SUMMARY Cerebral blood flow autoregulation (CBFA) to changes in perfusion pressure has not been previously reported in the rat. A modification of the Kety and Schmidt technique employing I33Xenon was used to measure cerebral blood flow (CBF) in paralyzed adult Sprague Dawley rats passively ventilated with 70% nitrous oxide and 30% oxygen. At a mean arterial blood pressure (MABP) of 121 ± 19 mm Hg, and a mean arterial Pco 2 of 36.2 ± 2.9 mm Hg, mean CBF was 103 ± 22 ml/min/100 gm of brain. CBF responses to hypercarbia were 4.9 ml/min/100 gm per mm Hg change in arterial Fco 2 . CBF was measured during steady state levels of hypo-and hypertension induced by phlebotomy, or by intravenous metaraminol, over the MABP range of 48-205 mm Hg. From a MABP of 80 to 160 mm Hg, CBF remained nearly constant, indicating the presence of CBFA. However, when MABP exceeded 160 mm Hg, CBF became pressure dependent, indicating a "breakthrough" of autoregulation in acute severe hypertension.CEREBRAL BLOOD FLOW autoregulation (CBFA) denotes the adaptive reaction whereby blood flow to the brain is maintained nearly constant despite variations in perfusion pressure.1 In most mammalian species, including man, CBFA has been characterized within the mean arterial blood pressure (MABP) range of approximately 70 to 150 mm Hg.2 ' 5 However, cerebral circulatory responses to blood pressures beyond this range in acute hypertension have not been extensively studied. Some investigators have recently reported that cerebral autoregulatory mechanisms fail at high perfusion pressures, with a so-called "breakthrough" of CBFA taking place. 59Most studies of the cerebral circulation have been carried out in man or in large experimental animals. More recently, CBF has also been studied in the most widely used laboratory animal, the albino rat, by a variety of methods, and values for basal CBF under conditions of normotension have been reported.10 "" However, pressure-flow relationships for the cerebral circulation have not been defined in this species. In the present study we have measured CBF in rats during induced alterations in arterial blood pressure. We have examined a wide range of systemic pressures, paying particular attention to the state of cerebral circulation during acute hypertension. Methods Animal PreparationSprague-Dawley rats of both sexes, weighing 300-600 gm, were employed in this study. Each rat was rapidly tracheotomized under ether anesthesia, paralyzed with tubocurarine (0.5 mg/kg, administered subcutaneously), and passively ventilated with a mixture of 70% nitrous oxide and 30% oxygen by a small animal respirator. Atropine (0.05 mg/kg) was injected subcutaneously to minimize tracheobronchial secretion. Ventilatory rate and tidal volume were adjusted to ensure arterial blood normoxia and normocarbia. The caudal artery was exposed and catheterized with a 30 gauge Teflon catheter. This catheter served to monitor arterial blood pressure with a pressure transducer (Statham, Model P23Dc), and to allow anaerobic withdrawal of arterial blo...

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Cerebral blood flow (CBF) and cerebral metabolic rates (CMR) were studied in newborn dogs during insulin-induced hypoglycemia. Pups were anesthetized, paralyzed, and artificially ventilated with a mixture of 70% nitrous oxide and 30% oxygen to maintain normoxia and normocarbia. Experimental animals were given regular insulin (0.3 units/gm IV); controls received normal saline. CBF was determined using a modification of the Kety-Schmidt technical employing 133Xe as indicator. Arteriovenous differences for oxygen, glucose, lactate, and beta-hydroxybutyrate (beta-OHB) were also measured, and CMRO2 and CMRsubstrates calculated. Two groups of hypoglycemic dogs were identified; those in which blood glucose levels were greater than 0.5 mM (group 1), and those in which they were less than 0.5 mM (group 2). CBF did not change significantly from control values of 23 +/- 10 ml/min/100 g (mean +/- S.D.) at both levels of hypoglycemia. Similarly, hypoglycemia did not alter CMRO2 significantly from its initial level of 1.05 +/- 0.37 ml O2/min/100 g. Glucose consumption in brain during normoglycemia accounted for 95% of cerebral energy supply with minimal contributions from lactate (4%) and beta-OHB (0.5%). During hypoglycemia, CMRglucose declined by 29 and 52% in groups 1 and 2, respectively, while CMRlactate increased to the extent that this metabolite became the dominant fuel for oxidative metabolism in brain. The cerebral utilization of beta-OHB was unaltered by hypoglycemia. The findings indicate that insulin-induced hypoglycemia in the newborn dog is associated with an increase in cerebral lactate utilization, supplementing glucose as the primary energy fuel and thereby preserving a normal CMRO2. These metabolic responses may contribute to the tolerance of the immature nervous system to the known deleterious effects of hypoglycemia.

Cerebral blood flow (CBF), CBF responses to changes in arterial CO2 tension, and cerebral metabolic rate for oxygen (CMRO2) were measured in newborn dogs, by means of a modification of the Kety and Schmidt technique employing 133Xe. Mongrel dogs of 1-7 days of age were paralyzed and passively ventilated with 70% N2O and 30% O2. CBF was derived by analysis of paired serial 20-microliter samples of arterial and of cerebral venous blood from the superior sagittal sinus. At an arterial PCO2 of 36.9 +/- 3.7 Torr and a mean arterial blood pressure of 62 +/- 10 Torr, CBF was 23 +/- 8 ml/min per 100 g. The arteriovenous oxygen content difference averaged 5.6 vol%, and CMRO2 was 1.13 +/- 0.30 ml O2/min per 100 g. CBF increased or decreased by 0.58 ml/min/100 g per Torr change in PCO2. Our results suggest that in the newborn, basal CBF and CBF responses to CO2 are considerably lower than in the adult and parallel the lower metabolic needs of the newborn brain.

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The cerebrovascular response of newborn animals to hypotension has not been defined on a regional basis. Using an autoradiographic technique employing 14C-iodoantipyrine as indicator, we studied the cerebral physiological responses of newborn dogs to hypotension induced by exsanguination or by administration of Escherichia coli endotoxin. Regional cerebral blood flow (rCBF) to all gray matter structures was preserved, even at mean arterial pressures as low as 20 mm Hg. In contrast, rCBF to periventricular and occipital white matter decreased significantly during severe hypotension. The selective hypoperfusion of cerebral white matter during severe hypotension may provide a mechanistic explanation for the pathogenesis of periventricular leukomalacia.

Abstract:The Effect of Sympathetic Denervation on Cerebral C Sensitivitv