Objective: To study the changes between cerebral oxygen (O 2) delivery and uptake in dogs resuscitated under normotension or hypertension for 4 h. Methods: The model of ventricular fibrillation of 8 min in 12 dogs was...Objective: To study the changes between cerebral oxygen (O 2) delivery and uptake in dogs resuscitated under normotension or hypertension for 4 h. Methods: The model of ventricular fibrillation of 8 min in 12 dogs was made, followed by open cardiopulmonary resuscitation, reperfusion with normal or high mean arterial pressure (MAP), and controlled ventilation to 4 h. Animals were randomly assigned into Group NT (normotensive reperfusion, n=6) and Group HT (hypertensive reperfusion, n=6). Cerebral arteriovenous (sagittal sinus) O 2 content difference (Ca-ssO 2) and venous (sagittal sinus) PO 2 (PssO 2) were determined before cardiac arrest (CA) and 30, 60, 120, and 240 min after CA. Results: In Group NT, Ca-ssO 2 was lower at 30 min (P<0.05) but higher at 240 min (P<0.01) after CA than that before CA. In Group HT, Ca-ssO 2 was not significantly different from that in Group NT before CA but was lower than that in Group NT at 30 min after CA (P<0.01). Ca-ssO 2 was not significantly different in Group NT and HT thereafter. In both groups, PssO 2 was both higher at 30 min after reperfusion (P<0.01) and at 240 min after reperfusion lower (P<0.05) than those before CA .At 30 min after reperfusion, PssO 2 was higher (P<0.01) in Group HT than that in Group NT, with insignificant difference between two groups. Conclusion: Cerebral O 2 delivery and uptake are mismatched after CA and resuscitation. Hypertensive reperfusion improves oxygen delivery to the brain early after CA.展开更多
文摘Objective: To study the changes between cerebral oxygen (O 2) delivery and uptake in dogs resuscitated under normotension or hypertension for 4 h. Methods: The model of ventricular fibrillation of 8 min in 12 dogs was made, followed by open cardiopulmonary resuscitation, reperfusion with normal or high mean arterial pressure (MAP), and controlled ventilation to 4 h. Animals were randomly assigned into Group NT (normotensive reperfusion, n=6) and Group HT (hypertensive reperfusion, n=6). Cerebral arteriovenous (sagittal sinus) O 2 content difference (Ca-ssO 2) and venous (sagittal sinus) PO 2 (PssO 2) were determined before cardiac arrest (CA) and 30, 60, 120, and 240 min after CA. Results: In Group NT, Ca-ssO 2 was lower at 30 min (P<0.05) but higher at 240 min (P<0.01) after CA than that before CA. In Group HT, Ca-ssO 2 was not significantly different from that in Group NT before CA but was lower than that in Group NT at 30 min after CA (P<0.01). Ca-ssO 2 was not significantly different in Group NT and HT thereafter. In both groups, PssO 2 was both higher at 30 min after reperfusion (P<0.01) and at 240 min after reperfusion lower (P<0.05) than those before CA .At 30 min after reperfusion, PssO 2 was higher (P<0.01) in Group HT than that in Group NT, with insignificant difference between two groups. Conclusion: Cerebral O 2 delivery and uptake are mismatched after CA and resuscitation. Hypertensive reperfusion improves oxygen delivery to the brain early after CA.
