Focal ischemia due to reduction of cerebral blood flow (CBF), creates 2 zones of damage: the core area, which suffers severe damage, and penumbra area, which surrounds the core and suffers intermediate levels of injury. Objectives: A novel method is introduced, which evaluates mitochondrial function in the core and in the penumbra, during focal cerebral ischemia. Methods: Wistar rats underwent focal cerebral ischemia by middle cerebral artery occlusion (MCAO) for 60 minutes, followed by 60 minutes of reperfusion. Mitochondrial function was assessed by a unique Multi-Site – Multi-Parametric (MSMP) monitoring system, which measures mitochondrial NADH using fluorometric technique, and CBF using Laser Doppler Flowmetry (LDF). Results: At the onset of occlusion, CBF dropped and NADH increased significantly only in the right hemisphere. CBF levels were significantly lower and NADH significantly higher in the core than in the penumbra. After reperfusion, CBF and NADH recovered correspondingly to the intensity of ischemia. Conclusion: Application of the MSMP system can add significant information for the understanding of the cerebral metabolic state under ischemic conditions, with an emphasis on mitochondrial function.

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We examined the reflex effect of brief left circumflex coronary artery occlusion (CAO) on renal blood flow (RBF) and renin secretion (RS). Studies were conducted in alpha-chloralose-anesthetized dogs maintained on a salt-free diet for at least 3 days. A snare was placed around the left circumflex artery near its origin. The left renal artery and vein were exposed via flank incision, a flow probe was placed around the artery, and a curved needle was inserted into the vein for collection of renal venous blood. Values of blood pressure (BP), RBF, and RS were obtained for a 30-min control period, 4 min after the completion of a 10-ml/kg hemorrhage, 1 and 5 min after CAO, and 15 min after reinfusion. The CAO consisted of two 1-min occlusions separated by a 1-min interval. The results indicate that CAO reflexively inhibits the RS response to nonhypotensive hemorrhage and prevents renal vasoconstriction (P less than 0.05, n = 7). Both effects were completely abolished after vagotomy (n = 5). Renal denervation also abolished the response (n = 5). No response was observed during identical time controls (n = 5). The response was more pronounced in dogs with carotid sinus denervation, even though CAO resulted in marked reductions in BP (20%) under these conditions. These results demonstrate the presence of a cardiorenal reflex that can be activated by myocardial hypoxia and that acutely suppresses RS. This response is more pronounced in the absence of carotid sinus buffering.