✓ The relationship of cerebral blood volume (CBV) to cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and the cerebral metabolic rate for oxygen (CMRO2) was examined in rhesus monkeys. In vivo tracer methods employing radioactive oxygen-15 were used to measure CBV, CBF, and CMRO2. Cerebral perfusion pressure was decreased by raising the intracranial pressure (ICP) by infusion of artificial cerebrospinal fluid (CSF) into the cisterna magna. The production of progressive intracranial hypertension to an ICP of 70 torr (CPP of 40 torr) caused a rise in CBV accompanied by a steady CBF. With a further increase in ICP to 94 torr, CBV remained elevated without change while CBF declined significantly. Cerebral metabolic rate for oxygen did not change significantly during intracranial hypertension. For comparison, CPP was lowered by reducing mean arterial blood pressure in a second group of monkeys. Only CBF was measured in this group. In this second group of animals, the lower limit of CBF autoregulat...

Effects of increased intracranial pressure on cerebral blood volume, blood flow, and oxygen utilization in monkeys

Catheterization of Labbe's vein and of a pial branch of the middle cerebral artery has been performed on anesthetized baboons. Closure of the skull has enabled the reaction of the venous outflow from Labbe's vein to be monitored in response to pressure step increases in the pial arterial pressure induced by gas compression of a perfusion mixture connected to the arterial line. Rapid changes in cerebrovascular resistance with swift emergence of regulatory constancy have been shown, and the time characteristics of the resistance changes strongly suggest that they are primarily myogenic in origin. Induction of hypercapnia did not interfere with this autoregulatory mechanism to increased perfusion pressure, which indeed appeared to be more effective at raised arterial PCO2, but the mechanism was abolished by the induction of ischemia from middle cerebral occlusion.

A Study of Regional Autoregulation in the Cerebral Circulation to Increased Perfusion Pressure in Normocapnia and Hypercapnia

CBF and related parameters were studied in 68 patients before, during, and following cardiopulmonary bypass. CBF was measured using the intraarterial 133Xe injection method. The extracorporeal circuit was nonpulsatile with a bubble oxygenator administering 3-5% CO2 in the main group of hypercapnic patients (n = 59) and no CO2 in a second group of hypocapnic patients. In the hypercapnic patients, marked changes in CBF occurred during bypass. Evidence was found of a brain luxury perfusion that could not be related to the effect of CO2 per se. Mean CBF was 29 ml/100 g/min just before bypass, 49 ml/100 g/min at steady-state hypothermia (27 degrees C), reached a maximum of 73 ml/100 g/min during the rewarming phase (32 degrees C), fell to 56 ml/100 g/min at steady-state normothermic bypass (37 degrees C), and was 48 ml/100 g/min shortly after bypass was stopped. Addition of CO2 evoked systemic vasodilation with low blood pressure and a rebound hyperemia. The hypocapnic group responded more physiologically to the induced changes in hematocrit (Htc) and temperature, CBF being 25, 23, 25, 34, and 35 ml/100 g/min, respectively, during the five corresponding periods. Carbon dioxide was an important regulator of CBF during all phases of cardiac surgery, the responsiveness of CBF being approximately 4% for each 1-mm Hg change of PaCO2. The level of MABP was important for the CO2 response. At low blood pressure states, the CBF responsiveness to changes in PaCO2 was almost abolished. An optimal level of PaCO2 during hypothermic bypass of approximately 25 mm Hg (at actual temperature) is recommended. A normal autoregulatory response of CBF to changes in blood pressure was found during and following bypass. The lower limit of autoregulation was at pressure levels of approximately 50-60 mm Hg. CBF autoregulation was almost abolished at PaCO2 levels of greater than 50 mm Hg. The degree of hemodilution neither affected the CO2 response nor impaired CBF autoregulation, although, as would be expected, it influenced CBF: In 33 women CBF was 55 ml/100 g/min at an Htc of 24%, as compared with 42 ml/100 g/min in 35 men (Htc = 28%). High PaO2 was a vasoconstrictor, the autoregulatory plateau being narrowed. The lower limit of autoregulation was shifted to a higher pressure when PaO2 was low.

https://journals.sagepub.com/doi/pdf/10.1038/jcbfm.1986.61

Brain Luxury Perfusion During Cardiopulmonary Bypass in Humans. A Study of the Cerebral Blood Flow Response to Changes in CO2, O2, and Blood Pressure

Object. The aim of this study was to analyze how the main values extrapolated from the transcranial Doppler (TCD) waveform (systolic, mean, and diastolic velocity; velocity peak-to-peak amplitude; and pulsatility index [PI]) are affected by changes in intracranial pressure (ICP), systemic arterial pressure (SAP), autoregulation, and intracranial compliance. Methods. The analysis was performed using a mathematical model of the intracranial dynamics. This model includes a passive middle cerebral artery, the biomechanics of large and small pial arteries subjected to autoregulatory mechanisms, a collapsing venous cerebrovascular bed, the cerebrospinal fluid circulation, and the ICP—volume relationship. The results indicate that there are approximately three distinct zones characterized by different relationships between cerebral perfusion pressure (CPP) and velocity parameters in patients with preserved autoregulation. In the central autoregulatory zone (CPP > 70 mm Hg) the mean velocity does not change with ...

Relationships among cerebral perfusion pressure, autoregulation, and transcranial Doppler waveform: a modeling study

Publisher Summary This chapter discusses the local control of microvascular perfusion, which has been described as “the maintenance of appropriate tissue blood flow despite changes in arterial pressure, changes in local rate of metabolism, changes in nutrient concentrations in the blood, or changes in any other [local] factor that might affect the tissue demand for nutrients”. The discussion includes the phenomena of flow/pressure regulation, reactive hyperemia, functional hyperemia, and the underlying mechanisms of each. The chapter focuses on recent insights into metabolic and myogenic control mechanisms. Substantial progress has been made on two additional mechanisms that contribute to local control of microvascular perfusion: flow-induced responses and conducted responses. The chapter also addresses some of the interactions between flow-induced dilation and myogenic/metabolic responses focusing on selected aspects of conducted vasodilation as they relate to functional hyperemia and to the coordination of segmental control mechanisms.

Local Regulation of Microvascular Perfusion

The mechanism of cerebral autoregulation is still open to discussion [4]. One important factor involved is described by the myogenic theory. From our recent experimental work dealing with the influence of extracorporeal circulation upon CBF and cerebral metabolism we obtained results which, we think, support the myogenic theory. The term autoregulation in its restricted sense describes the intrinsic ability of cerebral circulation to maintain a constant blood flow at varying perfusion pressures. This fact is usually demonstrated in the familiar pressure-flow diagram, where CBF is plotted against an arbitrary mean pressure. This procedure however neglects the fact that normal blood pressure is pulsatile. If one agrees to the concept of transmural pressure as the important factor in myogenic autoregulation a different response to normal pulsatile and to a constant non-pulsatile perfusion pressure can be expected.

Gottstein U

Papers

CBF in Non-Pulsatile Perfusion