Effects of permissive hypercapnia on cerebral blood flow in ventilated newborn swine / 中华急诊医学杂志

ABSTRACT

Objective To investigate the effects of permissive hypercapnia (PHC) strategy used in ventilated newborn swine with respiratory failure on cerebral blood flow (CBF) and tissue metabolism. Method Eighteen newborn swine were randomly (random number) divided into 3 groups (n = 6) PHC, normocapnia (NC) and normal control groups. In PHC (PaCO2 50～60 mmHg) and NC (PaCO2 35 ～ 45 mmHg) groups, newborn swine were ventilated for treating respiratory failure induced by meconium aspiration. CBF was measured by using colored microsphere tracking technique. Cerebral oxygen metabolism rate (CMRO2), cerebral glucose metabolism rate (CMRGlu), and cerebral lactate production (CLP) were measured. Results After ventilation for 6 hours and 12hours, CBF in NC group decreased more significantly than those did in control group, and CMRGlu and CLP increased more significantly than those did in control group. In NC group, CMRO2 decreased more prominently than it did in control group 12 hours later. The CBF/CMRGlu and CBF/CLP ratios in NC group were lower than those in control(P＜0.05). There was no significant difference in CBF/CMRO2 ratio between NC and control groups. After ventilation for 6 hours, CBF in PHC group was lower than those in control group. But after ventilation for 12hours, CBF in PHC group increased and there was no significant difference in CBF between PHC group and control group (P＞O.05). There were no significant differences in CMRGlu, CLP and CMRO2 between PHC group and control group. The CBF/CMRGlu and CBF/CLP ratios in PHC group were lower than those in control, but higher then those in NC group (P＜0.05). There was no significant difference in CBF/CMRO2 ratio between PHC and control groups. Conclusions The reduction of cerebral blood flow and the disturbance of CBF autoregulation disturbance occur in ventilated newborn swine with hypoxemia respiratory failure. PHC may attenuate the reduction in CBF and the disturbance of CBF autoregulation.