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Biomedical subjects

I J Chen

Publications and source records attributed to I J Chen.

At least 55 records · Page 3Linked to original sources

Spinal adenosine modulates capsaicin-induced depressor reflex: involvement of adenosine A2 receptor.

1. The depressor responses to i.a. and i.v. injection of capsaicin (CAP) were blocked following intrathecal (i.t.) perfusion of [D-Pro2, D-Trp7,9] substance P, a specific substance P antagonist. This confirmed that the CAP-elicited depressor reflex is mediated by substance P-containing afferent fibres. 2. The regulatory roles of spinal adenosine in the CAP-evoked substance P release and the possible involvement of adenosine A2 receptors were analyzed by analyzing the changes in cardiovascular responses to i.a. and i.v. injection of CAP after various pretreatments with adenosine agonists and antagonists, administered subcutaneously or intrathecally.

Adenosine↗

Xanthonolol: a calcium channel and beta-adrenoceptor blocker with vasodilating properties.

1. Xanthonolol (0.1-5.0 mg/kg, i.v.) reduced the blood pressure, heart rate, and L-isoproterenol (0.05 microgram/kg, i.v.)-induced tachycardia in rats. 2. In the isolated guinea-pig right atrium, xanthonolol (10(-6)-3 x 10(-4) M) produced long-lasting negative, inhibited L-isoproterenol-induced positive chronotropic effects, prevented the rate-increasing effects of increased extracellular Ca2+ (3.0-9.0 mM), and inhibited Ca2+ (3.0-9.0 mM)-induced heart rate-increase. 3. In the isolated guinea-pig thoracic aorta, the contractions induced by CaCl2 (0.1-5.0 mM) were inhibited by xanthonolol (10(-6)-10(-4) M). 4. Xanthonolol is suggested to have a calcium channel and beta adrenergic blocking effect with vasodilating properties.

Adrenergic beta-Antagonists↗

Cardiovascular interactions of nonivamide, glyceryl nonivamide, capsaicin analogues, and substance P antagonist in rats.

Nonanoyl vanillylamide-4-o-glycerol (glyceryl nonivamide, GLNVA) a nonpungent ether-linked derivative of nonanoyl vanillylamide (nonivamide, NVA) was compared to capsaicin (CAP) and NVA with regard to its depressor response in rats. IV injection of CAP and NVA (10(-1) to 10(-4) mg/kg) in Wistar rats elicit a triphasic blood pressure response, bradycardia, and aponea. However, IV injection of GLNVA results in a monophasic reduction in blood pressure, with little effect on heart rate and respiration. The depressor response to GLNVA was not diminished by bilateral vagotomy or by systemic pretreatment with atropine. Following the CAP pretreatment, the delayed hypotension induced by CAP, NVA, and the hypotension of GLNVA was almost abolished. Injection of CAP, NVA (10 micrograms/kg), or GLNVA (100 micrograms/kg) into one femoral artery elicited a fall in blood pressure in the rat. This effect was abolished following intrathecal injection of substance P antagonist [D-Pro2,D-Trp7,9]-SP. Microejections of CAP, NVA, or GLNVA into the nucleus tractus solitarii (NTS) evoked hypotension, the bradycardia following microejection of CAP and NVA into the NTS occurred only at higher doses of GLNVA. From these results it is suggested that GLNVA appears to act more exclusively than CAP by stimulating peripheral perivascular small diameter C-fiber sensory nerves.

Animals↗

[Studies on antiaggregating drugs of horseshoe crab amebocytes].

The effects of drugs on amebocyte spontaneous aggregation and endotoxin induced aggregation were studied. N-Ethylmaleimide, ethylenediamine tetraacetate, propranolol, verapamil and lidocaine but not dibutyryl cyclic AMP could reduce the aggregating rate of amebocytes. The speed of degranulation induced by endotoxin was reduced by N-ethylmaleimide, ethylenediamine tetraacetate, propranolol, verapamil and caffeine. These results suggest that Ca+2 and c-AMP may play an important role in amebocyte spontaneous aggregation and endotoxin induced aggregation. The blocking agent of Ca+2 and c-AMP can also antagonize the aggregation of amebocytes.

Animals↗

Vanidil: a newly synthesized antiangina nonvolatile organic solid nitrate.

Newly synthesized Vanidil (4-o-(1,2-dinitroglyceryl)-6-nitrovanillic acid) is a nonvolatile organic solid nitrate, mp: 85 degrees C. In in vitro tests, Vanidil can inhibit 3,4-diaminopyridine (2 x 10(-2) M) induced pig coronary rhythmic vasocontraction, a prelude to coronary vasospasm, and nonrhythmic tonic vasocontraction. Vanidil is suggested as a potential antiangina agent.

Angina Pectoris↗

Cardiovascular effects of nonivamide succinate.

Intravenous injection of nonivamide or nonivamide succinate (25, 250 nmol/kg) into Wistar rats induced bradycardia, hypotension, apnea and a triphasic blood pressure response: an initial short fall (effect A), an intermediate rise (effect B), and a subsequent delayed fall (effect C) of blood pressure. This blood pressure response remained unchanged after treatment with propranolol or phentolamine. In atropine-pretreatment rats the initial effect A was markedly decreased and effect C was slight increased. Effect A was absent after bilateral vagotomy. Unilateral microinjection of nonivamide succinate (3, 30 fmol) into the nucleus tractus solitarii produced a marked reduction in blood pressure and heart rate. In the isolated aorta of the guinea pig, application of either nonivamide or its succinate (10(-8) to 10(-5) M) eliminated the smooth muscle tone produced by phenylephrine (10(-6) M). Re-exposure to these agents, however, produced an immediate tachyphylactic relaxing response and prolonged rebound contractile response. Both compounds induced a vascular contraction rather than relaxation during tachyphylaxis. The potency of nonivamide succinate was found to be slightly greater than that of nonivamide.

Animals↗

[Comparative study on the pharmacokinetics and bioequivalence of two brands of norfloxacin preparation].

The pharmacokinetics and bioequivalence of two norfloxacin, Gentle capsule and Baccidal tablet, were compared in eight healthy male volunteers. A 400 mg dose of norfloxacin was given orally after an overnight fasting to volunteers in a balanced two-way cross-over study. Blood samples were obtained at 0, 0.5, 1.0, 2.0, 4.0, 8.0, 12.0 and 24.0 hours after the dosing. Norfloxacin concentration in serum was assayed by a high pressure liquid chromatographic method using an UV detector. All the data was processed by KMCP computer software and the pharmacokinetic parameters were calculated, based on one-compartment model. The results revealed that the maximal concentration (Cmax) of Gentle and Baccidal was 0.96 +/- 0.089 and 0.99 +/- 0.110; the time to reach maximal concentration (Tmax) was 2.0 +/- 0.0 for both; the elimination constant (Kel) was 0.101 +/- 0.006 and 0.098 +/- 0.005 hr-1; the elimination half life (T1/2, beta) was 6.909 +/- 0.483 and 7.094 +/- 0.350 hr; the absorption constant (Ka) was 2.444 +/- 0.188 and 2.490 +/- 0.096 hr-1; the absorption half life (T1/2, alpha) was 0.278 +/- 0.019 and 0.277 +/- 0.010 hr; the area under curve (from 0 to 12 hours) (AUC0-12) was 7.106 +/- 1.065 and 7.380 +/- 1.044 micrograms.hr/ml; and the area under curve (from 0 hour to infinity) (AUC0-infinity) was 9.183 +/- 1.257 and 9.550 +/- 1.300 micrograms.hr/ml respectively. There were no significant difference found between the two groups after statistical analysis with two-way ANOVA (p greater than 0.05). A series of statistical parameters including d%, delta, and 95% C.I. were calculated by a bioequivalence test computer software of Yamaoka Simi. In order to strengthen the statistical evidence, the power of the test (1 - beta) was also calculated. After evaluating all the parameters, there was no significant difference found between the two groups. Therefore, the high similarity of these two formulations is suggested by the authors.

Adult↗

Halothane-inhalation system for using atracurium in rats.

This report describes an inhalation anesthetic technique employed in rats. Polyethylene-glycol 400 (PEG 400) was first designed to combine with halothane to produce a slow-releasing system of vaporized halothane. This design provided adequate anesthetic levels for treating with atracurium, a new neuromuscular blocking agent. Furthermore, isoflurane was also used in this study to examine this inhalation system for treating with atracurium. The efficient concentrations of inhalated anesthetics for adequate anesthesia when combining with PEG were 0.15% and 0.1% for halothane and isoflurane, respectively. This safe efficient state of anesthesia was maintained throughout the experimental course for treating atracurium, and might be used in clinical trials.

Anesthesia, Inhalation↗

Edema formation and degranulation of mast cells by a basic phospholipase A2 purified from Trimeresurus mucrosquamatus snake venom.

The basic phospholipase A2 (PLA2) purified from Trimeresurus mucrosquamatus snake venom was injected into the subplantar in order to induce edema formation in the rat hind paw. The maximum edema induced by PLA2 was induced at 1-2 hr after injection, and the per cent swelling curve showed a dose-dependent increase by PLA2 injection (2.5-10.0 micrograms). The rate of edema formation is different from the acute swelling induced by T. mucrosquamatus venom (TMV). Pretreatment with dexamethasone (4 mg/kg, s.c.), indomethacin (10 mg/kg, per 05) and diphenhydramine (100 mg/kg s.c.) inhibited the edema induced by the purified phospholipase A2. The injection of purified PLA2 or venom into rabbit skin resulted in an increase in vascular permeability which could be decreased by pretreatment with three antiinflammatory drugs. However, the pharmacological effect of dexamethasone (4 mg/kg) demonstrated a more effective inhibition than the other drugs in the PLA2-induced edema and vascular permeability change. Injection (i.p.) of PLA2 caused marked degranulation of mast cells in the rat mesentery which was facilitated by addition of calcium ion (10 mM) but antagonized by pretreating with three antiinflammatory agents. After incubating peritoneal mast cells with PLA2 (1.0 micrograms/ml), the release of histamine from the mast cell was approximately 36%, this effect was inhibited by preincubating the mast cell with three antiinflammatory agents.

Animals↗

[The role of ADP-cyclic AMP system in horseshoe crab amebocytes aggregation and gel formation].

A study of the effects of ADP and cyclic AMP related drugs on gel formation induced by endotoxin and amebocytes aggregation was conducted. The gel formation induced by endotoxin could be inhibited by ADP, cyclic AMP, ATP and aminophylline. Conversely, Phosphodiesterase enhanced gelation rate. A calmodulin antagonist, trifluoperazine, also inhibited endotoxin-induced gel formation, but this agent was able to induce potentiation in amebocytes aggregation. These results suggest that the cyclic AMP phosphodiesterase system may play an important role in endotoxin-induced gel formation, and it was concluded that, in the presence of both Ca++ and endotoxin, the calmodulin-like protein will activate the cyclic AMP phosphodiesterase system and decrease the concentration of cyclic AMP, thus promoting gel formation.

3',5'-Cyclic-AMP Phosphodiesterases↗

[Cultivation of horseshoe crab amebocytes].

The in vitro and in vivo cultivation of horseshoe crab amebocytes is studied. Partial bleeding promotes the proliferation of horseshoe crab amebocytes, and could be a useful method for amebocyte production in vivo. The optimal conditions of in vitro cultivation of amebocytes were incubation at 15 degrees C and pH delta 6.8-7.2. The best medium was the hemolymph of the horseshoe crab. Measuring DNA synthesis of amebocytes by 3H-thymidine uptake showed that no proliferation of amebocytes occurs during in vitro cultivation. Because some protozoa were found in the hemolymph, primaquine, quinine, pyrimethamine and metronidazole were used in the culture medium. Primaquine and metronidazole have a protozoacidal effect on the protozoa parasitising in the horseshoe crab.

Animals↗

[Comparative pharmacokinetics of two sulpiride formulations in healthy volunteers].

Six healthy male volunteers (age: 27.6 +/- 4.7; weight: 74.6 +/- 7.7) participated in a "repeated measure" design for comparing the bioavailability and pharmacokinetic behaviours of the brand-name drug of Dogmatyl and a generic sulpiride formulation. Each subject received a single 400-mg dose of Dogmatyl in tablet form during the first dosing period. After two weeks of washout period, the same dose of a generic preparation was then administered. Blood samples were obtained at 0, 0.5, 1, 1.5, 2, 4, 6, 12 and 24 hours after initial dosing. The concentration of sulpiride was measured by a high pressure liquid chromatographic method using a UV detector. All the data were processed by Keith K.H. Chan and Kenneth Wnuck's method which utilizes KMCP computer software. Pharmacokinetic parameters were calculated, based on one compartment model. The results revealed that the maximal concentration (Cmax) of Dogmatyl and the generic preparation was 1.468 +/- 0.631 and 1.472 +/- 0.608 mcg/ml, the time to reach maximal concentration (Tmax) was 1.5 +/- 0.63 and 1.25 +/- 0.61 hours, the half life (T 1/2) was 8.369 +/- 1.953 and 8.013 +/- 2.602 hours, the area under curve (from 0 to 24 hours) (AUC0-24 hr) was 11.03 +/- 6.78 and 8.27 +/- 2.99 mcghr/ml, and the area under curve (from 0 hour to infinity) (AUC0-hr) was 13.56 +/- 9.09 and 10.11 +/- 4.61 mcghr/ml, respectively. Based on the data, there was no significant difference found between the two groups after statistical analysis with paired t-test (p greater than 0.05). Therefore, the similarity of these two formulations is then suggested by the authors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Cyclooxygenase--independent pathway of phospholipase activation in carrageenan--induced platelet aggregation.

Carrageenan induced aggregation and ATP release of washed rabbit platelets. The aggregation was resistant to indomethacin or creatine phosphate/creatine phosphokinase system but sensitive to mepacrine or p-bromophenacyl bromide. Chlorpromazine, verapamil or tetracaine inhibited carrageenan-induced aggregation, ATP release reaction and membrane-bound calcium redistribution in washed platelets. Agents elevating cyclic nucleotides selectively inhibited the release reaction without affecting the aggregation. The mechanism of carrageenan-mediated platelet responses may be due to both activation of phospholipases A2 and C. Platelet activating factor, protein kinase C and inositol triphosphate or phosphatidic acid could be mediated by carrageenan to accomplish the cyclooxygenase-independent events.

Animals↗