engleski

Cerebral flow response to acute hypoxia in normal and cocaine fetuses (an ovine model)

Introduction: Cocaine exerts its drug action on the nervous system primarily by blocking the presynaptic reuptake of the monoamines (norepinephrine, epinephrine, dopamine and serotonin). Cocaine passes rapidly into fetal circulation from the maternal blood-stream and there are evidences of its teratogenic effects on the fetal brain development. Also cocaine may lead to destructive lesions like intracranial hemorrhages by inducing hypoxemia. In normal fetuses the cardiovascular response to hypoxia consists in a heart rate (HR) increase and cerebral vasodilatation with redistribution of fetal blood brain flow. This adaptation can be quantified by using parameters obtained by Doppler. Normally the cerebral vascular resistance index (CRI) and the cerebro-umbilical resistance index ratio (C/U) change in proportion with the pO2 level. Objective: To check if the long-term exposure to cocaine during pregnancy impairs fetal cardiac and cerebral reactivity in an ovine model. Study design: Heart rate and cerebral flow responses were measured in pregnant ewes during two acute hypoxic tests – cord compression and maternal aortic compression. The ewes were divided in 3 groups: control (received daily placebo of 2ml isotonic solution) and two cocaine groups treated daily from day 60 to day 134 of the gestation with 70mg or 140mg of cocaine intramuscularly. The ovine fetuses were instrumented with Doppler sensors for the cerebral and umbilical blood flow recording and a catheter in the femoral artery for blood gases measurement (pO2, pCO2, pH). Results: I cord compression (3min) The cerebral vascular resistance index and the cerebro-umbilical ratio decreased significantly less in the both cocaine groups (CRI p<0.05; C/U p<0.01). During the test the fetal heart rate increased less in cocaine groups (p<0.001). II maternal aortic compression (1min) The CRI decreased in the control and cocaine 70mg groups, but not in the cocaine 140mg group (p<0.01). The C/U decreased less in the both cocaine groups than in the control (p<0.05). The amplitude of the bradycardia was significantly higher in the cocaine groups (p<0.05). Conclusions: Long-term exposure to cocaine induces fetal blood flow disorders and hypoxia. It reduces the capability of the cerebral vessels to vasodilatate and the heart rate to increase during acute hypoxia.

cocaine; fetal hypoxia; Doppler

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