Experimental Study Of The Haemodynamics Effects Of Norepinephrine And Epinephrine In Actue Severe Hemorrhagic Shock

Background: Cute massive hemorrhage is a sudden and seriouscondition of the body. The probability of survival decreases by8%for everyminute of hesitation. In order to prevent cardiopulmonary arrest and win enoughtimes to save the patient though urgent surgical repair, appropriate resuscitationand application of vasoactive agents are measures conducive to lowering rate ofcardiopulmonary arrest. The key point of anesthesia is to increase the coronaryarterial blood flow,decrease totalcoronary arterial resistance and improvemyocardial blood andoxygensupply. If cardiac arrest happened,seriouscomplications rate increased and the survival rate will decreasecorrespondingly,even if cardiopulmonary resuscitation sucssfully. To objectivelyappraise the effect and mechanism of epinepHrine. NorepinepHrine (NE) isrecommended as first-line therapy to restore arterial pressure in septic andhaemorrhagic shock. As a catecholamines,epinepHrine is commonly used forthe cardiovascular support of these patients when shock and hypotension develop after resuscitation.Generally, it is also injected first for therapy ofanapHylactic shock. In our clinical work, epinepHrine is often used fortreatment of life-threatening hypotension, and the patientsrecovered well after resuscitation, with fewer complication cases. Although itsmechanism of keeping effective circulation may merit evaluation. The purposeof this study was to determine the effects of norepinepHrine vs. epinepHrine onhemodynamic variables in an animal model of actue severe hemorrhagic shockand delayed fluid resuscitation through animal experiment.Methods: The anesthetized rats were randomly divided into3groups,namely,the normal saline (NS) group, norepinepHrine(NE) group andepinepHrine (E)group. Three groups were subjected to a30-min controlledhemorrhage(withdrawal of3ml blood/100g body mass) followed by a30-minuncontrolled hemorrhage (Femoral artery bleeding), which resulted in a mean±sem loss of45%±5%of estimated whole blood volume within15mins andmean arterial pressures of <35mmHg. When mean arterial pressure declinedprogressively, rats randomly received a different bolus dose and continuousinfusion of either norepinepHrine (50ug～200ug/kg and50ug·g-1·h-1, n=20), orepinepHrine (50μg～200ug/kg and50μg·g-1·h-1, n=20), respectively. In the twohypotensive resuscitation groups (n=20), mean arterial pressure was not allowedto fall below35mmHg by infusion of vasoactive drugs. The endpoint was at60mins, all surviving animals were fluid resuscitated while bleeding wassurgically controlled.Results:1. Mean±sem arterial blood pressure at55%blood loss wassignificantly (P<0.05) higher after norepinepHrine vs. epinepHrineThe difference between the two groups in survival times had significant statistically difference.2. Mean arterial pressure and Heart rate was significantly higher in theepinepHrine group than norepinepHrine group throughout the study. There wasa significant difference (P <0.05) in>70%blood loss between the two groups.Despite several bolus doses, rats in the two groups treated with vasoactive drugscardiac arrested within30mins after drug administration.3.The difference between the two groups in theplasma biochemical indices were not statistically significant.Conclustions::1. We established a stable ASHS rat modelwhich maintained the stability of blood pressure in35±5mmHg during theresearch.2. EpinepHrine, compared with nepinepHrine, maintain bloodpressure effectively and win golden time for the further treatment in a ratmodel of uncontrolled hemorrhagic shock after main artery injury when surgicalintervention and fluid replacement was delayed.3. It is indicated that to some degree shock associated with hepaticand renal function damage with or without vasoactive agent.