Autoregulation of cerebral blood flow: influence of the arterial blood pressure on the blood flow through the cerebral cortex.

Abstract

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 (...

Hypercapnia during the first 3 days of life is associated with severe intraventricular hemorrhage in very low birth weight infants

“…17,18 Further, hypercapnia may abolish or impair cerebral autoregulation, causing the cerebral vasculature to be at risk for ischemia or hyperperfusion during fluctuations of blood pressure. [4][5][6] Consistent with our results, most studies examining the relationship between hypercapnia and IVH identified a positive univariate association. It was first demonstrated in 1978 that umbilical PaCO 2 was significantly greater in premature infants subsequently diagnosed with IVH compared to those without IVH.…”

“…4 Further, hypercapnia in animals has been shown to abolish intact cerebral autoregulation. 5,6 In addition to low gestational age, low birth weight, male gender, worse acute lung disease, etc., hypercapnia has also been identified as an important risk factor for intraventricular hemorrhage (IVH), [7][8][9][10][11][12][13][14][15][16] the most common acute brain injury of premature infants. Although it is unclear whether hypercapnia causes IVH or results from circulatory disturbances that follow severe IVH, hypercapnia may influence the development of IVH by causing vasodilation of cerebral resistance arterioles, increasing CBF, and by impairing intact cerebral autoregulation.…”

“…Although it is unclear whether hypercapnia causes IVH or results from circulatory disturbances that follow severe IVH, hypercapnia may influence the development of IVH by causing vasodilation of cerebral resistance arterioles, increasing CBF, and by impairing intact cerebral autoregulation. [4][5][6]17,18 A majority of the published studies reporting an association between hypercapnia and IVH were performed in the pre-surfactant era, where goals for ventilation 19,20 were different than that currently recommended. 21 Before the surfactant era, hypercapnia was likely a proxy for the sickest infants with the most severe respiratory distress syndrome.…”

Graded Hypotension and MCA Occlusion Duration: Effect in Transient Focal Ischemia

“…The pressure flow relationships for the cerebral circulation have been weII defined, and the cerebral perfusion pres sure is 80 mm Hg in humans under normal condi tions. However, autoregulation keeps CBF rela tively constant when the BP is within the range of 60 to 150 mm Hg in the rat (Hernandez et al, 1978), similar to that of other species, including primates and humans (Harper, 1966). The hypotension to 40 mm Hg in our study is absolutely out of the range of autoregulation, and it is not surprising that infarc tion was 25 ± 14% and 40 ± 12% at MCAO dura tions of 60 and 120 min, respectively, compared to 5 ± 3% and 19 ± 15% with the same MCAO dura tion when the BP was 80 mm Hg, Although MCAO at BP >80 mm Hg was not feasible in this series of experiments, 60 min of MCAO produced only mild scattered ischemic cell change in a similar model using Wi star rats at normal BP (Nagasawa and Kogure, 1989).…”

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

“…Together, the components of NVU detect physiological needs of the neural tissue and respond accordingly to supply these demands [112]. Consequently, under normal conditions, cerebral blood flow is maintained constant despite wide changes in perfusion pressure [114], a phenomenon called autoregulation of cerebral blood flow [115].…”