthesia, captopril (0.1-0.3 mg/kg i.v.) inhibited the potentiation of the pressor effects of the ganglion stimulant McNeil-A-343 caused by intravenous infusion of angiotensin I (0.1 microgram/min). 2. In both cats and rats under chloralose anaesthesia captopril (0.01-1.0 mg/kg i.v.) depressed pressor responses to McNeil-A-343 whilst not modifying those to bilateral occlusion of the carotid arteries, or intravenous injection of the ganglion stimulant dimethylphenylpiperazinium or adrenaline. 3. It is concluded that in the cat and rat captopril depresses cardiovascular responses to sympathetic postganglionic nerve activation, both in the presence and absence of exogenous angiotensin I by an action which is proximal to the terminal synapse.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1981

Cigarette smoke inhalation specifically inhibits depressor responses to prostacyclin in the rat.

Studies have been made of the effects of prior exposure to cigarette smoke on cardiovascular responses of the anaesthetized rat to arachidonic acid, prostaglandin E2 (PGE2), PGF2 alpha and PGI2. When compared with a control group, falls in systolic and diastolic blood pressure and tachycardia following intravenous PGI2 were significantly reduced in those animals exposed to smoke 1 and 24 h previously. Responses 48 h after exposure were not significantly different. Pressor effects of PGF2 alpha and depressor responses to arachidonic acid and PGE2 were not significantly affected these times. It is suggested that the specific and long lasting attenuation of the effects of PGI2 which occurs following cigarette smoke inhalation could contribute to both acute cardiovascular changes and the circulatory diseases associated with smoking.

Animals↗
PubMed1979

A study of the changes in motor behaviour caused by TRH on intracerebral injection.

20 microgram TRH injected bilaterally into the caudate-putamen, tuberculum olfactorium, nucleus accumbens, amygdala, lateral ventricles, midbrain or cerebral cortex failed to induce any increase in locomotor activity (measured using photocells), although other behavioural changes were observed after each injection, and included body shakes, limb tremor, repetitive head and limb movements, biting, scratching and an alert appearance. These behavioural changes could result in positive readings from equipment used to measure locomotor activity, but careful investigations focussing on the nucleus accumbens used photocell boxes, activity wheels and Animex recorders to emphasise the inability of intracerebral TRH (10--40 microgram) to enhance locomotor activity. Intraaccumbens TRH also failed to enhance amphetamine hyperactivity or reduce the motor depression caused by haloperidol and analeptic drugs. The data do not support a central locomotor stimulant action of TRH.

Animals↗
PubMedDate not supplied

Captopril potentiates depressor responses to arachidonic acid in the rat.

1. In chloralose anaesthetized rats intravenous administration of captopril (0.5 mg/kg) was followed by an approximately 100-fold decrease in sensitivity to the pressor actions of angiotensin I. Concomitantly there was a 100-fold increase in sensitivity to the depressor effects of bradykinin. 2. Depressor responses to intravenous prostacyclin (PGI2), prostaglandin E2 (PGE2) or a low dose of arachidonic acid (1 mg/kg) were not changed by captopril administration, but responses to a high dose of arachidonic acid (3 mg/kg), given either intravenously or into the aortic arch, were enhanced for up to two hours afterwards. 3. Depressor responses to arachidonic acid, both before and after captopril, were inhibited after intravenous indomethacin (1 mg/kg). 4. These results support the hypothesis that increased synthesis of prostaglandins in the circulation contributes to the hypotensive action of captopril.

Angiotensin I↗
PubMedDate not supplied

Attenuation by captopril of pressor responses to peripheral sympathetic nerve stimulation in rats is abolished after bilateral nephrectomy and during mineralocorticoid hypertension.

Intravenous administration of captopril (0.1-0.3 mg/kg) to normotensive pithed rats, with or without unilateral nephrectomy, was followed by a sustained fall in arterial blood pressure. Concomitantly pressor responses to electrical stimulation of the spinal sympathetic outflow (T11-L3), ganglion stimulation with McNeil-A-343 (4-(m-chlorophenylcarbamoyloxy)-2-butynyl-trimethylammonium chloride) or intravenous injection of noradrenaline were reduced. Attenuation by captopril (1 mg/kg) of pressor responses to McNeil-A-343 persisted after intravenous propranolol (1 mg/kg). Tachycardia caused by electrical stimulation of the spinal sympathetic nerves (C7-T2) was unchanged after 3.0 mg/kg captopril. After procedures reducing the activity of the renin angiotensin system, bilateral nephrectomy or induction of mineralocorticoid hypertension by unilateral nephrectomy and administration of desoxycorticosterone acetate, pressor responses to McNeil-A-343 or noradrenaline were unchanged after 1 mg/kg captopril. It is concluded that in the pithed rat, basal arterial blood pressure and the height of pressor responses to either postganglionic sympathetic nerve activation or intravenous noradrenaline depend on converting enzyme activity maintaining circulating angiotensin II levels.

Animals↗
PubMedDate not supplied

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↗