The influences of morphine or ketamine pre-treatment on hemodynamic, acid-base status, biochemical markers of brain damage and early survival in rats after asphyxial cardiac arrest

Abstract

BackgroundIn different models of hypoxia, blockade of opioid or N-methyl-D-aspartate (NMDA) receptors shows cardio- and neuroprotective effects with a consequent increase in animal survival. The aim of the study was to investigate effects of pre-treatment with Morphine or Ketamine on hemodynamic, acid-base status, early survival, and biochemical markers of brain damage in a rat model of asphyxial cardiac arrest (ACA).MethodsUnder anaesthesia with Thiopental Sodium 60 mg/kg, i.p., Wistar rats (n = 42) were tracheostomized and catheters were inserted in a femoral vein and artery. After randomization, the rats were pre-treated with: Morphine 5 mg/kg i.v. (n = 14); Ketamine 40 mg/kg i.v. (n = 14); or equal volume of i.v. NaCl 0.9% as a Control (n = 14). ACA was induced by corking of the tracheal tube for 8 min, and defined as a mean arterial pressure (MAP) < 20 mmHg. Resuscitation was started at 5 min after cardiac arrest (CA). Invasive MAP was recorded during experiments. Arterial pH and blood gases were sampled at baseline (BL) and 10 min after CA. At the end of experiments, all surviving rats were euthanised, brain and blood samples for measurement of Neuron Specific Enolase (NSE), s100 calcium binding protein B (s100B) and Caspase-3 (CS-3) were retrieved.ResultsAt BL no differences between groups were found in hemodynamic or acid-base status. After 3 min of asphyxia, all animals had cardiac arrest (CA). Return of spontaneous circulation (MAP > 60 mmHg) was achieved in all animals within 3 min after CA. At the end of the experiment, the Ketamine pre-treated group had increased survival (13 of 14; 93%) compared to the Control (7 of 14; 50%) and Morphine (10 of 14; 72%) groups (p = 0.035). Biochemical analysis of plasma concentration of NSE and s100B as well as an analysis of CS-3 levels in the brain tissue did not reveal any differences between the study groups.ConclusionIn rats after ACA, pre-treatment with Morphine or Ketamine did not have any significant influence on hemodynamic and biochemical markers of brain damage. However, significantly better pH level and increased early survival were found in the Ketamine pre-treated group.

Inhibition of mast cell tryptase attenuates neuroinflammation via PAR-2/p38/NFκB pathway following asphyxial cardiac arrest in rats

“…Neurologic deficits were associated with the status of the neuroinflammation. The mortality rate of the present work was in line with previous reports evaluating ACA in rodents [65][66][67] Several potential limitations should be considered while interpreting the results of the present study. For example, in this study, we focused on the role of MCtryptase in neurologic dysfunction following CA, but not MC itself.…”

Effect of Thiopental on Ischemic Stroke in Rat Brain in Spontaneously Hypertensive Rats

“…A context of the longer period of hypertension among the selected animals has reported a higher risk potential related to the damaged condition of the brain cells [ 19 ]. The advantage is that thiopental is responsible for less effect on the context of damaging rat brain for lower rate of the involvement in focal cerebral ischemia for hypertensive rats.…”

Analgesic Use in Patients during Cardio-Pulmonary Resuscitation

“…Two retrospective studies have shown that patients receiving opioids before or during cardiac arrest had statistically significantly higher survival rates and better neurological outcomes compared to untreated patients [ 47 , 48 ]. Fentanyl is considered hemodynamically neutral whereas morphine can cause hypotension through peripheral vasodilation [ 49 , 50 ].…”