Determination of cerebral cortical blood flow: a thermal technique.

A mathematical model for tissue thermodilution was developed to study cerebral cortical perfusion before and after controlled perfusion arrest. Cerebral cortical perfusion rates are readily determined by this method. A thermistor was introduced into the subdural space and secured in direct contact with the frontal cortex in 12 dogs on ketamine and gallamine anesthesia. A 22-gauge angiocath was placed in the right superior thyroid artery and directed into the carotid artery on the same side as the thermistor. The dogs were placed on cardiac bypass using a circuit from the right atrium to the pulmonary artery and a second circuit from the left ventricular apex to the left femoral artery. Arterial pressure, central venous pressure (CVP), intracranial pressure (ICP), and left atrial pressure (LAP) were monitored directly. A heat exchanger was used to maintain a constant blood temperature of 37 C in the output of the left side bypass circuit. Thermal flow curves were generated in the cerebral cortex by injecting 2 to 4 cc of cold saline into the common carotid artery through the injection catheter. Preliminary evaluation of this flow method in comparison to radioactive microspheres indicates that this method can be used in a reliable and reproducible fashion to determine cerebral cortical blood flow.

Effect of flunarizine on canine cerebral cortical blood flow and vascular resistance post cardiac arrest.

Twelve dogs were anesthetized and instrumental for determination of CVP, arterial pressure, intracranial pressure, left atrial pressure, and frontal cerebral cortical blood flow (CCBF) by the thermal method. A catheter was introduced into the venous return of the cerebral confluence to allow determination of cerebral A-V oxygen saturation differences. The animals were placed on cardiac bypass using a circuit from the right atrium to the pulmonary artery and a second circuit from the left ventricular apex to the left femoral artery. A heat exchanger was used to maintain a constant blood temperature of 37 C in the output of the left side bypass circuit. All animals were heparinized during bypass. Ventricular fibrillation was induced after completion of the bypass surgery. Two dogs served as controls. Pre-arrest determinations of hemoglobin, glucose, CCBF, and cerebral A-V oxygen differences were taken. Full circulatory arrest was carried out for 20 minutes by shutting off the cardiac bypass. Resuscitation was achieved by resumption of bypass perfusion. Acid-base balance was corrected quickly, and pre-arrest perfusion pressure was achieved and maintained for 90 minutes. All pressure parameters were monitored continuously. All pre-arrest determinations were repeated at 20, 40, 60, and 90 minutes post resuscitation. Five dogs were treated with 6 microgram/kg flunarizine administered IV drip over 10 minutes immediately post reperfusion. Five dogs were not treated post arrest. Treated animals had a prompt return of CCBF rates equal to or greater than pre-arrest flow, which persisted throughout the period of post-arrest observation. Untreated animals had markedly reduced CCBF and increased resistance. CCBF uniformly proceeded to near zero flow by 90 minutes. The ICP was not significantly altered by treatment.

Canine cerebral cortical blood flow and vascular resistance post cardiac arrest.

seven dogs were anesthetized and instrumented for determination of central venous pressure (CVP), arterial pressure, intracranial pressure (ICP), left atrial pressure (LAP), and frontal cerebral cortical blood flow by the thermal method. A catheter was introduced into the venous return of the cerebral confluence to allow determination of cerebral A-V oxygen saturation differences. The animals were placed on cardiac bypass using a circuit from the right atrium to the pulmonary artery, and a second circuit from the left ventricular apex to the left femoral artery. A heat exchanger was used to maintain a constant blood temperature of 37 C in the output of the left-side bypass circuit. All animals were heparinized during bypass. Ventricular fibrillation was induced after completion of the bypass surgery. Two dogs served as controls for stability of the measured parameters on prolonged bypass. Pre-arrest determinations of hemoglobin, cerebral cortical blood flow, and cerebral A-V oxygen saturation differences were taken. Full circulatory arrest was carried out for 20 minutes in 5 dogs by shutting off the cardiac bypass. Resuscitation was achieved by resumption of bypass perfusion. Acid-base balance was corrected and pre-arrest perfusion pressures were achieved and maintained for 90 minutes. All pressure parameters were monitored continuously. Pre-arrest determinations were repeated at 20, 40, 60, and 90 minutes post resuscitation. A 50% reduction in cerebral cortical blood flow 20 minutes post resuscitation progressed to near zero flow 90 minutes post resuscitation. The changes in net cerebral perfusion pressure produced by the slowly rising intracranial pressure do not account for this flow reduction. Calculation of cerebral vascular resistance reveals a ten-fold increase in resistance post-arrest and -resuscitation.