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Biomedical subjects

S C Hui

Publications and source records attributed to S C Hui.

At least 19 recordsLinked to original sources
PubMed2000

Development of normative values for resting and exercise rate pressure product.

PURPOSE: The purpose of this study was to develop multivariate models to quantify resting, submaximal, and maximal rate pressure products (RPP). METHODS: A validation sample (N = 1623) was randomly selected from a clinically healthy population, and four cross-validation samples were randomly selected from a clinical cohort. The cross-validation samples were patients who had a negative exercise ECG with (Neg-Med, N = 179) and without cardiovascular drug (Neg-NoMed, N = 350), and patients who had a positive exercise ECG with (Pos-Med, N = 60) and without cardiovascular drug (Pos-NoMed, N = 75). Men made up 83% of the validation sample (mean age = 44.2+/-8.7) and women 17% (mean age = 39.7+/-10.1). The validation sample was used to develop multiple regression equations to quantify resting, submaximal, and maximal RPP. RESULTS: Results indicated that gender, body mass index (BMI), and physical activity level (Ex-code) were significantly related with resting RPP. Gender, age, BMI, and Ex-code were significantly related with maximal RPP. Gender, age, BMI, Ex-code, and percent of maximal heart rate at submaximal exercise (%HRmax) were significantly related with submaximal RPP. The multiple correlations for the resting, submaximal, and maximal models were 0.29 (SE = 16.75 beats x min(-1) x mm Hg), 0.87 (SE = 29.04 beats x min(-1) x mm Hg), and 0.31 (SE = 42.41 beats x min(-1) x mm Hg), respectively. The accuracy of the models was confirmed when applied to the Neg-NoMed and Pos-NoMed samples but not the Neg-Med and Pos-Med samples. This result suggest that the regression models developed from this study can be generalized to other populations where patients were not taking cardiovascular medication. Microcomputer programs were suggested to evaluate RPP at rest, maximal exercise, and submaximal exercise. CONCLUSION: Normative RPP for resting and exercise relies on multiple fitness parameters. Practical regression models are developed and can be applied to patients without cardiovascular medication.

Adult↗
PubMed1999

Inhibition of endothelium-dependent vascular relaxation by tetrandrine.

The effects of tetrandrine, a Ca2+ antagonist of bis-benzylisoquinoline alkaloid origin, on endothelium-dependent and -independent vascular responsiveness were investigated in perfused rat mesenteric artery. In endothelium-intact preparations pre-contracted with 3 microM phenylephrine and fully relaxed by 0.3 microM acetylcholine tetrandrine caused a rapid transient contraction. In endothelium-denuded preparations, tetrandrine caused only vasorelaxation of phenylephrine-contraction. The biphasic effect of tetrandrine in acetylcholine-relaxed preparations could also be mimicked by sequential applications of atropine/tetrandrine or N(G)-nitro-L-arginine-methylester (L-NAME)/tetrandrine, but atropine or L-NAME alone caused only vasoconstriction. This tetrandrine-induced transient vasoconstriction was also observed in preparations relaxed with ATP, histamine or thapsigargin (TSG), but not those relaxed with A23187, sodium nitroprusside or nifedipine. The present results suggest that tetrandrine, in addition to its known inhibitory effects on vascular smooth muscle by virtue of its Ca2+ antagonistic actions, also inhibits NO production by the endothelial cells possibly by blockade of Ca2+ release-activated Ca2+ channels.

Acetylcholine↗
PubMed1996

Influence of repeated prazosin administration on cardiovascular responses in rats and rabbits.

Prazosin was injected i.v. at a dose of 50 micrograms/kg every 2 h for 8 h in conscious rats. Its hypotensive action significantly declined. A similar effect was also observed in rabbits pretreated with prazosin (40 micrograms/kg, i.v.) every 1 h for 4 h. In prazosin-treated rabbits, the total peripheral resistance became less responsive to phentolamine stimulation. Repeated prazosin administration abolished its ability to block receptors in a model of anococcygue muscle contraction after noradrenaline (NA) stimulation. The alpha-adrenoceptors in anococcygue muscle exhibited lower pD2 to NA and lower pA2 to prazosin in prazosin-treated rats. The results demonstrate that repeated prazosin administration reduces the effectiveness of alpha-adrenoceptors blockers.

Animals↗
PubMed1996

Tetrandrine, a calcium antagonist of Chinese herbal origin, interacts with vascular muscle alpha 1-adrenoceptor.

The effects of tetrandrine (TET) on the contractile responses of rat aortic rings and perfused rat mesenteric arteries to phenylephrine (PE) were investigated. TET inhibited the maximal contraction to PE in a concentration-dependent manner. TET significantly inhibited the transient contraction in Ca(2+)-free medium presumably due to release of intracellular Ca2+ after activation of alpha 1-adrenoceptors. However, it caused a stronger inhibition of the sustained contraction in Ca(2+)-containing medium presumably the result of Ca2+ influx. TET has no inhibitory effect on caffeine-induced transient contraction. Radioligand receptor binding study using isolated dog aortic muscle membranes indicated that TET inhibited the binding of 3H-prazosin in a competitive manner, hence showing that TET interacted directly with the alpha 1-adrenoceptors. Thus, TET affected PE-induced aortic contractions by multiple mechanisms, inhibiting interaction of PE with alpha 1-adrenoceptors and interfering with PE-induced responses involving both Ca2+ entry and release.

Alkaloids↗
PubMed1996

Prevention by the 5-HT3 receptor antagonist, ondansetron, of morphine-dependence and tolerance in the rat.

1. The effect of ondansetron, a selective 5-hydroxytryptamine3 (5-HT3) receptor antagonist, was studied in morphine-addicted rats. Morphine-dependence and tolerance, induced by drinking increasing concentrations of morphine sulphate in 5% sucrose solution for 3 weeks, were demonstrated by the naloxone-precipitated withdrawal syndrome and tail flick response to a thermal noxious stimulus (water at 50 degrees C), respectively. 2. Morphine-dependence, assessed by naloxone precipitated withdrawal, was undetectable by the 6th day, when the animals drank only tap water for 7 days after the 3-week induction period. 3. When detoxified rats were offered sucrose and morphine solutions for 10 days, the recurrence of opiate solution preference with relapse to dependence and tolerance was observed. 4. Giving ondansetron (0.1 or 1 microgram kg-1; i.p.; twice daily) on the 14th day of, or 7 days prior to, the 3-week induction period reduced dependence and tolerance seen during the 3-week morphine induction and the 10-day drinking preference periods. 5. 5-Hydroxytryptamine2 (5-HT2) receptor antagonism by cyproheptadine (100 or 250 micrograms kg-1; i.p.; twice daily) did not influence morphine-dependence and tolerance. 6. These findings suggest that ondansetron may be useful for treating opiate addiction and lowering the recidivism rate.

Animals↗
PubMed1996

Tetrandrine differentially inhibits aggregation and ATP-release of rat platelets.

AIM: To examine the effects of tetrandrine (Tet) on the aggregation and ATP-release of rat washed platelets induced by several platelet activators. METHODS: Gel-filtration (Sepharose 2B) was used to isolate washed platelets from adult rats and the platelet aggragation and ATP-release were measured simultaneously. RESULTS: In the presence of Ca2+ 1 mmol.L-1, Tet 300 mumol.L-1 inhibited the aggregation induced by ADP (25 mumol.L-1), collagen (2.5 g.L-1), and thrombin (103 unit.L-1) by 62%, 60%, and 34%, respectively. It also inhibited arachidonic acid (1 mmol.L-1)-induced aggregation. Elevating intracellular Ca2+ concentration with the Ca2+ ionophore, calcimycin (30 mumol.L-1), or by blocking the intracellular calcium pump with cyclopiazonic acid (5 mumol.L-1) initiated platelet aggregation, which was also inhibited by Tet. In Ca(2+)-free medium, Tet still elicited an inhibitory effect on aggregation induced by ristocetin (2.5 g.L-1). Lower concentrations of Tet (30 nmol.L-1 to 3 mumol.L-1) failed to inhibit the aggregation (requiring Tet 10-300 mumol.L-1), but strongly suppressed ATP-release induced by ADP 10 mumol.L-1, both of which were measured simultaneously in a single sample. CONCLUSION: Tet elicits a nonselective inhibitory effect on platelet aggregation not solely due to its Ca2+ antagonism and may act on a final common pathway leading to platelet aggregation. Furthermore, Tet is a much potent inhibitor of the release of ATP in platelets.

Adenosine Triphosphate↗
PubMed1995

Mechanisms mediating NG-nitro-L-arginine methyl ester-induced hypophagia in mice.

NG-Nitro-L-arginine methyl ester (50 mg/kg s.c.), an inhibitor of nitric oxide (NO) synthase, has been reported to increase brain serotonin (5-hhydroxytryptamine, 5-HT) metabolism and induce hypophagia. Conversely, enhanced NO synthase activity is found to be accompanied by a decrease in 5-HT level. This negative correlation between NO and 5-HT in the regulation of food intake was further studied in mice. 5-HT depletion by p-chlorophenylalanine (250 mg/kg i.p., twice daily for 2 days) failed to antagonize the hypophagic effect of NG-nitro-L-arginine methyl ester. Similarly, treatment with the NO synthesis precursor, L-arginine (1000 mg/kg s.c.), did not reverse the anorexia induced by fenfluramine (10 mg/kg s.c.), a 5-HT releaser/uptake inhibitor. Pretreatment with (-)-pindolol, methylsergide and ritanserin had no effect on the hypophagic action of NG-nitro-L-arginine methyl ester, suggesting the lack of involvement of 5-HT1 and 5-HT2 receptors. The selective neuronal NO synthase inhibitor, 7-nitroindazole (12.5-50.0 mg/kg i.p.), however, did not exhibit any hypophagic effect whilst NG-nitro-L-arginine methyl ester increased gastric retention, which may subsequently induce satiety. Moreover, the hypophagic effect of NG-nitro-L-arginine methyl ester, which was unassociated with changes in water intake and malaise induction, was also unattenuated by cholecystokinin (CCK) receptor antagonists, devazepide (10 mg/kg i.p.) and PD 135,158 ([1S-[1 alpha,2 beta[S*(S*)],4 alpha ]]-4-[[2-[[3-(1 H-indol-3-yl)-2-methyl-1-oxo-2-[[[(1,7,7- trimethylbicyclo[2.2.1]hept-2-yl)oxy]carbonyl]amino]propyl]amino] -1-phenylethyl] amino]-4-oxo-butanoic acid N-methyl-D-glucamine salt; 1 mg/kg i.p.).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

The influence of peripheral or central administration of ondansetron on stress-induced gastric ulceration in rats.

Ondansetron (0.08, 0.15 or 0.3 mg/kg) injected s.c., every 12 h with the fourth dose given 0.5 h before experiments, dose-dependently lessened gastric glandular mucosal ulceration produced by cold-restraint stress for 2 h. When given intracerebrally (i.c.) (0.1, 0.5 or 1 microgram), using the same treatment regimen, infusion of ondansetron 1 microgram into the nucleus amygdaloideus centralis decreased stress-evoked ulcers; in contrast, injection of the same dose into the nucleus accumbens intensified these lesions. The associated stress-induced stomach wall mast cell degranulation was unaffected by all s.c. or i.c. doses of ondansetron. Pretreatment with disodium cromoglycate i.p. alone, or concurrently with ondansetron s.c., prevented not only ulceration but also mast cell degranulation. 5-Hydroxytryptamine3 receptor antagonism appears to inhibit stress-evoked ulcers mainly by blocking the peripheral effects of the amine after its release from the gastric mucosal mast cells.

Animals↗
PubMed1995

Effects of small-volume infusion of 7.5% hypertonic saline/6% dextran-70 on the cardiovascular function of traumatic-hemorrhagic shock rats at high altitude.

This study was designed to evaluate the effects of small-volume infusion of 7.5% hypertonic saline/6% dextran-70 (HSD) on the cardiovascular function of traumatic-hemorrhagic shock rats at simulated high altitude. 32 rats were randomly divided into four groups: 1) normal saline (NS)-treated group, 2) .9% NaCl/6% dextran-70 (Dex)-treated group, 3) 7.5% hypertonic saline (HS)-treated group, and 4) 7.5% hypertonic saline/6% dextran-70 (HSD)-treated group. The rats were exposed to a simulated high altitude of 4,000 m in a hypobaric hypoxic chamber, and traumatic-hemorrhagic shock was inflicted through fracture of the shaft of the left femur and bleeding from femoral vein to reduce mean arterial pressure (MAP) to 6.00 +/- .67 kPa within 5 min. The MAP was kept at this level for 1 h, and then a bolus intravenous injection of 4 mL/kg NS, Dex, HS, or HSD were given to the rats, respectively. In the 5 h period after treatment, it was found that MAP, left ventricular systolic pressure, maximal rate of left ventricular pressure rise and drop (+/- dp/dtmax) were significantly higher in HSD group than in the NS, Dex and HS groups. It can be concluded that 1) HSD can improve the cardiovascular function and hemodynamics of traumatic-hemorrhagic shock rats at simulated high altitude and 2) HSD is more effective than HS.

Altitude↗
PubMed1993

5-HT3 antagonists reduce morphine self-administration in rats.

1. The effects of the 5-HT3 receptor antagonists, ondansetron and tropisetron, on morphine consumption were studied in naive and morphine-dependent rats. 2. The administration of ondansetron (1 microgram kg-1, i.p. twice daily) 7 days prior to, and during a 21-day period of, morphine availability (increasing concentration from 0.1 to 0.4 mg ml-1) in 5% sucrose solution reduced opiate intake from the 9th day of morphine treatment. 3. The administration of ondansetron (0.1 microgram kg-1, i.p. twice daily) or tropisetron (0.1 microgram kg-1, i.p. twice daily) on the 14th day of the 21-day period of morphine treatment failed to reduce opiate consumption. Administration of the larger doses of tropisetron (1 microgram kg-1) or ondansetron (1 microgram kg-1) reduced morphine consumption. 4. After receiving 21 days of treatment with morphine alone or with the ondansetron or tropisetron regimens identified above, the sucrose solutions were substituted with tap water for 7 days. These detoxified rats were then allowed a free choice of sucrose or morphine for 10 days. Animals that had received concomitant treatment with ondansetron or tropisetron showed reduced morphine intake when compared with the controls treated with morphine only or with vehicle-treated controls. 5. The administration of cyproheptadine (100 or 250 micrograms kg-1, i.p. twice daily) on the 14th day of 21-day morphine treatment failed to modify morphine intake and also failed to influence the subsequent intake of the opiate in the free choice situation. 6. It is concluded that ondasetron and tropisetron can reduce morphine intake in both naive and morphine-dependent rats.

Animals↗
PubMed1992

Arachidonic acid metabolism in nicotine-treated rats and nicotine-incubated rabbit aortic smooth muscle cells.

1. The changes in plasma levels of thromboxane-B2 (TXB2) and 6-keto-prostaglandin-F1 alpha (6-keto-PGF1 alpha) were examined in rats given 5, 25, 50 or 100 micrograms/mL nicotine in drinking water for 10 days. 2. The effect of nicotine on prostacyclin (PGI2) synthesis from endogenous arachidonic acid by cultured rabbit aortic smooth muscle cells was also studied. 3. Plasma levels of TXB2 were increased dose-dependently by treatment for 10 day with nicotine. 4. 6-Keto-PGF1 alpha values were lowered dose-dependently, both in the plasma of nicotine-treated rats and in rabbit aortic smooth muscle cells incubated with the alkaloid. 5. The results suggest that endogenous synthesis of thromboxane-A2 and PGI2, as reflected by TXB2 and 6-keto-PGF1 alpha levels, respectively, is influenced by nicotine treatment. These findings may be related to cardiovascular diseases associated with cigarette smoking, but further studies are needed.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Chronic nicotine intake increases the responses to muscarinic receptor stimulation.

Chronic nicotine administration depresses the autonomic ganglia, but its effects on the muscarinic receptors at the neuroeffector sites remain unclear. The present study, using rats, examines the influence of chronic treatment with nicotine (25 micrograms/ml drinking water) for 10 or 15 days on muscarinic receptor responses, as reflected by bethanechol-evoked gastric secretion or by acetylcholine-induced decreases in mean blood pressure. Bethanechol, 0.4, 0.8, 1.6 or 3.2 mg/kg injected subcutaneously, dose-dependently increased the basal gastric secretory volume and acid output in pylorus-ligated control animals which normally drank tap water. Rats given nicotine in their drinking water for 10 or 15 days showed a further marked increase in both the volume of gastric secretion and acid output in response to bethanechol injections. Although bethanechol dose-dependently increased acid secretion, the ulcer index was very small and there was no significant difference between the control and nicotine-treated groups. The basal mean blood pressure remained normal after the 10-day nicotine treatment. Acetylcholine, 0.1, 0.3, 1 or 3 micrograms/kg given intravenously, decreased the mean blood pressure; this acetylcholine-evoked blood pressure fall was intensified by nicotine pretreatment. The findings suggest that the responses to muscarinic receptor stimulation are increased by chronic nicotine treatment for 10 or 15 days. These exaggerated effects are possibly the consequence of persistent autonomic ganglion blockade by chronic nicotine treatment.

Acetylcholine↗
PubMed1992

5-Hydroxytryptamine3-receptor blockade protects against gastric mucosal damage in rats.

Ondansetron, a specific 5-hydroxytryptamine3 (5-HT3)-blocker, injected s.c. (0.038, 0.075, 0.15 or 0.3 mg/kg) every 12 h with the fourth dose given 0.5 h before restraint at 4 degrees C (stress) or oral administration (p.o.) of 1 ml 80% ethanol, dose-dependently prevented gastric mucosal damage in female Sprague-Dawley rats (160-180 g); the animals were killed 2 or 1 h after stress or ethanol p.o., respectively. A similar pretreatment regimen with cyproheptadine (0.1, 0.25 or 0.5 mg/kg) or ketanserin (15, 30, or 75 micrograms/kg), both being 5HT2-receptor antagonists, also dose-dependently lowered the severity of stress- or ethanol-induced mucosal lesions. Only the higher doses of phenobarbitone (25 or 50 mg/kg given s.c. in a single dose 0.5 h beforehand) inhibited stress-induced gastric ulcers; however, even the lowest non-antinuclear dose (12.5 mg/kg), effectively produced CNS depression. These preliminary findings suggest that 5HT3-receptor blockade not only can antagonise stress- or ethanol-evoked gastric mucosal damage, but also may act through a peripheral mechanism.

Animals↗
PubMed1991

Chronic nicotine treatment enhances the depressor responses to arachidonic acid in the rat.

The depressor responses to intravenous injections of arachidonic acid, prostacyclin (PGI2), prostaglandin E2 (PGE2) and sodium nitroprusside were studied in chronically nicotine-treated rats. Arachidonic acid, PGI2, PGE2 and sodium nitroprusside decreased the diastolic blood pressure dose-dependently in the control animals. The vasodepressor effect of arachidonic acid was significantly enhanced in rats given nicotine 5 and 25 micrograms/ml in their drinking water for 10 days but remained unchanged in the animals treated with 1 microgram/ml nicotine for 10 days or given 1 mg/kg i.v. nicotine 10 min before administration of arachidonic acid. Indometacin abolished arachidonic-acid-induced depressor responses in both the control and nicotine-treated rats. Hypotension induced by PGI2, PGE2 and sodium nitroprusside was of similar magnitude in the control and nicotine-treated animals. It is suggested that the enhancement by chronic nicotine treatment of depressor responses to arachidonic acid could be due to changes in the formation and/or removal of its vaso-active metabolites (i.e. prostacyclin and/or thromboxane A2).

Administration, Oral↗
PubMed1989

Changes in arachidonic acid metabolite patterns in alloxan-induced diabetic rats.

The vasodepressor responses to intravenous injections of arachidonic acid, and the formation of its metabolites, were studied in rats made diabetic 1 or 2 weeks after a 1-dose alloxan treatment. Arachidonic acid dose-dependently decreased the diastolic blood pressure in normal animals, but this hypotensive effect was significantly weaker in 2-week postalloxan-treated rats. Indometacin abolished arachidonic-acid-induced depressor responses in both normal and diabetic animals. Hypotension induced by sodium nitroprusside was of the same magnitude in non-diabetic and insulin deficient rats. Plasma levels of thromboxane B2 were significantly increased in both the 1- and 2-week diabetic rats, being greater in the latter group; those of 6-keto-PGF1 alpha remained unchanged during the 2-week diabetic period. It is concluded that the attenuation by diabetes of depressor responses to arachidonic acid could be due to changes in the thromboxane/prostacyclin balance, with thromboxane formation being elevated whereas prostacyclin generation remains unaffected.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Mechanisms of captopril-induced potentiation of the depressor responses to arachidonic acid in rats.

The mechanisms underlying potentiation by captopril of the depressor responses to arachidonic acid were studied in chloralose-anaesthetized rats. Captopril, in a dose (0.5 mg/kg, i.v.) which inhibited the pressor responses to angiotensin I (0.03-1 microgram/kg, i.v.), enhanced the depressor responses to bradykinin (3-300 micrograms/kg, i.v.) and potentiated the hypotensive action of arachidonic acid (3 mg/kg, intravenously). This phenomenon was observed not only when captopril and arachidonic acid were administered intravenously, but also when these compounds were injected directly into the aortic arch. The enhancement of arachidonic acid-induced hypotension by captopril was not significantly affected by pretreatment with a low dose of aprotinin (3 mg/kg, i.v.), but was abolished by bilateral nephrectomy or by pretreatment with a higher dose of aprotinin (6 mg/kg, i.v.). It is suggested that captopril augments the depressor responses to arachidonic acid by inhibiting angiotensin converting enzyme. This results in accumulation of bradykinin which in turn increases release of vasodilator prostaglandins, originating most probably, from the kidneys. The possibility that blockade of angiotensin II formation by captopril may leave the vasodilator action of prostaglandin unopposed cannot be excluded.

Angiotensin I↗