Biomedical subjects

S X Fu

Publications and source records attributed to S X Fu.

At least 19 recordsLinked to original sources

PubMed2000

[Clinical analysis of 318 cases of new-mode cesarean section].

OBJECTIVES: To study types of new mode cesarean section (CS) and its clinical value. METHODS: Four hundred and sixty-eight pregnant women with operative indications were randomly divided into three groups: the new mode CS group whose peritoneum was not sewed, the new mode CS group whose peritoneum was sewed, and the lower segmental CS group. The duration of operation, bleeding volume, morbidity after operation, and B type ultrasound for examining the incision were observed. RESULTS: There were significant difference in the duration of operation, bleeding volume, and morbidity after operation between the lower segmental CS and the two types of the new mode CS (P < 0.05). There was no significant differences in the bleeding volume and morbidity after operation between the two types of the new mode CS (P > 0.05), but there were significant difference in the duration of operation and the incision examined by B type ultrasound (P < 0.05). CONCLUSION: The new mode CS has shorter operative period, less bleeding, weak pain, faster recovery of peristalsis, and lower incidence of post-operative morbidity.

Cesarean Section↗

PubMed2000

Urethane-induced hyperglycemia.

AIM: To study the effects of urethane, at anesthetic dose, on the blood glucose levels in normal rats and hyperglycemic rats, and its effects on the hypoglycemic action of exogenous insulin in alloxan-treated rats. METHODS: Blood glucose concentration was measured with the glucose oxidase method. RESULTS: Urethane at anesthetic dose 1.5 g.kg-1 increased the blood glucose levels in fasting (to 2.6 +/- 0.3 g.L-1, P < 0.01) or glucose-loaded (to 3.9 +/- 0.4 g.L-1, P < 0.01) rats. It did not modify the hyperglycemia induced by epinephrine (normal islet beta-cells) or alloxan (impaired islet beta-cells). In the rats treated with alloxan, blood glucose level decreased to 1.8 +/- 0.7 g.L-1 at 200 min after administration of insulin from control level of 7.0 +/- 2.3 g.L-1, but the hypoglycemic action of exogenous insulin was abolished by urethane. CONCLUSION: Hyperglycemic action of urethane was due to its inhibiting effect on the hypoglycemic effect of insulin, except for its known mechanism of increased sympathetic release.

Alloxan↗

PubMed1999

Selective effects of alfuzosin and doxazosin with intraduodenal administration on urethral pressure of cats.

AIM: To observe the selective effects of alfuzosin (Alf) and doxazosin (Dox) on the urethral pressure by different administration routes. METHODS: The urethral pressure of the anesthetized cat was increased by electric stimulation of the hypogastric nerve. The different effects of Alf or Dox on the arterial blood pressure and urethral pressure between intraduodenal administration (i.d.) and intravenous infusion (i.v.) were compared. RESULTS: When the hypogastric nerve was stimulated by electric stimulation (10 Hz, 25 V), the ratios of ED20(BP)/ED50(UP) i.d. to ED20(BP)/ED50(UP) i.v. were 10.9:4.3 for Alf, and 3.1:2.1 for Dox. The reduction in urethral pressure induced by i.d. Alf was greater than that by i.v. Alf. Dox did not show any difference in its effects by 2 administration routes. CONCLUSION: Intraduodenal administration of Alf, but not Dox, selectively decreased the urethral pressure elevated by electric stimulation. The uroselectivity of i.d. Alf was not due to the species difference in its bioavailability and biotransformation.

Adrenergic alpha-Antagonists↗

PubMed1995

Effects of 3-morpholinosydnonimine-N-ethylcarbamide on hypoxia-induced mechanical and electric responses of isolated pig coronary artery.

AIM: To study effects of 3-morpholinosydnonimine-N -ethylcarbamide (SIN-1) on hypoxia-induced mechanical and electric activities of the isolated pig coronary artery. METHODS: Mechanical tension and membrane potential were measured simultaneously. RESULTS: Hypoxia initially caused a transient vascular smooth muscle cell membrane hyperpolarization followed by a membrane depolarization in isolated pig coronary artery. Subsequent addition of SIN-1 100 mumol . L-1 or verapamil (Ver) 10 mumol . L-1 led to membrane repolarization and relaxation of the vascular smooth muscle. Nitro-L-arginine (NLA) 0.2 mmol . L-1 and KCI 40 mmol . L-1 also induced membrane depolarization and vasoconstriction, which were similarly suppressed by SIN-1 or Ver. CONCLUSION: Hypoxic contractile response in isolated pig coronary artery is mediated by an increased Ca2+ influx via suppression of nitric oxide release.

Animals↗

PubMed1994

[Effects of m-nisoldipine on arterial baroreflex sensitivity in anesthetized rats].

Baroreflex sensitivity (BRS) in anesthetized rats was measured as the slope of the regression line of the concomitant maximal change in heart rate (delta R-R) and blood pressure (delta BP) induced by bolus i.v. phenylephrine or sodium nitroprusside, m-nisoldipine (m-Nis) i.v. 5, 10, 20 micrograms.kg-1 depressed the BRS (2.6 +/- 0.2, 2.4 +/- 0.3, 1.6 +/- 0.2, or 1.7 +/- 0.1, 1.6 +/- 0.2, and 1.4 +/- 0.2 ms.kPa-1, respectively) compared with before medication (P < 0.01). m-Nis may act directly on carotid sinus to depress the BRS, but not through cardiac beta or M receptor nor through central nervous system.

Animals↗

PubMed1994

Effects of inhibitor of endothelium-derived relaxing factor on hypoxic contraction of isolated pig coronary artery.

Exposure of isolated pig coronary artery with endothelium intact to hypoxia Krebs-Henseleit solution aerated with 95% N2 + 5% CO2 caused a transient contractile response, and the coronary artery without endothelium exhibited a gradual decrease in basal tension. The endothelium-dependent contractile response to hypoxia was almost completely blocked by nitro-L-arginine (0.2 mmol.L-1), and inhibited by methylthioninium chloride (10 mumol.L-1). The inhibitory effect of the NLA was partially reversed by L-arginine (2 mmol.L-1). Sodium nitroprusside (10 mumol.L-1) was also completely antagonized and nicorandil (0.3 mol.L-1) remarkably reduced the hypoxic contractile response. Tetraethylammonium (10 mmol.L-1) and glibenclamide (1 mumol.L-1) had little effect on hypoxia-induced vascular contraction, whereas cromakalim (1 mumol.L-1) produced obvious relaxing effect on hypoxic response. These results suggest that suppression of basally released nitric oxide (NO) is an important mechanism of coronary vasoconstriction induced by hypoxia.

Animals↗

PubMed1994

Effects of m-nisoldipine on contraction and 45Ca influx in isolated rat aorta.

m-Nisoldipine caused a concentration-dependent depression of the contractile response and 45Ca influx evoked by KCl in isolated rat thoracic aorta. The IC50 value for contraction and 45Ca influx were 0.69 (95% confidence limits 0.32-1.5) nmol.L-1 and 0.35 (95% confidence limits 0.06-2.0) nmol.L-1, respectively. There was a positive correlation between the inhibition of KCl-evoked contraction and 45Ca influx (r = 0.996). m-Nisoldipine (0.1-10 mumol.L-1) did not influence the 45Ca influx into resting cells and failed to inhibit noradrenaline (1.0 mumol.L-1)-evoked contraction and 45Ca influx. The results suggest that the relaxant effect of m-nisoldipine on rat aorta may be closely related to the blockade of Ca2+ entry through a potential-dependent calcium channel.

Animals↗

PubMed1993

Effects of hydrochlorothiazide on contraction and 86Rb efflux in rat aorta.

Hydrochlorothiazide (HCT) (0.1, 0.3 mmol.L-1) inhibited the contraction of rat aortic strips induced by low (< 40 mmol.L-1), not higher concentrations of KCl. HCT (0.3 mmol.L-1) did not inhibit the CaCl2-induced contraction of the aortic strips depolarized with high K+ (KCl 80 mmol.L-1). The inhibitory effect of HCT (0.1 mmol.L-1) on KCl (20 mmol.L-1)-induced contraction was markedly antagonized by BaCl2 (0.1 mmol.L-1) and tetraethylammonium (TEA) (0.3 mmol.L-1), but not by glibenclamide (Gli, 0.01 mmol.L-1). With norepinephrine (NE) or 5-HT as agonists, HCT (0.3 mmol.L-1) also inhibited the contractions of rat aortic strips. In the 2 components of NE-induced contraction, HCT inhibited only the tonic component depending on Ca2+ influx, but not the phasic component elicited by the release of intracellular Ca2+. The inhibitory action of HCT was endothelium-independent. That the HCT (3 mmol.L-1) increased the 86Rb efflux rate coefficient was antagonized by BaCl2 (0.1 mmol.L-1), but not by Gli (0.01 mmol.L-1). The results indicated that the inhibitory effect of HCT on the contraction of rat aorta was attributable to the opening of membrane potassium channels.

Animals↗

PubMed1992

Antihypertensive effects of m-nisoldipine and nisoldipine on conscious renal hypertensive rats and dogs.

The antihypertensive effects of m-nisoldipine (m-Nis) and nisoldipine (Nis) by ig 0.3, 1.0, 3.0 and 1.0, 3.0, 9.0 mg.kg-1 respectively on renal hypertensive rats (RHR) and 0.1, 0.3, 1.0 mg.kg-1 orally (for both drugs) on renal hypertensive dogs (RHD) were studied. Both m-Nis and Nis depressed blood pressure (BP) dose-dependently in RHR and RHD. The reduction of blood pressure correlated well with the m-Nis concentration in plasma of RHD. On the basis of ED20 (HR)/ED20 (BP), the hypotensive effect of m-Nis on systolic blood pressure (SBP) was only 1.6 times as great as that of Nis on RHR (P less than 0.05), but in RHD, both drugs showed the same potency (P greater than 0.05). In both models, m-Nis showed much more potent effect on diastolic blood pressure (DBP) than Nis (P less than 0.01), and possessed stronger hypotensive effects on DBP than on SBP (P less than 0.05 and P less than 0.01); but for Nis, its effects on SBP and DBP appeared to be in the same order (P greater than 0.05). The fall in BP was accompanied by a transient increase of heart rates (HR) with m-Nis and Nis in RHR and RHD. The chronic antihypertensive effects of m-Nis and Nis were also remarkable with 1.0 mg.kg-1 daily at 9 AM for 21 d. During this period, the BP and HR lowered to nearly normal level. After withdrawal of m-Nis and Nis, the hypotensive effects lasted nearly 1 wk.

Animals↗

PubMed1992

[Effects of m-nisoldipine and nisoldipine on isolated uterine muscle].

m-Nisoldipine (m-Nis) and nisoldipine (Nis) inhibited spontaneous contraction of isolated non-pregnant human myometrium, IC50 being 3.7 +/- 0.7 mumol.L-1 for m-Nis and 6.0 +/- 0.9 mumol.L-1 for Nis. Both drugs also suppressed spontaneous and oxytocin-induced contraction of isolated pregnant rat uterus. In isolated uterus from virgin rat, both drugs inhibited the contractions induced by KCl, acetylcholine (ACh), and oxytocin (Oxy), the values of pD'2 against KCl, ACh, Oxy being 9.0 +/- 0.2, 6.1 +/- 0.1, and 5.9 +/- 0.1 for m-Nis and 9.1 +/- 0.3, 5.7 +/- 0.2, and 5.6 +/- 0.1 for Nis respectively. The results indicate that both m-Nis and Nis may be clinically useful for the treatment of dysmenorrhea and premature labour.

Acetylcholine↗

PubMed1991

Effect of ubiquinone on ischemic arrhythmia in conscious rats.

Ubiquinone 6.2, 12.5 or 2.5 mg.kg-1 respectively twice iv 24 h and 30 min before coronary artery ligation, ameliorated the ischemic arrhythmia in conscious rats, and there was a close positive correlation between the ubiquinone concentration in myocardium and plasma and its anti-arrhythmic effect. Ubiquinone iv 3.1, 6.2, and 12.5 mg.kg-1 increased, while 25 mg.kg-1 decreased 6-keto-PGF1 alpha, and 12.5 and 25 mg.kg-1 decreased TXB2, which was in accordance with inhibitory effects on the synthesis of 6-keto-PGF1 alpha and TXB2 in vitro. But the ratio of metabolites of PGI2/TXA2 in vivo was increased in all ubiquinone groups. These results indicated that ubiquinone possesses protective effects on ischemic arrhythmia of conscious rats and the beneficial effects on myocardial ubiquinone content and PGI2/TXA2 seem to contribute to its myocardial protective action.

6-Ketoprostaglandin F1 alpha↗

PubMed1991

Effects of glibenclamide and tolbutamide on ischemia- and ouabain-induced arrhythmias and membrane potentials of ventricular myocardium from rat and guinea pig.

Glibenclamide (Gli) 0.3, 1, 3 mg.kg-1 and tolbutamide (Tol) 3, 10, 30 mg.kg-1 iv 10 min before ischemia or ouabain infusion prevented ventricular fibrillation induced by ischemia in rat and arrhythmias induced by ouabain in guinea pig. Gli 10 mumol.L-1 and Tol 1 mmol.L-1 increased APD and ERP in rat ventricular muscle. Gli 0.1, 1, 10 mumol.L-1 and Tol 0.01, 0.1, 1 mmol.L-1 prevented and reversed the shortening of APD and ERP induced by hypoxia in guinea pig ventricular muscle. These effects of Gli and Tol were dose-dependent. The results confirmed that Gli and Tol were effective on arrhythmias induced by ischemia and ouabain by blocking ATP-sensitive potassium channel.

Animals↗

PubMed1990

[Histamine and early ischemic arrhythmia in anesthetized cats].

Ligation of left anterior descending coronary artery caused various arrhythmias and reduced histamine content in ischemic myocardium in anesthetized cats. Intracoronary injection of compound 48-80 100 micrograms shortened the onset of VT and VF from 13 +/- 5, 18 +/- 5 min (n = 7) in control to 7.2 +/- 1.1 (P less than 0.01), 11 +/- 5 min (P less than 0.05) (n = 6) respectively, elevated the histamine concentration of plasma after acute coronary artery occlusion (15 +/- 3, 26 +/- 10 ng/ml, P less than 0.05, before and after ligation respectively). Iv chlorpheniramine (5, 10 mg/kg) or cimetidine (20, 40 mg/kg) dose-dependently reduced arrhythmia score, incidence of VF and mortality after myocardial ischemia, but with little influence on histamine content in ischemic myocardium and plasma. These results suggest that release of histamine from the ischemic myocardium is involved in the generation of early arrhythmias through H1 and H2 receptors in anesthetized cats subjected to acute coronary artery occlusion.

Animals↗

PubMed1990

Pharmacokinetics of m-nisoldipine in rabbits and rats.

A reverse phase HPLC method was devised for determination of m-Nis in plasma. A mobile phase of methanol-KH2PO4 with a flow rate of 1 ml/min was used. Diazepam was used as the internal standard. A two-compartment model featured the pharmacokinetic process of m-Nis after its iv injection to rats (30 micrograms/kg) and rabbits (50 micrograms/kg). The pharmacokinetic parameters were: T 1/2 alpha = 4.3 min, T 1/2 beta = 63.6 min, Vd = 0.805 L/kg, Cl = 9 ml/(min.kg) in rats; T 1/2 alpha = 5.0 min, T 1/2 beta = 78.3 min, Vd = 1.191 L/kg, Cl = 11 ml/(min.kg) in rabbits. The pharmacokinetics for m-Nis after ig 200 micrograms/kg to rats described one-compartment model with parameters: T 1/2 = 84.8 min, Tmax = 31.2 min, Cmax = 49.97 micrograms/L, Vd = 0.792 L/kg and Cl = 25 ml/(min.kg).

Animals↗

PubMed1990

Effects of m-nisoldipine on anoxia-potentiated histamine and acetylcholine-induced contractions of the porcine isolated coronary artery.

Anoxia (95% N2 + 5% CO2) potentiated the contractile response to KCl 20 mmol/L, histamine (His) 5 mumol/L and acetylcholine (ACh) 0.5 mumol/L in isolated porcine coronary arterial rings. Calcium antagonists m-nisoldipine (m-Nis) and nisoldipine (Nis) 0.4-250 nmol/L produced a concentration-dependent decrease in both KCl, His and anoxia-potentiated KCl2 His or ACh-induced contractions. Chlorpheniramine 10 mumol/L but not cimetidine 10 mumol/L and atropine 10 mumol/L abolished contractions induced by His and ACh respectively. All 3 agents did not affect KCl response and the anoxia facilitation. Indomethacin 10 mumol/L markedly attenuated the further increase in tension by anoxia but failed to inhibit the response by these vasoconstrictors.

Acetylcholine↗

PubMed1990

Acute toxicity of dipfluzine and its effects on isolated vascular smooth muscle.

Dipfluzine (Dip) is a new derivative of cinnarizine (Cin) first developed by Department of Chemistry, Beijing University. Dip showed a dose-dependently inhibitory effect on both KCl- and NE-induced contraction in the rabbit aortic rings. It was more effective in suppressing the contractile response evoked by KCl than that by NE. Dip also inhibited the KCl-induced contraction in porcine basilar, coronary and radial arteries. Their pD2' values were 5.7 +/- 0.6, 5.4 +/- 0.4 and 4.6 +/- 0.5 respectively. The selectivity of Dip for vasodilation was proved by higher pD2' value of the basilar artery than that of the coronary and radial arteries, and this selectivity of Dip was more significant than that of Cin. The acute iv LD50 of Dip and Cin in mice were 37 and 36 mg/kg, respectively.

Animals↗

PubMed1989

[Acute toxicity testing (LD50) of Chinese mineral drugs].

Acute toxicity and LD50 of 62 mineral drugs were determined by ig, ip or iv in mice, in order to provide some guidelines for safety in clinical use, as well as for pharmacological and toxicological studies. In the present investigation, the difference in the acute toxicity and LD50 between raw drugs and medicines prepared by roasting is explained.

Animals↗

PubMed1989

[Protective effects of m-nisoldipine and nisoldipine on myocardial damage in working rabbit hearts after ischemia-reperfusion].

m-Nisoldipine 4, 8, 16 nmol/L, nisoldipine 1, 4 nmol/L and nifedipine 4, 8, 16, 50 nmol/L enhanced the recoveries of functional parameters of working rabbit hearts after ischemia-reperfusion, as well as prevented the development of contracture and the release of CPK from the reperfused hearts. m-Nisoldipine 8 nmol/L, nisoldipine 1 nmol/L and nifedipine 8 nmol/L attenuated the reduction of myocardial Na+-K+-ATPase and 5'-nucleotidase activity induced by ischemia-reperfusion. The breakdown of membrane phospholipids and elevation of the myocardial Ca2+-ATPase activity and the free fatty acids level were also prevented.

Animals↗