It is well known that the cerebral blood flow alters in response to changes in the arterial carbon dioxide tension. However, it is not yet clear whether there are upper and lower limits of Paco, beyond which the cerebral vessels do not react. In addition, there have been no reports on the response of cerebral blood flow to alterations in Paco, in hypotensive states.The recent development by Ingvar (1961, 1962) of a rapid, easily repeatable, and relatively untraumatic method of estimating the blood flow through the cerebral cortex has enabled us to make multiple estimations of blood flow in lightly anaesthetized dogs at varying tensions of arterial carbon dioxide and varying arterial blood pressures. METHODThree hundred and two measurements of blood flow through the cerebral cortex were made on 41 unselected mongrel dogs. The animals were anaesthetized with thiopentone. A cuffed endotracheal tube was inserted and connected to a Starling respiratory pump, through which a 4:1 mixture of N20 and oxygen was delivered in open circuit. Suxamethonium chloride was administered at intervals. Repeated small doses of thiopentone were given during the actual operation. A cannula was inserted into the femoral artery and connected to a damped mercury manometer for the measurement of the systemic blood pressure. This cannula was also used for the withdrawal of arterial blood samples.The thyroid branch of the common carotid artery was cannulated centripetally, the distal end being tied. The temporal muscle was excised and a trephine hole made over the parietal bone. A cruciate incision was made in the dura and the exposed brain cortex was covered with a plastic membrane (Melinex) 6,& in thickness. A thin lead shield was placed over the surrounding dura and bone, leaving exposed only the area of cortex covered by the membrane. An end window Geiger counter, mounted 1 mm. above the exposed cortex, was connected to a ratemeter and a direct writing recorder. After the operation was completed, thiopentone administration was discontinued and the preparation remained undisturbed for one hour before the first measurements of blood flow were made. Plasma substitute (Dextran), saturated with 85 Krypton, was injected, rapidly at first and then more slowly, into the carotid artery over two to three minutes. The blood flow through the brain cortex was calculated from the half-life of the initial slope of a semilogarithmic plot of the clearance curve using the formula of Lassen and Ingvar (1961, 1962
Until fairly recently it 'was believed that cerebral blood flow followed more or less passively the mean arterial blood pressure, and the stability of the cerebral circulation under physiological conditions reflected only the relative constancy of the arterial pressure maintained by the homeostatic pressor reflex mechanism ' (Sokoloff, 1959). That there might also be an intrinsic regulation of cerebrovascular tone was suggested by Fog (1934Fog ( , 1938 and by Forbes, Nason, and Wortman (1937). These workers observed that the blood vessels of the pia mater constricted in response to a rise in arterial blood pressure and dilated in response to a fall in pressure.Although more recent studies in man (summarized by Lassen, 1959) seem to refute the idea of a passive pressure/flow relationship for the cerebral circulation, there is still conflict on the precise role of the arterial blood pressure in the control of the cerebral blood flow.The experiments reported in this paper were undertaken to measure the effect of gradual reduction of the mean arterial blood pressure on the blood flow through the cerebral cortex under 'normal' respiratory conditions (that is a PaCO2 of 40 mm. Hg) and under conditions of hypercapnia (CO2 being added to the respiratory mixture). METHODOne hundred and seventeen measurements of blood flow through the cerebral cortex were made on 12 unselected mongrel dogs. The animals were anaesthetized with thiopentone. A cuffed endotracheal tube was inserted and connected to a Starling respiratory pump, through which a 4:1 mixture of N20 and oxygen was delivered in open circuit. Suxamethonium chloride was administered at intervals. Repeated small doses of thiopentone were given during the actual operation. A cannula was inserted into the femoral artery and connected to a damped mercury manometer for the measurement of the systemic blood pressure. This cannula was also used for the withdrawal of arterial blood samples.The thyroid branch of the common carotid artery was cannulated centripetally, the distal end being tied. The temporal muscle was excised and a trephine hole made over the perietal bone. A cruciate incision was made in the dura and the exposed brain cortex was covered with a plastic membrane (Melinex) 6p in thickness. A thin lead shield was placed over the surrounding dura and bone, leaving exposed only the area of cortex covered by the membrane. An end window Geiger counter, mounted 1 mm. above the exposed cortex, was connected to a ratemeter and.a direct writing recorder. After the operation was completed, thiopentone administration was discontinued and the preparation remained undisturbed for one hour before the first measurements of blood flow were made. Plasma substitute (Dextran), saturated with 85 Krypton, was injected, rapidly at first and then more slowly, into the carotid artery over two to three minutes. The blood flow through the cerebral cortex was calculated from the half-life of the initial slope of a semi-logarithmic plot of the clearance curve using the formula of Ingvar (...
Acute hypertension was induced in 19 anesthetized cats by the intravenous administration of angiotensin. The caliber of pial arteries was measured by a television image-splitting technique and local cerebral blood flow by the hydrogen clearance technique. As the blood pressure was increased, pail arterioles constricted and cerebral blood flow remained relatively constant, showing that autoregulation of cerebral blood flow was intact. At mean arterial pressures of more than 170 mm Hg arteriolar dilation appeared. In smaller arterioles (initial diameter less than 100 mum) a segmental dilation (the "sausage'string" phenomenon) frequently preceded uniform dilation. This arteriolar dilation was associated with a marked increase in local cerebral blood flow indicating that the upper level of autoregulation had been breached. In no cat was vasospasm or a decrease in blood flow observed during induced hypertension. Hypertension also caused dysfunction of the bloodbrain barrier since, in 17 out of 19 of the cats examined, there was extravasation of protein-bound Evans blue into brain tissue. In only one of the 19 cats subjected to neuropathological analysis was ischemic brain damage identified and this was restricted to minimal ischemic cell change. The results indicate that severe, induced hypertension in cats produces cerebral arteriolar dilation, an increase of cerebral blood flow, and dysfunction of the blood-brain barrier. These observations may be of importance in understanding the pathogenesis of hypertensive encephalopathy.
The systemic administration of norepinephrine has minimal effects on the cerebral circulation, perhaps due to blood-brain barrier mechanisms. To test hypothesis, the cerebrovascular effects of norepinephrine beyond the blood-brain barrier were studied in anesthetized baboons, Intraventricular norepinephrine (40 mug/kg) resulted in significant increases in cerebral blood flow (40%), cerebral oxygen consumption (21%), and cerebral glucose uptake (153%). Intracarotid hypertonic urea opens the blood-brain barrier by osmotic disruption; Consequent to hypertonic urea, the intracarotid infusion of norepinephrine, 50 ng/kg-min, significantly increase cerebral blood flow (49%), cerebral oxygen consumption (21%), and cerebral glucose uptake (76%), It appears probable that the cerebrovascular responses to norepinephrine are dependent on the integrity of the blood-brain barrier; It is likely that the increase in cerebral blood flow, associated with norepinephrine when it bypasses the barrier, is secondary to an increase in cerebral metabolism.
The effect on the cerebral blood flow (CBF) (27:1-6,1972)
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