Biomedical subjects

C Y Hong

Publications and source records attributed to C Y Hong.

At least 91 records · Page 5Linked to original sources

PubMed1997

Portal hypotensive effects of tetrandrine and verapamil in portal hypertensive rats.

The portal hypotensive effects of tetrandrine and verapamil (both calcium-channel blockers) were assessed in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Both tetrandrine (4, 8, 16 and 24 mg kg-1) and verapamil (0.5, 1.0, 1.5 and 2.0 mg kg-1) induced dose-dependent decreases of portal venous pressure and mean arterial pressure after intravenous infusion. for example, infusion of tetrandrine (16 mg kg-1) induced a maximum reduction of portal venous pressure and mean arterial pressure approximately 1 min after the start of infusion. Portal venous pressure decreased from baseline (12.5 mmHg) to 10.0 mmHg, and mean arterial pressure from baseline (90 mmHg) to 80 mmHg. Heart rate decreased from 250 to 240 beats min-1. At 24 mg kg-1, tetrandrine reduced portal venous pressure and mean arterial pressure to 20.3 +/- 2.4% and 28.4 +/- 1.4% of baseline, respectively. Our results show that both tetrandrine and verapamil induce portal pressure reduction in portal hypertensive animals.

Alkaloids↗

PubMed1997

The hemodynamic effects of AT-112, an analog of ketanserin, in portal hypertensive rats.

A serotonin mechanism has been reported to contribute to the hyperdynamic circulation of portal hypertension. Different studies have demonstrated that serotonin antagonists decrease portal pressure in portal hypertensive patients and animals. The present study was undertaken to investigate the effect of AT-112, an analog of ketanserin, on portal hypertension induced by partial portal vein ligation in rats. Since ketanserin is known to possess alpha 1-adrenergic antagonistic activity, the effect of AT-112 was compared to that of prazosin. A single dose (prazosin 4.2 micrograms/kg, AT-112 1 mg/kg) was chosen to produce a similar hypotensive effect (-20 +/- 4% for prazosin and -24 +/- 4% for AT-112). At this dose, prazosin significantly decreased total peripheral resistance whereas AT-112 significantly decreased cardiac index and heart rate. Both agents significantly decreased the portal tributary blood flow and portal pressure. In rats receiving AT-112, a significant correlation was found between the magnitudes of decrease in cardiac index and the decrease in portal tributary blood flow. We also found that the magnitude of reduction in portal pressure was greater following AT-112 administration. This study suggested that AT-112 may have more beneficial hemodynamic effects than prazosin in portal hypertensive rats. Our results provide further support for the serotonergic mechanism in the pathogenesis of hyperdynamic circulation in portal hypertension.

Animals↗

PubMed1997

Hemodynamic effects of chronic tetrandrine and propranolol administration on portal hypertensive rats.

The purpose of this study was to investigate the therapeutic effects of tetrandrine and propranolol, alone or in combination, on portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Animals were allocated into one of the four groups: vehicle group (0.1 N.HCl, 0.7 ml/day), tetrandrine group (50 mg/kg/ day), propranolol group (30 mg/kg/day), and tetrandrine (50 mg/kg/day) plus propranolol (30 mg/kg/day) group. Drug or vehicle was administered by gavage for consecutive 9 days. After 9 days of treatment, the portal venous pressure and mean arterial pressure in each treatment group were significantly lower than those in the vehicle group. The cardiac index was not changed by tetrandrine alone, but reduced in the two groups receiving propranolol alone or in combination. Total peripheral resistance was significantly decreased in the tetrandrine group and significantly increased in the tetrandrine plus propranolol group as compared with the vehicle group. Our results suggested that tetrandrine or propranolol alone induced portal hypotensive effects, with propranolol achieving better antihyperdynamic effects in terms of cardiac index, and in combination propranolol effects predominated over those of tetrandrine.

Administration, Oral↗

PubMed1997

Effect of trilinolein on superoxide dismutase activity and left ventricular pressure in isolated rat hearts subjected to hypoxia and normoxic perfusion.

Oxygen-derived free radicals have been implicated in the development of myocardial injury during hypoxia/reperfusion. Antioxidants can effectively inhibit the formation of free radicals and ameliorate the myocardial damage which may occur during hypoxia/reperfusion. Trilinolein is a triacylglycerol recently purified from the traditional Chinese medicinal plant Panax pseudo-ginseng. It has linoleic-acid residues as the only type of fatty acid residue in all three esterified positions of the triacyglycerol. It has been proposed that decreased endogenous superoxide dismutase (SOD) activity may contribute to free radical-mediated reperfusion injury of the ischemic myocardium. In the present study, when isolated rat hearts were subjected to hypoxia for 10, 30, 60 and 90 min without normoxic perfusion, a significant decrease in Mn-SOD activity was shown throughout the period of hypoxia, whereas the Cu.Zn-SOD activity was increased at 10 and 30 min but was not different from the baseline at 60 and 90 min of hypoxia. In rat hearts pretreated with 10(-7) mol/l trilinolein and subjected to 60 min of hypoxia without normoxic perfusion, Cu.Zn-SOD was augmented compared with baseline and compared with hearts subjected to 60 min of hypoxia without trilinolein, whereas Mn-SOD activity was still reduced compared with baseline, although less so than after 60 min of hypoxia without trilinolein. Pretreatment with trilinolein was associated with better preservation of left ventricular function during hypoxia and more rapid return to recovery during normoxic perfusion. This myocardial protective effect may be related to an antioxidant effect through potentiation of SOD, particularly Cu.Zn-SOD during hypoxia.

Animals↗

PubMed1997

Postural stability in non-insulin dependent diabetics.

Postural stability in 55 non-insulin dependent diabetics was compared with 53 non-diabetic controls matched for age and gender. The study was conducted in a primary care clinic, using a computerised postural sway system. Changes in the centre of pressure while the subjects stood on a force platform were recorded, and sway parameters computed using customised software. Clinical data were obtained by interview, physical examination, and from case records. Results of the study showed that non-insulin dependent diabetics were more unstable than the non-diabetic controls for four out of the six parameters studied (namely L, length of sway path; Vel, average speed of centre of pressure along its path; Ao, area included within the path of the centre of pressure; and Ae, 95% confidence elliptical area), after adjusting for height, weight, adequate sleep and alcohol intake the night before, and history of bone or thyroid disorders. Amongst diabetic subjects, significant factors associated with postural stability were age, weight, presence of peripheral neuropathy or cataract, metformin, use, and HbAlc levels > 9%. Further studies are indicated to look into factors affecting postural stability (other than diabetic neuropathy) in greater depth.

Adult↗

PubMed1996

The in vitro antioxidant activity of trilinolein and other lipid-related natural substances as measured by enhanced chemiluminescence.

There is abundant evidence for the premise that oxygen-derived free radicals (OFR) mediate ischemia/reperfusion injury to the myocardium. OFR scavengers such as superoxide dismutase can effectively reduce damage through lipid peroxidation during ischemia/reperfusion. Enhanced chemiluminescence, which has been used to measure OFR, was used to measure the antioxidant activity of fatty acids (palmitic and linoleic acid) and triglycerides (triolein, tristearin) and natural plant antioxidants (magnolol, catechin, trilinolein). Trilinolein, which has recently been isolated from natural products, as well as the well-known water soluble analogue of vitamin E-Trolox, were used as control. During pretreatment with chemicals, at concentrations of 10(-9) to 10(-7) M, enhanced chemiluminescence of linoleic acid (C 18:2) showed a dose-responsive reduction of OFR with a maximal mean reduction of -31.9% when compared to baseline. A saturated fatty acid such as palmitic acid (C 16:0) showed only relatively weak antioxidant activity at concentrations of 10(-7) to 10(-6) M with a maximum reduction of OFR of- 15.2% only. control chemicals such as trilinolein and Trolox showed significant antioxidant activity. At concentrations between 10(-10) and 10(-6) M and trilinolein has the most potent antioxidant activity with a maximal mean reduction of OFR of -48.0%, whereas Trolox showed only -39.2%. As for the natural plant antioxidants, only catechin showed potent antioxidant activity (-40%). Polyunsaturated triglycerides such as triolein (oleic acid, C 18:1) also possess significant OFR scavenging effect (-31.9%) whilst saturated triglycerides such as tristearin (stearic acid, C 18:0) had only relatively weak antioxidant activity (-15.2%). Generally, the antioxidant activity of unsaturated compounds is stronger than saturated compounds; double-bond existence may partially explain this phenomenon.

Antioxidants↗

PubMed1996

Chronic administration of octreotide increases vascular responsiveness in rats with portal hypertension.

1. It has been reported that ortreotide partially corrects the hyperdynamic state in patients and animals with portal hypertension. The aim of the present study was to investigate whether chronic administration of octreotide can increase vascular responsiveness in rats with portal hypertension. 2. Portal hypertension was induced by partial portal vein ligation. Octreotide was given for 9 days subcutaneously (100 micrograms/kg every 12 h) starting 1 day before ligation. The aorta and mesenteric artery were then removed to study contraction after pressure recording. 3. Octreotide treatment significantly reduced portal pressure and plasma glucagon concentrations compared with the vehicle-treated group. Both phenylephrine and vasopressin induced concentration-dependent contractile responses in the aorta and mesenteric artery from both groups. The maximum contractile responses to phenylephrine and vasopressin in aorta and mesenteric artery were significantly greater in the octreotide-treated group than in the vehicle-treated group. The EC50 values for phenylephrine and vasopressin were significantly different in the aorta, but not in the mesenteric artery, but not in the mesenteric artery, between the two groups. In contrast, octreotide treatment did not alter the contractile responsiveness of arteries rom sham-operated rats. 4. These results show that, in rats with portal vein stenosis, octreotide increases arterial contractile responsiveness and reduces portal pressure.

Animals↗

PubMed1996

Myocardial protective effect of honokiol: an active component in Magnolia officinalis.

Honokiol is an active component of Magnolia officinalis. It was reported to be 1000 times more potent than alpha-tocopherol in inhibiting lipid peroxidation in rat heart mitochondria. In this study, we investigated the in vivo antiarrhythmic and antiischemic effects of honokiol in coronary ligated rats. Male Sprague-Dawley rats were anesthetized with urethane. Honokiol, at dosages of 10(-7) g/kg, 10(-8) g/kg, and 10(-9) g/kg, was administered intravenously 15 min before ligation of the coronary artery. Incidence and duration of ventricular tachycardia and ventricular fibrillation during 30 min coronary ligation were significantly reduced by 10(-7) g/kg honokiol. Ventricular arrhythmia during 10 min reperfusion after the relief of coronary ligation was also reduced. In rats subjected to 4 hours coronary ligation, 10(-7) g/kg, 10(-8) g/kg, and 10(-9) g/kg honokiol significantly reduced the infarct zone. We concluded that honokiol may protect the myocardium against ischemic injury and suppress ventricular arrhythmia during ischemia and reperfusion.

Animals↗

PubMed1996

Magnolol reduces infarct size and suppresses ventricular arrhythmia in rats subjected to coronary ligation.

1. Magnolol is an active component of Magnolia officinalis. It is 1000-times more potent than alpha-tocopherol in inhibiting lipid peroxidation in rat heart mitochondria. In the present study, the in vivo antiarrhythmic and anti-ischaemic effects of magnolol in coronary ligated rats were investigated. 2. Male Sprague-Dawley rats were anaesthetized with urethane. Magnolol, at dosages of 10(-7), 10(-8) and 10(-9) g/kg, was administered intravenously 15 min before ligation of the coronary artery. 3. The incidence and duration of ventricular tachycardia and ventricular fibrillation during 30 min coronary ligation were significantly reduced by magnolol. Ventricular arrhythmias during 10 min reperfusion after the relief of coronary ligation were also reduced. 4. In rats subjected to 4 h coronary ligation, 10(-7) and 10(-8) g/kg magnolol significantly reduced infarct size. 5. We conclude that magnolol may protect the myocardium against ischaemic injury and suppress ventricular arrhythmia during ischaemia and reperfusion.

Analysis of Variance↗

PubMed1996

In vitro and in vivo evaluations of LB20304, a new fluoronaphthyridone.

In vitro activity of LB20304 against 1,231 clinical isolates was evaluated and compared with those of ciprofloxacin, sparfloxacin, lomefloxacin, and ofloxacin. LB20304 demonstrated the most potent activity against gram-positive bacteria. It was 32- to 64-fold more active than ciprofloxacin against methicillin-susceptible Staphylococcus aureus, methicillin-resistant S. aureus, methicillin-resistant Staphylococcus epidermidis, and Streptococcus pneumoniae (penicillin G resistant). LB20304 was also highly active against most members of the family Enterobacteriaceae. Its activity was more potent than those of sparfloxacin, ofloxacin, and lomefloxacin and comparable to that of ciprofloxacin. The protective activities of LB20304 against systemic infections caused by gram-positive bacteria in mice were superior to those of ciprofloxacin and sparfloxacin. Against infections by gram-negative bacteria, LB20304 was slightly less active than ciprofloxacin.

Animals↗

PubMed1996

Trilinolein preserves mitochondria ultrastructure in isolated rat heart subjected to global ischemia through antioxidant activity as measured by chemiluminescence.

Oxygen-derived free radicals (OFR) have been proposed as the cause of myocardial damage through lipid peroxidation during ischemia and reperfusion. Antioxidants can effectively ameliorate the damage induced by lipid peroxidation. Trilinolein is a triacylglycerol recently purified from the well known traditional Chinese herb Panax pseudoginseng, which has been used in treating circulatory disorders among Chinese for hundreds of years; it has linoleate as the only fatty acid residue in all three esterified positions of glycerol. This chemical has recently been demonstrated to have antioxidant activity by enhanced chemiluminescence. The addition of phorbol myristic acetate (PMA) to medium containing leukocytes produces OFR; this phenomenon was measured by chemiluminescence. Addition of trilinolein to medium containing leukocytes preceding the addition of PMA suppressed the production of OFR. The control value of chemiluminescence of a medium containing leukocytes with addition of PMA was 9.23 +/- 1.19 x 10(3) mV. The most effective concentration of trilinolein was 10(-7) mol/l which decreased the signals to 4.59 +/- 0.02 x 10(3) mV (p < 0.001). The antioxidant effect had a concentration-response curve similar to alpha-tocopherol. After pretreatment for 15 min with trilinolein at a concentration of 10(-7) mol/l in isolated perfused rat heart which had been subjected to 60 min of global ischemia, the integrity of the rat heart mitochondria was preserved as examined under the electron microscope. No swelling of mitochondria occurred and there was good alignment of cristae and absence of amorphous density. Previous experiments have shown that trilinolein can also improve erythrocyte deformability in vitro. Infarct size reduction of about 50% was also demonstrated in in vivo rat heart subjected to 4 h coronary occlusion. The mechanism of myocardial protection, in addition to the antioxidant effect, is suggested as maintaining the membrane fluidity of cardiomyocytes.

Animals↗

PubMed1996

Vascular hyporesponsiveness in aorta from portal hypertensive rats: possible sites of involvement.

Vascular hyporesponsiveness in portal hypertension has been proposed to be due to postreceptor defect. The present study was aimed to investigate possible sites of involvement in such hyporesponsiveness. Portal hypertension was induced by partial portal vein ligation (PVL). Concentration-response curves to KCI and phenylephrine in both groups showed that the Emax values were significantly lower in the PVL group. The EC50 values were not different between the two groups. In Ca++ free condition, phenylephrine induced a phasic contraction, which was significantly smaller in the aorta from PVL rats. Cumulative readdition of CaCl2 (1.0-2.5 mM) induced tension increases, which were all significantly lower in the PVL group. Basal contents of [3H]inositol phosphates in the aorta were similar between the two groups. Phenylephrine induced concentration-dependent increase of [3H]inositol phosphates in the aorta from both groups. The responses at 10(-8), 10(-7), 10(-6) and 10(-5) M were significantly smaller in the PVL group than in the sham-operated group. Both okadaic acid and phorbol 12,13-dibutyrate induced slowly developing contractile responses in the aorta. The responses were similar between the two groups at all time points. Our results suggested that in the aorta from PVL rats, vascular hyporesponsiveness was observed, together with decreased contractile responses due to: voltage- and receptor-dependent calcium influx as well as intracellular calcium release, and decreased receptor-coupled inositol phosphate formation. Contractile responses due to activation of protein kinase C or phosphatase inhibition were not impaired.

Animals↗

PubMed1996

The advance directive--a review.

The advance directive is a document that enables a competent individual to specify the form of health care he would like to have, in the event that he is unable to make such decisions in the future. This review paper traces the development of the advance directive from 1967, when it was first proposed by Luis Kutner. The Karen Ann Quinlan case and the Nancy Cruzan case are cited as examples of the case for the advance directive. The argument is that advance directives assist doctors, patients, family members and other carers with the increasingly complex health care decision making. Reservations have been expressed about the anticipatory nature of the decision, possible conflict with personal and religious ethics and the risk of cost containment considerations being over-riding concerns. The advance directive in America has undergone changes since the California Natural Death Act 1976 was passed. In the 1980s, "terminal" included permanent unconsciousness and advanced dementia. The declarant was also given a wider choice of treatment procedures that they wish to be withheld. Proxy directives were also introduced. In the 1990s, the declarant is even allowed to request the use of life-prolonging procedures. When appropriately implemented, the advance directive can perform its intended functions of clarifying the patient's perspective on life, death and medical care. When it is vague in terminology or applied to patients with uncertain prognoses, it can cause confusion to the patient's carers; and when improperly used, it can become an instrument not of patient's preferences, but of economic purpose, family bias, or physician's values.

Advance Directives↗

PubMed1995

Endothelium-dependent vasorelaxant effect of trilinolein: mediated by nitric oxide and cyclic GMP.

At concentrations ranged from 0.1 nM to 1 microM, trilinolein concentration-dependently relaxed the phenylephrine-induced constriction of isolated rat aorta. Concentration-response curves for the interaction between trilinolein and phenylephrine showed that trilinolein was unlikely a competitive antagonist of phenylephrine. The vasorelaxant effect of trilinolein was dependent on the presence of intact endothelium. Both NG-nitro-L-arginine methyl ester and methylene blue antagonized this vasorelaxant effect. L-arginine partially reversed the effect of L-NAME on trilinolein. Linoleic acid had no vasorelaxant effect. We concluded that trilinolein is an endothelium dependent vasorelaxant and the underlying mechanism could be a stimulation of the nitric oxide and cyclic GMP pathway.

Amino Acid Oxidoreductases↗

PubMed1995

Fructus aurantii reduced portal pressure in portal hypertensive rats.

The purpose of this study was to investigate the effects of Fructus Aurantii (the unripe fruits of Citrus aurantium L.) on portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague-Dawley rats. Sham-operated (Sham) rats served as controls. Hemodynamic and in vitro contractile studies were performed at 14 days after surgery. Both the aqueous extract of Fructus Aurantii and synephrine, one of its purified principles with pressor activity, were infused into the conscious PVL and Sham rats via a syringe pump. Fructus Aurantii (1.25, 2.5, & 5.0 mg/kg/min) dose-dependently reduced portal pressure in PVL and Sham rats, with the percentage change in portal pressure more pronounced in PVL rats. Mean arterial pressure was dose-dependently elevated by Fructus Aurantii. Synephrine (0.095, 0.19, & 0.38 mg/kg/min) also dose-dependently reduced portal pressure and elevated mean arterial pressure in PVL and Sham rats. Fructus Aurantii (2.8-280 micrograms/ml) induced dose-dependent contractile responses mainly in aorta and mesenteric artery, but little response in portal vein. The results showed that Fructus Aurantii infusion reduced portal pressure, possibly by way of arterial vasoconstriction.

Animals↗

PubMed1995

The potencies of synthetic analogues of saxitoxin and the absolute stereoselectivity of decarbamoyl saxitoxin.

The potencies of synthetic saxitoxin (+/- STX) and six of its synthetic analogues, including the enantioselectively synthesized unnatural (-)enantiomer of decarbamoyl saxitoxin (dcSTX), were measured and compared to those of natural saxitoxin [(+)STX]. The analogues, all of which were racemic (+/-) mixtures except for dcSTX, varied in the substituents at the C6 position, the carbamoyl 'moeity', and the C12 position, the hydrated ketone. The ability of the toxins to inhibit the compound action potential (AP) and to displace radiolabeled natural saxitoxin (3H-STX) from nerve membranes at equilibrium were both used as potency assays. Biological activity of both (+)- and (-)dcSTX was analyzed by the kinetics of block of single Na+ channels reconstituted in planar lipid bilayer membranes, where it was demonstrated that only (+)dcSTX had biological activity. The potency of STX analogues fell markedly as the substituent at the C6 position became smaller; Ki values from the binding competition assay (at 4 degrees C) are: (+/-)6-methanolic-STX, 5 x 10(-10) M; (+/-)6-methyl-STX, 1 x 10(-6) M; (+/-)6-dihydro-STX, 3.5 x 10(-5) M. Replacement of the ketone at the C12 position by a methylene group was accomplished in two derivatives, although both also had substituents at the C6 position. The compound (+/-)6-methyl-12-deoxy-STX was about 0.03 as potent as (+/-)6-methyl-STX and only 10(-5) as potent as racemic (+/-)STX. In synthetic compounds where the benzyloxymethyl (-CH2OCH2C6H5) substituent occurred at the C6 position, the C12-methylene derivative still displayed some binding activity (Ki = 6 x 10(-4) M). However, when the same C6 derivatized compounds also contained a 6-membered heterocyclic group (-C3H8S2-) conjugated to carbon 12, the measured binding affinity was even further decreased (Ki = 2 x 10(-3) M). The findings show that substitutions on the carbon 6 position of STX have stronger effects on STX potency than previously believed, and that the toxin may form a hydrogen bond with the sodium channel at this site. Furthermore, the total removal of oxygen from the C12 position does not completely abolish the binding activity of the molecule.

Action Potentials↗

PubMed1995

Effect of anthraquinone derivatives on lipid peroxidation in rat heart mitochondria: structure-activity relationship.

Lipid peroxidation was induced in rat heart mitochondria with FeSO4 and the inhibitory effects of various anthraquinone derivatives were compared. Oxygen consumption and malondialdehyde formation were used to quantitate the amount of lipid peroxidation. Emodin [2], alizarin [13], and alizarin complexone [14] significantly inhibited lipid peroxidation; their potency as inhibitors of lipid peroxidation was higher than that of alpha-tocopherol. Structure-activity analysis showed that two hydroxyl groups arranged in either the ortho- or meta-position in the C ring of the anthraquinone nucleus are required for such derivatives to inhibit lipid peroxidation. The diphenyl-p-picrylhydrazyl test showed that alizarin [13] and alizarin complexone [14] are free-radical scavengers while emodin [2] is not. The mechanism for emodin [2] to inhibit lipid peroxidation is most likely due to inhibition on the propagation of lipid peroxyl radicals in the mitochondrial membrane.

Animals↗

PubMed1995

Effect of trilinolein on cyclic nucleotide formation in human platelets: relationship with its antiplatelet effect and nitric oxide synthesis.

1. Trilinolein, a triacylglycerol with linoleic acid as the only fatty acid residue in all three esterified positions of glycerol, was recently reported to have an inhibitory effect on adrenaline-induced platelet aggregation. In the present study, we found that trilinolein at concentrations ranging from 0.01 to 1 microM increased cyclic GMP formation and decreased cyclic AMP formation in washed human platelets. Both NG-nitro-L-arginine methyl ester (L-NAME) and methylene blue attenuated the trilinolein-induced increase in cyclic GMP. 2. Adrenaline decreased not only the production of cyclic AMP but also that of cyclic GMP. Trilinolein antagonized the inhibitory effect of adrenaline on cyclic GMP formation, but potentiated the inhibitory effect of adrenaline on cyclic AMP accumulation. 3. Both trilinolein and adrenaline enhanced intracellular calcium but the increment of intracellular calcium induced by them was much less than that produced by thrombin. 4. We propose that the anti-platelet effect of trilinolein is mediated through an increase in cyclic GMP, and that the change in cyclic GMP results from stimulation of nitric oxide synthesis in platelets. 5. We also propose that reduction of both cyclic AMP and cyclic GMP are involved in adrenaline-induced platelet aggregation.

Adult↗