Forty rots were randomized into 2 groups and naloxone or saline were injected to therats after they were inflicted with hemorrhagic shock at sea level and at a simulated altitude of4000m respectively to observe the ef...Forty rots were randomized into 2 groups and naloxone or saline were injected to therats after they were inflicted with hemorrhagic shock at sea level and at a simulated altitude of4000m respectively to observe the effects of naloxone on left ventricular systolic pressure(LVSP),left ventricular diastolic pressure(LVDP),the maximal changing rate of LVSP(dp/dt max),heartrate(HR),and survival time of the animals.Plasma β-endorphin(β-EP)was determined beforeand after hemorrhage to observe the relationship between β-EP and hemorrhagic shock.It wasfound that the circulatory parameters of hemorrhagic shock changed more markedly at high alti-tude than at sea level,naloxone could restore these parameters and prolong the survival time inboth the animals of the sea level and high altitude groups,and plasma β-EP level was elevatedafter hemorrhage especially in those animals at high altitude.These findings indicate:(1)Hemorrhagic shock at high altitude is usually accompanied with severe clinical manifestations,rapid progression,and high mortality.(2)β-EP seems to participate in the pathologicalmanifestafions of hemorrhagic shock at high altitude,and its depressive action on myocardialcontraction may be one of the factors inducing hemorrhagic shock.(3)Naloxone possesses defi-nite property to comet hemorrhagic shock at high altitude.展开更多
Objective: The aim of this study was to investigate the action of the arterial wall opioid receptor in vascular function regulation during shock in rats. Metbods : Experiments were performed on rat model of hemorrhagi...Objective: The aim of this study was to investigate the action of the arterial wall opioid receptor in vascular function regulation during shock in rats. Metbods : Experiments were performed on rat model of hemorrhagic shock in vivo and arterial strips in vitro. Results: The mean arterial pressure of the rat was reduced rapidly to 3. 99 kpa by bleeding and was managed to maintain at that level. The mean maximum bleeding volume of the naloxone group was 25. 90±4. 23 ml/kg. It was significantly more than that of the control group which was 20. 26 ± 4. 43 ml/kg (P<0. 05). The vasoconstrictive phase of shock was 50. 00± 11. 53 min in the naloxone group and 31. 68 ± 9. 98 min in the control group. The differences between the two groups were considered significant (P<0. 05). The contents of leucine enkephalin (L-ENK) in the rat's arteries were measured by radioimmunoassay , which increased greatly during hemorrhagic shock. We found that the contractions of the rat's thoracic aorta strip evoked by electric field stimulation decreased significantly in the hemorrhagic shock group as compared with the control's. After giving naloxone (1. 37 ×10-5mol/L) , the enhancement rates of contraction of the shocked rat's artery strips increased greatly as compared with the control strips (P<0.01). Conclusion : The results indicated that opioid receptors in the arterial wall played a role in the decrease of vasoconstriction during hemorrhagic shock. The increasing content of enkephalin in the artery wall during hemorrhagic shork could be one of the important causes why vasoconstriction declined in hemorrhagic shock.Naloxone could act directly on the opioid receptors to block the inhibitory effects of opioid peptide on vasoconstriction and so to increase blood pressure and defy shock.展开更多
文摘Forty rots were randomized into 2 groups and naloxone or saline were injected to therats after they were inflicted with hemorrhagic shock at sea level and at a simulated altitude of4000m respectively to observe the effects of naloxone on left ventricular systolic pressure(LVSP),left ventricular diastolic pressure(LVDP),the maximal changing rate of LVSP(dp/dt max),heartrate(HR),and survival time of the animals.Plasma β-endorphin(β-EP)was determined beforeand after hemorrhage to observe the relationship between β-EP and hemorrhagic shock.It wasfound that the circulatory parameters of hemorrhagic shock changed more markedly at high alti-tude than at sea level,naloxone could restore these parameters and prolong the survival time inboth the animals of the sea level and high altitude groups,and plasma β-EP level was elevatedafter hemorrhage especially in those animals at high altitude.These findings indicate:(1)Hemorrhagic shock at high altitude is usually accompanied with severe clinical manifestations,rapid progression,and high mortality.(2)β-EP seems to participate in the pathologicalmanifestafions of hemorrhagic shock at high altitude,and its depressive action on myocardialcontraction may be one of the factors inducing hemorrhagic shock.(3)Naloxone possesses defi-nite property to comet hemorrhagic shock at high altitude.
文摘Objective: The aim of this study was to investigate the action of the arterial wall opioid receptor in vascular function regulation during shock in rats. Metbods : Experiments were performed on rat model of hemorrhagic shock in vivo and arterial strips in vitro. Results: The mean arterial pressure of the rat was reduced rapidly to 3. 99 kpa by bleeding and was managed to maintain at that level. The mean maximum bleeding volume of the naloxone group was 25. 90±4. 23 ml/kg. It was significantly more than that of the control group which was 20. 26 ± 4. 43 ml/kg (P<0. 05). The vasoconstrictive phase of shock was 50. 00± 11. 53 min in the naloxone group and 31. 68 ± 9. 98 min in the control group. The differences between the two groups were considered significant (P<0. 05). The contents of leucine enkephalin (L-ENK) in the rat's arteries were measured by radioimmunoassay , which increased greatly during hemorrhagic shock. We found that the contractions of the rat's thoracic aorta strip evoked by electric field stimulation decreased significantly in the hemorrhagic shock group as compared with the control's. After giving naloxone (1. 37 ×10-5mol/L) , the enhancement rates of contraction of the shocked rat's artery strips increased greatly as compared with the control strips (P<0.01). Conclusion : The results indicated that opioid receptors in the arterial wall played a role in the decrease of vasoconstriction during hemorrhagic shock. The increasing content of enkephalin in the artery wall during hemorrhagic shork could be one of the important causes why vasoconstriction declined in hemorrhagic shock.Naloxone could act directly on the opioid receptors to block the inhibitory effects of opioid peptide on vasoconstriction and so to increase blood pressure and defy shock.
