Résumé
Objective To investigate the effects of propofol on mesenteric artery in SD rats and to observe whether the effect of propofol on the mesenteric artery relaxation is related to the gap. Methods Pressure myograph was used to examine the effect of 18β-GA and 2-APB on the relaxation induced by propofol 1×10 -7 ,3×10 -7 ,1×10 -6 ,3×10 -6 ,1 ×10 -5 ,3 ×10 -5 ,1 ×10 -4 and 3 ×10 -4 mol/L in acutely separated mesenteric arterioles of SD rat.Results The diameter of mesenteric arteri-oles were increased from (208.6±13.4)to (213.5±13.6),(21 9.7±13.2),(226.4±12.5),(234.9 ±12.3),(245.5±13.0),(267.4±1 5.2),(336.2±18.3)and (385.9 ±14.2)μm after application of 1×10 -7 ,3×10 -7 ,1 × 10 -6 ,3 × 10 -6 ,1 × 10 -5 ,3 × 10 -5 ,1 × 10 -4 and 3 × 10 -4 mol/L propofol,re-spectively.Propofol induced dilation of the rat mesenteric arterioles in a concentration-dependent man-ner (P < 0.01 ).After pretreatment with 18β-GA and 2-APB,1 × 10 -4 mol/L propofol induced dilation was absolutely decreased (P <0.01).Conclusion These results suggest that propofol relaxes mesenteric arterioles via gap junction.
Résumé
Objective To investigate the effects and mechanisms of hypoxia on the contraction of mesen-teric arteries induced by phenylephrine (PE) in guinea pig. Methods Pressure myograph system was used to study the effects of 20, 40 and 60 min hypoxia (mixed with 95% CO2 and 5% O2) on the constriction induced by PE in acutely separated mesenteric artery (300 ~ 400 μm) of guinea pig. Results PE (0.1 ~ 100 μmol/L) caused the contractions of the mesenteric arteries in guinea pig in a concentration-dependent way . Hypoxia de creased the pH value of perfusion fluid from 7.4 to 6.3. Hypoxia significantly inhibited PE-induced vasocon-striction, and the inhibition was hard to recover after reoxygenation. Hypoxia inhibited PE-induced vasoconstric-tion in a time-dependent way , with the inhibition rate reduced in the sequence of inhibition duration of 60 , 40 and 20 min. When its value was decreased to 6.3 , the perfusion fluid even inhibited PE-induced vasoconstric tion. Conclusion Hypoxia can inhibit PE-induced vasoconstriction in the mesenteric arteries of guinea pig in a time-dependent way. The mechanism may have something to do with the change of pH.
Résumé
Aim To establish a method for recording tension changes in small artery in vitro.Methods The vessel segments of intestine were dissected from the mesenteric artery of rats and mounted onto Myograph.The internal circumferences of the segments were normalized with Chart5 software.Then the internal diameters of the segments and initial setting of tension were calculated with self-made Excel file.Following these preparation steps, the tension changes induced by several stimulations were recorded by Myograph.Results Normalization procedure provided the data of lumen diameters of small arteries,which was convenient for initial setting of tension and guaranteed the uniformity of the experimental conditions.Myograph could record the tension changes of small arteries induced by several classic stimulations.Conclusion Precise recording method for tension changes in small arteries in vitro is successfully established.
Résumé
Cerebral blood vessels relax when extracellular K+ concentrations ((K+))e are elevated moderately (2~15 mM, K+-induced vasorelaxation). We have therefore studied the underlying mechanism for this K+-induced vasorelaxation in the isolated middle cerebral arteries (MCAs). The effects of ouabain and Ba2+ on K+-induced vasorelaxation were examined to determine the role of sodium pump and/or Ba-sensitive process (possibly, inward rectifier K current) in the mechanism. Mulvany myograph was used to study 24 rats, 18 rabbits, and 10 humans MCAs (216+/-3 mum, 347+/-7 mum, and 597+/-39 mum in diameter when stretched to a tension equivalent to 55 mmHg). High K+ (125 mM) and PGF2alpha (1~10 muM) induced concentration-dependent contractions in all 3 species, while histamine (10~50 muM) evoked contraction only in the rabbits and induced relaxation in the rats and humans. Addition of K+ (2~10 mM) to the control solution induced vasorelaxations. These effects were inhibited by the pretreatment with both ouabain (10 muM) and Ba2+ (0.1~0.3 mM) in the rat, but only with ouabain (10 muM) in the rabbit and human. These results suggest that K+-induced vasorelaxation occurs via the stimulation of electrogenic Na pump in the rabbit and human MCAs, while in the rat MCAs via the activation of both Na pump and Ba-sensitive process.