Aim To study the effect of hesperdin and synephrine on the isolated gastric smooth muscle cells.Method Gain isolated gastric smooth muscle cells by digesting gastric smooth muscle with collagenase(typeⅡ), measure long axis length of 25～50 cells randomly under microscope. Then, compare the contraction change of cells between before and after given drugs, the contraction change of cells is expressed with percent, negative expresses contraction, positive expresses relaxation.Results Hesperdine had no effect on the isolated gastric smooth muscle cells. The contractile response to synephrine was prompt, rising to a peak within 60 s and dose-dependent at the range of 0.001～1 g?L -1. Synephrine inhibited the excited cells caused by acetylcholine(P

AIM To investigate whether there is vasodilator nerve innervation in rat hind limb and what the nature of vasodilator nerve is. METHODS Wistar rats were treated with reserpine 1 mg?kg -1 ip at 24 h before experiment. The rats were pithed and the hind limb vascular bed was perfused with Krebs-Henseleite solution containing 1 mmol?L -1 phenylephrine at 2 ml?min -1 speed. The hind limb perfused pressure (HPP) as a main index was continuously recorded. Spinal cord electrical stimulation (SES) was repeatedly applied via an electrode at L 1～2 level of lumber vertebra. The various tool drugs were administered by iv or infusion by added to persusion solution. The data is expressed as decrease percentages of HPP increased by continuous infusion of phenylephrine. RESULTS HPP was increased from (5 7?1 5) to (21 6?3 7) kPa ( n =37) after phenylephrine perfusion. SES caused a fall of HPP in frequency dependent and voltage dependent manner. An optimum parameters of SES (10 Hz, 50 V and 1 msec) was selected to observe effects of various tool drugs on depressor response of HPP to SES. Tetrotodoxin (0 3 ?mol?L -1 ) abolished the effect completely. L NAME (10 ?mol?L -1 ), a NO synthase inhibitor, had no effect. Ganglion blocker arfonad (110 mg?kg -1 , iv, M R blocker atropine (10 ?mol?L -1 ), ? receptor blocker propranolol (1 ?mol?L -1 ) and P 1 receptor blocker aminophylline (10 ?mol?L -1 ) had also no effect. Glibenclamide (0 1 mmol?L -1 ), an ATP sensitive K + channel blocker, markedly abolished and slightly reversed the effect. CONCLUTION The nonadrenergic noncholinergic vasodilator nerve exists in rat hind limb and is not nitroxidergic or purinergic nerve. This nerve may be peptidergic nerve which releases some peptide such as CGRP and the major mechanism of vasodilatation probably activates the ATP sensitive K + channel.

Objective To investigate the protective effects of hypereapnia on acute lung injury(ALI)in an model of rabbits in vivo,and to observe its effect on oxygen free radicals in the lung tissue in order to uncover the potential mechanisms.Method In the laboratory of pharmacology,China Medical Univereity,twenty-two healthy New Zealand white rabbits were randomly assigned to control group(Group C,n=6)with the injection of normal saline(0.1 ml/kg),and sixteen rabbits were injected with oleic acid(0.1ml/kg)intravenously,and then were randomly dirided into normocapnia group(Group N,n=8)and hypercapnia group(Group H,n=8,FiCO2=8%).Then tracheostomy was performed,and the experimental animals were ventilated for 3 hours after oleic acid or sterile normal saline administration.Lung mechanics,hemodynamics,blood-gas analysis were monitored.The rabbits were exsangninated.and the lungs and heart were taken out from the thorax.The concentration of superoxide dismutase(SOD)and malondialdehyde(MDA)in the lung tissue were assayed.Lung tissue wet/dry ratio and pulmonary permeability index were measured and histologic damage was assessed after three hours'mechanical ventilation.Results Peak airway pressure in Group H was significantly lower than that in Group N and the dynamic lung comphance Was significantly higher than that in Group N(P＜0.05).PaO2 in Group H was significantly higher than that in Group N(P＜0.05).The concentration of MDA in the lung tissue in group H was significantly lower than that in Group N(P＜0.05),and SOD in group H was significantly higher than that in Group N(P＜O.05).Lung tissue wet/dry ratio and pulmonary permeability in group H were significantly lower than that in Group N(P＜0.05).Histological tissus damage in Group N wassignificantly severer than that in Group H.Conclusions Hypercapnia induced by inhalation of high concentration of carbon dioxide(8%)plays protective role in this in vivo model of ALI.The mechanisms may be associated with enhanced SOD activity and the attenuation of lipid peroxidation in the lung tissue.

AIM: To investigate whether hypercapnia is protective against acute lung injury (ALI) in a rabbit model, and study it's potential mechanisms. METHODS: Twenty-two healthy New Zealand white rabbits were involved in this study, and randomly allocated to control group (group C), normocapnic group (group N) and hypercapnic group (group H). Oleic acid (0 1 mL/kg) was injected intravenously to establish ALI model. Lung mechanics, hemodynamics, blood-gas analysis, the content of malondialdehyde (MDA) and superoxide dismutase (SOD) activity in lung tissue were measured. Apoptosis was analyzed after 3h mechanical ventilation. RESULTS: (1) Peak airway pressure in group H was significantly lower than that in group N (P