Because of rheological factors and cellular swelling that restricts capillary diameter, restoration of CBF after complete cerebral ischemia initially requires higher perfusion pressure than that anticipated from a CBF autoregulatory curve. Thus, the low cerebral perfusion pressures typically attained during chest compressions with cardiopulmonary resuscitation are generally inadequate for restoring cerebral energy metabolism (13,14). Moreover, delaying the onset resuscitation after cardiac arrest from 0 min to 1.5, 3, 6, and 12 min progressively worsens the level of CBF attained at low reperfusion pressures (15). Once cardiac function is restored, arterial pressure may transiently increase above normal levels because of the persistent action of endogenously released and exogenously administered vasopressors during resuscitation. It has been argued that brief hypertension after resuscitation may be beneficial for the brain by washing out the poorly deform-able leukocytes and reestablishing flow in all capillaries (16,17).
Full reperfusion leads to recovery of oxidative phosphorylation and ATP. Full recovery of ATP lags behind recovery of the transcellular Na+ gradient by several minutes as additional ATP is required for enhanced ionic pump activity (3). However, complete ischemia of long durations, such as 30 min, results in incomplete recovery of ATP (9), presumably because of mitochondrial dysfunction, loss of adenine nucleotide base and nicotinamide adenine dinuclotide (NAD+), and microcirculatory patches of poor reflow. A secondary delayed loss of ATP at several hours or days of reperfusion is thought to be related to opening of the mitochondrial transition pore and loss of mitochondrial membrane potential. Recovery of intracellular pH lags the initial recovery of ATP (Fig. 1), and recovery of electrical conduction as assessed by evoked potentials lags recovery of pH (9). A relationship between tissue acidosis during early reperfusion and evoked potential recovery is suggested by the observations that augmenting carbonic acidosis during reperfusion suppresses evoked potential recovery (18), while accelerating intracellular pH recovery with antioxidant treatment improves evoked potential recovery (19 ).
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...