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C C Pang

Publications and source records attributed to C C Pang.

At least 19 recordsLinked to original sources
PubMed2001

Antibiotic treatment for threatened abortion during the early first trimester in women with previous spontaneous abortion.

BACKGROUND: We retrospectively examined the usefulness of antibiotic therapy for management of first-trimester threatened abortion in women with previous spontaneous abortion. METHODS: From 1993 through 1999, women with first-trimester threatened abortion received antibiotic therapy. Only those with gestational age less than 9 weeks and previous spontaneous abortion were included in this analysis. Women with mild abdominal cramping received amoxicillin plus erythromycin for 1 week; those with severe abdominal pain received amoxicillin plus clindamycin for 1 week. Recurrence was documented on the basis of either lower abdominal pain or vaginal bleeding. RESULTS: Of the 23 women included, 15 (65%) had abnormal vaginal flora (a score above 4, Nugent's criteria). Seven of 16 women who received amoxicillin plus clindamycin and three of seven who received amoxicillin plus erythromycin had complete resolution of lower abdominal pain and vaginal bleeding without recurrence (p=1). The recurrence rate was higher, though not significantly, in women with abnormal bacterial vaginal flora (8/15 vs. 2/8, p=0.379). Twenty-two (96%) of the 23 pregnancies were carried to term, with no identifiable neonatal anomalies. CONCLUSIONS: These results suggest the usefulness of early antibiotic therapy in preventing pregnancy loss in women with threatened abortion early in the first trimester, and warrant further clinical trials.

Abortion, Spontaneous↗
PubMed2001

Oxidative stress in the fetal lamb brain following intermittent umbilical cord occlusion: a path analysis.

OBJECTIVE: To evaluate the relative contribution of cord occlusion length intervals between occlusions and experimental duration on oxidative stress in the fetal lamb brain. DESIGN: Acute, partially exteriorised fetal lambs with intermittent total cord occlusion. SETTING: The Vivarium of Westmead Hospital, University of Sydney, Australia and The Chinese University of Hong Kong. MAIN OUTCOME MEASURES: Arterio-venous differences in the concentration of organic hydroperoxides, measured in paired samples of carotid arterial and jugular venous blood, as an index of oxidative stress in the brain. METHODS: Thirty-two fetal lambs were exposed to graded hypoxia, induced by intermittent total umbilical cord compression of 30 seconds, 60 seconds and 90 seconds duration, occurring every minute for a total of 27 occlusions over 81 minutes. Three sham experiments were also performed. In addition to organic hydroperoxides, carotid arterial blood samples were also assayed in 15 animals (two sham) for oxygen saturation, pH, hypoxanthine, xanthine and urate concentrations. A causal model for oxidative stress was defined: occlusions leading to hypoxia with a rise in hypoxanthine; reperfusion during intervals between occlusions leading to the accelerated production of xanthine and uric acid and the generation of oxygen free radicals, which in turn, are responsible for the rise in lipid peroxidation. Path analysis was performed to assess the strength of the relationships between these variables and the cord occlusion length, the interval between occlusions and the duration of the experiment. RESULTS: Sham experiments showed no change in organic hydroperoxide production. Following 30-second umbilical cord occlusions a sixfold drop in mean organic hydroperoxides was observed between carotid arterial and jugular venous levels. In contrast, following occlusions of 60 seconds duration (or longer) a median 20-fold increase in organic hydroperoxide production was observed. Path analysis revealed a strong indirect pathway from occlusion length --> hypoxanthine --> urate and weak positive pathways from oxygen saturation --> urate and from interval between occlusions --> urate. After accounting for these pathways reflecting oxidative stress, a strong direct path remained from time from first occlusion --> organic hydroperoxide production. CONCLUSIONS: Peroxidation of lipids in the brain occurs under conditions of severe hypoxia and reperfusion associated with intermittent umbilical cord occlusions of 60 seconds or longer. The path analysis supported the causal model as originally defined, with the exception that the indirect pathway via pH was found to be trivial.

Animals↗
PubMed2000

In vivo venodilator action of fenoldopam, a dopamine D(1)-receptor agonist.

The effects of the dopamine D(1)-receptor agonist fenoldopam were compared with those of the D(2)-receptor agonist R(-)-propylnorapomorphine and vehicle on mean arterial pressure (MAP), mean circulatory filling pressure (MCFP, the driving force of venous return), arterial resistance (R(a)), venous resistance (R(v)), heart rate (HR) and cardiac output (CO) in groups of thiobutabarbitone-anaesthetized rats pre-treated with i.v. injection of mecamylamine (3.7 micromol kg(-1)) and continuously infused with noradrenaline (6.8 nmol kg(-1) min(-1)). The vehicle did not alter any haemodynamic variables. All doses of fenoldopam (0.5, 2 and 16 microgram kg(-1) min(-1)) reduced MAP, R(a) and R(v), and increased CO. At the highest dose, fenoldopam also increased HR and reduced MCFP. All doses of R(-)-propylnorapomorphine (0.5, 2 and 16 microgram kg(-1) min(-1)) increased MAP but did not significantly alter CO, R(v) and MCFP. Both R(a) and HR were increased by the highest dose of R(-)-propylnorapomorphine. Our results indicate that fenoldopam reduces MAP and MCFP, and markedly increases CO through reductions of arterial and venous resistances. The effects of fenoldopam in dilating arterial resistance and capacitance vessels were similar. In contrast, R(-)-propylnorapomorphine elevates MAP through an increase in arterial resistance but has minimal effects on CO, MCFP and venous resistance. Both drugs have a small direct, positive chronotropic action at the highest dose.

Animals↗
PubMed2000

Vasodilator effects of organotransition-metal nitrosyl complexes, novel nitric oxide donors.

Nitrovasodilators cause endothelium-independent relaxation of blood vessels by generating nitric oxide (NO). We examined the relaxation and depressor effects of two organotransition-metal nitrosyl complexes, CpCr(NO)2Cl and CpMo(NO)2Cl, relative to those of the prototypal nitrovasodilators, nitroglycerin, and sodium nitroprusside (SNP), in phenylephrine-preconstricted aortic rings and conscious, unrestrained rats. CpCr(NO)2Cl, CpMo(NO)2Cl, nitroglycerin and SNP caused dose-dependent relaxation of aortic rings at maximal responses (Emax) of -118+/-4, -113+/-4, -104+/-1, and -128+/-5% and EC50 of 0.14+/-0.04, 22+/-4, 1.23+/-0.65, and 0.063+/-0.013 microM, respectively. The dose-response curve of CpCr(NO)2Cl was displaced to the right by hemoglobin, as well as methylene blue, showing involvement of the NO/cGMP pathway. Unlike nitroglycerin, preexposure for 1 h to CpCr(NO)2Cl did not alter subsequent relaxation response to the compound. Intravenous bolus injections of CpCr(NO)2Cl, CpMo(NO)2Cl, nitroglycerin, and SNP caused dose-dependent decreases in MAP with Emax of -42+/-2, -51+/-8, -56+/-6, and -58+/-2 mm Hg and EC50 of 0.041+/-0.010, 13+/-4, 1.6+/-0.4, and 0.037+/-0.004 micromol/kg, respectively. These results show that CpCr(NO)2Cl and CpMo(NO)2Cl are efficacious nitrovasodilators in vitro and in vivo.

Animals↗
PubMed2000

Effects of estrogen on venous function in rats with chronic heart failure.

The effect of 17beta-estradiol on venous function was investigated in ovariectomized rats with heart failure. Rats (50-60 days old) were ovariectomized and implanted with 60-day-release pellets that contain 17beta-estradiol (1.5 mg) or vehicle. The left coronary artery was ligated 7 days later. Another group of ovariectomized rats was given vehicle pellets and then a sham operation was performed. The rats were studied while under pentobarbital anesthesia at 7 wk after ligation. Ligated rats, relative to sham groups, had lower mean arterial pressure (MAP, -34 mmHg) and cardiac output (CO, -38%); higher arterial resistance (R(A), +12%) and venous resistance (R(V), +116%); mean circulatory filling pressure (MCFP, +40%) and left ventricular end-diastolic pressure (LVEDP, +11 mmHg); and similar cardiovascular responses to norepinephrine (NE). Treatment of ligated rats with 17beta-estradiol increased CO (+16%); reduced R(A) (-16%), R(V) (-35%), MCFP (-23%), and LVEDP (-3 mmHg); and augmented MAP, R(V,) and MCFP responses to NE. Therefore, 17beta-estradiol reduced MCFP, and this reduced preload (LVEDP). 17beta-Estradiol decreased R(V), which, along with decreased R(A) (afterload), led to an increase in CO. 17beta-Estradiol likely augmented vasoconstriction to NE through an improvement on the cardiovascular status.

Animals↗
PubMed1999

Bilateral kidney ligation abolishes pressor response to N(G)-nitro-D-arginine.

We have shown that N(G)-nitro-D-arginine (D-NNA) is 50% as potent as N(G)-nitro-L-arginine (L-NNA) in causing pressor response and 2-3% as potent as L-NNA in inhibiting endothelium-dependent relaxation in vitro. These results suggest in vivo activation of D-NNA. Furthermore, the potency of D-NNA was markedly increased after it had been incubated with homogenate of the kidney, but not plasma or homogenate of the aorta, lungs or liver. This study examined if bilateral ligation of the kidneys attenuated the biological action of D-NNA. I.v. bolus of D-NNA (16 mg/kg), L-NNA (3 mg/kg) and norepinephrine (0.25-16 microg/kg) increased arterial pressure in sham-operated rats. Bilateral ligation of the kidneys abolished pressor response to D-NNA, but not L-NNA and norepinephrine. I.v. bolus D-NNA in sham-operated rats, but not kidney-ligated rats, inhibited relaxation response to acetylcholine in pre-constricted aortic rings ex vivo. These results indicate that the kidney is the primary organ which activates D-NNA.

Acetylcholine↗
PubMed1999

Presence of donor- and recipient-derived DNA in cell-free urine samples of renal transplantation recipients: urinary DNA chimerism.

BACKGROUND: Previous studies have indicated that microchimerism is present in body tissues, peripheral blood, and plasma of recipients after organ transplantation. We hypothesize that donor-derived DNA may also be present in cell-free urine of renal transplant recipients and that the concentrations of urine DNA may be correlated with graft rejection. METHODS: Thirty-one female patients who had renal transplantation were enrolled in the study. In women with male organ donors, the SRY gene on the Y chromosome was used as a marker for donor-derived DNA. Real-time quantitative PCR for the SRY and beta-globin genes was carried out on cell-free urinary DNA from these patients. Serial urine samples from a female renal transplant recipient undergoing an acute rejection episode were also collected and analyzed with the beta-globin quantitative PCR system. RESULTS: SRY sequences were detected in the urine of 14 of 17 female patients with male organ donors. None of the 14 patients with female organ donors had detectable SRY sequences in urinary DNA. The median fractional concentration of donor-derived DNA was 8.7% (interquartile range, 1.9-26.4%). During the acute rejection episode, urinary concentrations of the beta-globin gene were markedly increased, with the concentrations returning rapidly to normal following antirejection treatment. CONCLUSIONS: Our results demonstrate that urinary DNA chimerism is present following renal transplantation. The measurement of urinary DNA using quantitative PCR may be useful for the diagnosis and monitoring of graft rejection.

Biomarkers↗
PubMed1998

Zaprinast, a type V phosphodiesterase inhibitor, dilates capacitance vessels in anaesthetised rats.

The effects of zaprinast (a type V phosphodiesterase inhibitor) on mean arterial pressure, heart rate, cardiac output, mean circulatory filling pressure, arterial and venous resistances were compared to those of sodium nitroprusside in three groups, each of intact or ganglion-blocked, Inactin-anaesthetised rats. In intact rats, zaprinast (1.5, 3.0 mg kg(-1) min(-1)) and sodium nitroprusside (8.0, 64.0,microg kg(-1) min(-1)) dose-dependently reduced mean arterial pressure and arterial resistance, but did not alter cardiac output and venous resistance. Both increased heart rate, with the effect of zaprinast less than that of sodium nitroprusside. Mean circulatory filling pressure was elevated by both doses of zaprinast but only the high dose of sodium nitroprusside. In rats given mecamylamine (3.7 micromol kg(-1), i.v. bolus) and noradrenaline (7.3 nmol kg(-l) min(-1)), zaprinast and sodium nitroprusside elicited dose-dependent reductions in mean arterial pressure, arterial and venous resistances, and mean circulatory filling pressure. Both increased cardiac output, with the effect of zaprinast greater than that of sodium nitroprusside at the low dose. Zaprinast but not sodium nitroprusside reduced heart rate. Our results indicate that zaprinast, similar to sodium nitroprusside, dilates both resistance and capacitance vessels in ganglion-blocked rats infused with noradrenaline to restore vasomotor tone. Zaprinast but not sodium nitroprusside has a direct, negative chronotropic effect on the heart.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1998

Pressor and vasoconstrictor effects of methylene blue in endotoxaemic rats.

Nitric oxide (NO) is a primary mediator of hypotension in sepsis. We examined the effects of methylene blue (MB), an inhibitor of the NO/cGMP pathway, on mean arterial pressure (MAP), cardiac output (CO), total peripheral resistance (TPR), mesenteric blood flow (MBF) and renal blood flow (RBF) in pentobarbitone-anaesthetised rats injected with lipopolysaccharide (LPS, 7.5 mg/kg). MB (1, 3 or 10 mg/kg x h) or vehicle was i.v. infused into four groups at 2.5 h after i.v. injection of LPS. Two other groups received MB or vehicle at 2.5 h after receiving saline. LPS reduced MAP, CO, RBF as well as MBF at 2.5 and 4 h, and increased TPR at 2.5 but not 4 h. Whereas MB alone had no effects on measured variables in control rats at 4 h, in LPS-treated rats, it elevated TPR at all doses and attenuated the fall in MAP at the two low doses. CO was unaltered by low doses of MB but reduced by the high dose. MBF was unaltered, but RBF was increased by the lowest dose but decreased by the highest dose of MB. Therefore, in endotoxaemia, a low dose of MB increases MAP and TPR but does not alter CO; a high dose of MB does not raise MAP but increases TPR and reduces CO.

Animals↗
PubMed1998

Chronic 17beta-estradiol augments relaxant role of basal nitric oxide in blood vessels from rats with heart failure.

The effects of chronic 17beta-estradiol on endothelium-dependent relaxation to acetylcholine (ACh) and contraction to NG-nitro-L-arginine methyl ester (L-NAME), and endothelium-independent relaxation to sodium nitroprusside (SNP) were examined on blood vessels from rats with chronic heart failure (CHF). Two groups of ovariectomized female (50-60 days) rats were implanted with pellets containing 17beta-estradiol (25 microg/day) or vehicle, and given ligation of the left main coronary artery 1 week later. Another group of ovariectomized rats was implanted with vehicle pellets, and sham-operated. After 7 weeks, thoracic aortic rings, pulmonary artery rings, and portal vein strips were prepared for in vitro studies. Relative to sham-operated rats treated with the vehicle, vessels from vehicle-treated, coronary-ligated rats had similar relaxation to ACh and SNP but reduced response to L-NAME that was significant (P<0.05) for the aorta and portal vein but not pulmonary artery. Treatment of ligated rats with 17beta-estradiol augmented responses to L-NAME in the aorta, pulmonary artery and portal vein to values above those in sham-operated rat. 17beta-Estradiol did not affect relaxation of any vessels to SNP and increased maximum relaxation to ACh only in the portal vein. Hence, 17beta-estradiol enhances the relaxant role of basal nitric oxide in CHF.

Acetylcholine↗
PubMed1998

Endothelin ET(B) receptors counteract venoconstrictor effects of endothelin-1 in anesthetized rats.

The inhibitory effects of BQ 788 (3 mg/kg, i.v., ET(B)-receptor antagonist) on endothelin-1 (ET-1)- or IRL 1620 (ET(B)-receptor agonist)-induced changes in mean arterial pressure (MAP), mean circulatory filling pressure (MCFP, driving force of venous return), arterial resistance (RA), venous resistance (RV) and cardiac output (CO) were characterized in 6 groups of pentobarbital-anesthetized rats. ET-1 or IRL 1620 (0.5, 1 and 2 nmol/kg, i.v.) dose-dependently increased MAP, RA, RV and MCFP and decreased CO. Maximum changes in RA, RV and CO elicited by ET-1 were greater than those by IRL 1620. Equimolar doses of ET-1 and IRL 1620 also caused similar initial transient decreases in MAP. BQ 788 alone slightly elevated MCFP, but did not alter other variables. The ET(B)-blocker abolished all changes elicited by IRL 1620, but only partially inhibited its responses on MCFP, showing the presence of BQ 788-insensitive receptors. BQ 788 also abolished ET-1's depressor response, partially inhibited its effect on MCFP, and markedly augmented its effects on RA, RV and CO. Thus, ET(B)-receptors counteract the sustained constrictor effects of ET-1 on arterial and venous resistance vessels Our results indicate a substantial arterial and venous dilator role for ET(B) receptors.

Anesthesia↗
PubMed1998

Venous versus arterial actions of diethylamine/nitric oxide (DEA/NO) complex and S-nitroso-N-acetylpenicillamine (SNAP) in vivo.

We studied the effects of diethylamine/NO complex (DEA/NO) and S-nitroso-N-acetylpenicillamine (SNAP), relative to those of sodium nitroprusside (SNP) and nitroglycerin (NTG), on mean arterial pressure (MAP), mean circulatory filling pressure (MCFP), arterial resistance (Ra), venous resistance (Rv), heart rate (HR), cardiac output (CO) and stroke volume (SV) in groups of Inactin-anaesthetized rats pre-treated with i.v. mecamylamine (3.7 micromol kg(-1)) and noradrenaline (6.8 nmol kg(-1) min(-1)). Doses of each that reduced MAP by 30%, 80% and the lowest dose that maximally reduced MAP were examined to allow a comparison of the compounds' dilator actions at equivalent effective depressor doses. DEA/NO (4, 32 and 256 microg kg(-1) min(-1)), SNAP (4, 32 and 256 microg kg(-1) min(-1)) and SNP (8, 32 and 128 microg kg(-1) min(-1)) caused similar dose-dependent reductions in MAP and Ra, and increases in CO and SV. NTG (0.2, 0.8 and 6.4 microg kg(-1) min(-1)) dose-dependently reduced Ra, and increased CO and SV, but lowered MAP only at the highest dose. DEA/NO, SNAP and SNP but not NTG lowered MCFP with efficacy: DEA/NO > SNAP > SNP. All four drugs reduced Rv with efficacy: DEA/NO approximately equal to SNAP > SNP approximately equal to NTG. Therefore, all compounds lowered Ra and Rv. DEA/NO, SNAP and SNP but not NTG reduced MCFP. The pharmacological profiles of DEA/NO and SNAP resemble SNP more than NTG.

Animals↗
PubMed1998

Protective effects of ethynylestradiol on the hemodynamic changes induced by lipopolysaccharide in anesthetized rats.

Estrogen pretreatment has been reported to protect rats from death induced by endotoxin. We investigated the effects of posttreatment with a synthetic estrogen, ethynylestradiol, on arterial pressure and hemodynamics in thiobutabarbitone-anesthetized rats challenged with Escherichia coli lipopolysaccharide. Rats were i.v. injected with lipopolysaccharide (1 mg/kg) followed by vehicle or a single dose of ethynylestradiol (0.25, 0.5, or 1 mg/kg) 1 h later. Another group (time-matched control) was given the vehicle. In the time-control group, there was a slight decrease in mean arterial pressure (-10 +/- 3 mm Hg) but no significant changes in cardiac output, total peripheral resistance, or heart rate over the 6-h study period. Lipopolysaccharide progressively reduced mean arterial pressure and cardiac output (-27 +/- 8 mm Hg and -52 +/- 6 ml/min, after 6 h) and increased total peripheral resistance and heart rate (+0.33 +/- 0.10 mm Hg/min/ml and +21 +/- 13 beats/min, after 6 h). None of the time-control rats died, but 36% of the rats treated with lipopolysaccharide died between 3 and 6 h after endotoxin challenge. Ethynylestradiol, at 0.25 and 0.5 completely, and at 1 mg/kg partially, restored mean arterial pressure and cardiac output at 6 h after injection of lipopolysaccharide. Ethynylestradiol at 0.5 and 1 mg/kg, but not 0.25 mg/kg, completely reversed the increase in total peripheral resistance at 6 h after injection of lipopolysaccharide. Mortality was 14% in each of the three groups of rats given ethynylestradiol 1 h after lipopolysaccharide. Therefore posttreatment with ethynylestradiol attenuated hemodynamic changes in endotoxic shock.

Administration, Oral↗
PubMed1998

Estrogen restores role of basal nitric oxide in control of vascular tone in rats with chronic heart failure.

This study examined the cardiovascular effects of 17beta-estradiol in ovariectomized rats with heart failure. Two groups (50-60 days old) were implanted with 60-day-release pellets containing 17beta-estradiol (25 microg/day) or vehicle at 7 days before ligation of the left coronary artery. Another group was sham operated and given vehicle pellets. After 7 wk, they were studied under pentobarbital anesthesia. Relative to sham-operated rats, ligated rats had reduced mean arterial pressure (MAP, -24 +/- 6 mmHg), cardiac output (-27 +/- 4 ml/min), left ventricular (LV) end-systolic pressure (-29 +/- 8 mmHg), depressor responses to ACh (-6 +/- 4 mmHg at 7.2 microg/kg) and sodium nitroprusside (SNP, -22 +/- 6 mmHg at 9 microg/kg), and pressor responses to NG-nitro-L-arginine methyl ester (L-NAME, -14 +/- 6 mmHg at 8 mg/kg) and increased LV end-diastolic pressure (LVEDP, 10.3 +/- 0.8 mmHg) but no change in total peripheral resistance (TPR). Treatment of ligated rats with 17beta-estradiol reduced TPR (-0.19 +/- 0.06 mmHg . min . ml-1), LVEDP (-3.6 +/- 1 mmHg), and responses to ACh (-16 +/- 4 mmHg) and augmented responses to L-NAME (14 +/- 3 mmHg) but did not alter other variables. Therefore, 17beta-estradiol reduces preload and afterload and restores the vasodilator role of basal nitric oxide in ovariectomized rats with chronic heart failure.

Acetylcholine↗
PubMed1998

Incidence and predictive value of congenital hypertrophy of retinal pigment epithelium in Chinese familial adenomatous polyposis patients.

OBJECTIVE: To investigate the incidence and predictive value of congenital hypertrophy of retinal pigment epithelium (CHRPE) in the Chinese familial adenomatous polyposis (FAP) patients. METHODS: Eleven FAP patients and 28 at risk relatives from 7 families were examined for CHRPE lesions. RESULTS: CHRPE was present in all 11 FAP patients. Nine CHRPE lesions were found in 9 of the 28 at risk relatives. There were great intra and inter-familial variations of the CHRPE lesions. Two at risk relatives were diagnosed to have FAP only after our screening and subsequent proctosigmoidoscopy. Nine at risk relatives were put under high surveillance because of the presence of CHRPE. CONCLUSION: The incidence of CHRPE in the FAP patients in our study is 100%. Eye examination for CHRPE for FAP patients and their at risk relatives is of very high value. A central FAP registry is thus recommended.

Adenomatous Polyposis Coli↗