| The typical human cardiovascular response to septic shock is characterized by hypotension, lower systemic vascular resistance, the early development of myocardial depression, decrease blood flow of multiple splanchnic organ and incriminated function. Despite the continuous advances in monitor technologic and synthetic treatment, the mortality from septic shock remains high. This suggests the presence of septic mediators during septic shock that may be not inhibited. NO is known to play a major role. Many studies on septic animals or human, inhibiton or blockade of NO was beneficial, since it improved shock hemodynamic status. However, other documents described that NO blockaded was hazardous, since it worsened oxygen availability and blood perfusion of the splanchnic organ. How to remain the benefit of blockade NO in hemodynamics without an impairment in oxygen availability to the tisues are the unresolved problems in clinical practice. NO induces dilation of vascular and hypotension by activing soluble guanylate cyclase (sGC). In recently crimental studies on septic shock, NO synthase and sGC activation in splanchnic vascular tone are different, these differences may be result in improvement of hemodynamics without side effections of splanchnic oxygenation, which can be increased by increasing perfusion pressure.MB is an inhibitor of sGC. To blockade the effect of NO by inhibiting sGC with MB may represent a safer option. Effections of MB on hemodynamics and oxygenation of multiple splanchnic organs were observed in our study at first. Hemodynamics, blood flow of splanchnic organs, oxygenation and organ functions were recorded at status. Aim of the study was to predict the benefits which should be obtained with MBtreatment in septic shock.Parti. Experimental model of septic shock in dogs induced by endotoxin: a review and an evaluationObjective: To establish septic shock dog model by injection higher dose of endotoxin intravenously, then make a review and an evaluation of the animal model. Methods: In twelve anaesthetized and muscle relaxed mongrel dogs, 250~500μg/kg endotoxin were infused intravenously within 20-40 minutes. In order to determine whether septic shock was obtained during 2.5 hour, the parameters of hemodynamics and oxygenation were observed every 0.3 hour by Swan-Ganz catheter and blood gas was analysed. Results: After (1.5±0.3)hours of endotoxin infusion, eleven dogs satisfied septic shock criteria. Mean arterial pressure decreased after 0.3 hour of endotoxin infusion, then increased at low-moderate level and decreased significantly after 0.6 hour of administration endotoxin(P<0.01). It reached constant after one and half hours of endotoxin infusion. Cardiac output, left ventricular stroke work, systemic vascular resistance, oxygen delivery and oxygen uptake decreased remarkably below baseline(P<0.01). Conclusion: It is a practical and ideal model of dogs with septic shock which is characterized by hypodynamic and by deteriorating oxygenation through infusing higher dose of endotoxin intravenously.Part2. Effects of liquid resusciation on hemodynamics and oxygen metabilish in dogs with septic shock.Objective: To study the effects of liquid resusciation on hemodynamics and oxygen metabilish in dogs with septic shock. Methods; A model of septic shock was established by infusion 250ug/kg Escherichia coli endotoxin during 20 min in eleven dogs, which received isotonic salinefor resusciation. Hemodynamics was measured at baseline, shocked for 1 h and the different levels of pulmonary artery wedge pressure (PAWP) by Swan-Ganz catheter. Blood gas was analysed, then oxygen metabilish was calculated. Results: (l)Mean arterial pressure (MAP), cardiac output(CO), left ventricular stroke work (LVSW) and systemic vascular resistance (SVR) decreased significantly below baseline (decreased by 35.7%, 29.2%, 65.2% and 14.0%, respectively, P<0.01), Oxygen delivery (DO2) decreased by 46.9% (P<0.01), Oxygen uptake (VO2) decreased by 54.4% (P<0.01). (2)MAP, CO and LVSW increased signi...
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