Abstract:Global Ischemia in Dogs: Intracranial Pressures, Brain Blood Flow and Metabolism • Our earlier studies showed no secondary postischemic (PI) rise in cisterna magna pressure (CMP) for ten hours and no significant reduction in CBF (integrated N,O desaturation technique) for three and one-half hours after 15 minutes of systemic circulatory arrest. However, transtentorial pressure gradients may have developed, and CBF changes may have been masked by limitations of the N,O method in low flow states. In this study, 12 dogs were subjected to 15 minutes of aortic occlusion and studied for two hours PI. Immediately after restoration of circulation, cisterna magna, supracortical and lateral ventricle pressures rose to 35 to 40 torr, concomitant with a threefold increase in cerebral blood flow ^"Xe clearance technique). By 30 minutes postischemia, cisterna magna and supracortical pressures had returned to control values but lateral ventricular pressures normalized slower. CBF decreased to and remained at 50% of preischemic values after 40 minutes PI. Cerebral glucose uptake increased markedly immediately PI, then fell significantly below control values at 45 minutes. Cerebral O, uptake was significantly reduced, although less than for glucose, between 30 and 60 minutes PI. Global ischemia for 15 minutes is followed neither by a secondary rise in intracranial pressure nor by a cerebrospinal fluid pressure gradient but rather by hypoperfusion and defective glucose metabolism.Additional Key Word* circulatory arrest glucose uptake brain ischemia postischemic encephalopathy intracranial dynamics cerebral circulation postischemic no-reflow

SUMMARY Sympathetic nerve activity and in particular renal sympathetic nerve activity were monitored in six conscious dogs subjected to 6 days of intravenous angiotensin (ANG II) infusion (20 ng/kg/min). This was accomplished by measurement of both arterial and renal venous plasma catecholamine concentration. During the initial 4 hours of ANG II infusion, mean arterial pressure (MAP) increased 35 ± 8 mm Hg from a control value of 101 ± 4 mm Hg. Although there were no significant changes in arterial plasma norepinephrine (NE) concentration at this time (control = 148 ± 40 pg/ ml), arterial plasma epinephrine (E) concentration increased threefold (control 42 ± 15 pg/ml). After 24 hours of ANG II infusion, MAP remained elevated (132 ± 5 mm Hg), but plasma E concentration returned to control levels. From Days 2 through 6 of ANG II infusion, MAP was elevated approximately 40 mm Hg, but there were no chronic increases in either arterial plasma E or NE concentrations. In contrast to arterial plasma catecholamine concentration, renal vein plasma NE concentration (control = 216 ± 27 pg/ml) actually decreased during both the acute (122 ± 12 pg/ml) and chronic (103 ± 26 pg/ml) phases of ANG II infusion. Moreover, renal NE overflow (renal venous plasma NE concentration-arterial plasma NE concentration x effective renal plasma flow), an index of renal sympathetic nerve activity, was depressed during the chronic phase of ANG II hypertension. These results, therefore, do not support the contention that the sympathetic nervous system mediates the hypertension produced by elevated plasma levels of ANG II. In fact, the finding that renal NE overflow is chronically depressed during long-term ANG II infusion suggests that changes in renal sympathetic activity may serve to attenuate the development of elevated arterial pressure during ANG II hypertension. The proposed peripheral actions of ANG II include: 1) facilitation of evoked norepinephrine (NE) release from adrenergic nerve endings; 2) inhibition of NE reuptake from adrenergic nerve terminals; and 3) po-

Abstract:Global Ischemia in Dogs: Cerebrovascular COi Reactivity and Autoregulation• One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO 2 , and (2) cerebral blood flow (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO 2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing Paco 2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant Paco 2 . These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO 2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.

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SummaryBackground: There is disagreement regarding the anatomy of the pediatric airway,