The influences of ketamine or morphine on hemodynamics, acid-base status and early survival in rats after asphyxia cardiac arrest: a pilot study

2017

Толық мәтін Ашық қол жеткізу: Gold Метадеректер (CSL-JSON)
DOI 10.7490/f1000research.1113806.1
Деректер сенімділігі 70 орташа
Бұл баға қалай есептеледі

Ол жазбаның өзінің тексерілетін белгілерінен құралады: мақаланың DOI-і бар ма, оның деректерін қанша тәуелсіз дереккөз растады, міндетті өрістер толтырылған ба және соңғы растау қаншалықты жаңа. Дереккөздер арасындағы алшақтық пен идентификатордың болмауы бағаны төмендетеді. 80-нен бастап мән жазбаның қосымша тексерусіз жарияланғанын, 60-тан 79-ға дейін — оның сенімділігі төмен күйде жарияланғанын және қолмен тексеру ұсынылатынын білдіреді. Редактор қолмен тексерген жазбаны қайта есептеу 90-нан төмен түсірмейді. Бұл — мақаланың өзіне емес, ол туралы деректерімізге берілген баға.

Аңдатпа

Introduction: Acute hypoxia results in uncontrolled release of glutamate and the consequent stimulation of NMDA receptors, which affects the whole ionic homeostasis and finally activates apoptosis of neurons A potential therapeutic approach to prevent this sequence of events is a blockade of NMDA receptors. Meanwhile, in different models of acute hypoxia, activation of delta-opioid receptors by morphine demonstrates cardioprotective effect with a consequent increase in animal survival. Thus, we aimed to test the effects of morphine or ketamine on hemodynamics, acid-base status and early survival in rats after asphyxia cardiac arrest (ACA). Methods: After instrumentation under anaesthesia with Thiopental sodium (60 mg/kg, i.p.), Wistar rats (n=21) weighing between 350–400 g were randomly assigned to three groups where: 1. Morhpine 5 mg/kg iv (n=7) was given 10 min before ACA; 2. Ketamine 40 mg/kg iv (n=7) was given 10 min before ACA; 3. Control (n=7), the same amount of NaCl 0,9% iv was given 10 min before ACA. The rats were asphyxiated by clamping the tracheostomia tube at the end of expiration for 5 min. Resuscitation included epinephrine (0.02 mg/kg, iv), manual thoracic compressions (180 per min) and mechanical ventilation (21% O2, 80 breaths/min). Invasive MAP was recorded at the baseline (BL), every 1 min during ACA and every 5 min in post-resuscitation (PR) period. Blood gas samples were taken at the BL and 10 min at the PR period. Early survival was determined at the 20 min after ACA. Results: No differences in MAP between the rats was found at the BL period. The rats pre-treated by ketamine got significantly higher MAP during PR period (133,9±30,4 vs 52,7±37,3 and 60,0±26,2 mm Hg, respectively, p < 0,002) and had significantly lower production of lactate (11,8±2,2 vs 13,5±1,5 and 15,6±1,2 mmol/l, respectively, p < 0,002) when compared to the rats treated by morhpine and only saline. Six of the seven rats survived at the 20 min after ACA in the ketamine group while four of the seven and two of the seven rats survived in the morphine and Control groups respectively (P=0,122). Conclusions: Pre-treatment with ketamine attenuated significantly disturbances in hemodynamics and lactate after ACA, but it did not improve early survival when compared to the rats pre-treated by morphine or saline.