Acute effects of nimodipine on the cerebral blood flow and intracranial pressure

We determined how alterations in systemic hemodynamics, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and brain electrical conductive function, as assessed by somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was less than 50 mmHg. CMRO2 fell when CBF fell greater than 30-40%. Mean aortic pressure and cardiac output increased when CBF fell greater than 40%, i.e., at approximately the level at which CMRO2 fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMRO2. SEP latency did not increase unless CBF fell greater than 55-65%, corresponding to a 20-30% reduction of CMRO2. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of greater than 65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO2.

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Interaction among autoregulation, CO2 reactivity, and intracranial pressure: a mathematical model

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1998.274.5.h1715 ◽

1998 ◽

Vol 274 (5) ◽

pp. H1715-H1728 ◽

Cited By ~ 50

Author(s):

Mauro Ursino ◽

Carlo Alberto Lodi

Keyword(s):

Mathematical Model ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Intracranial Pressure ◽

Nonlinear Interaction ◽

Cerebral Blood Volume ◽

Cerebral Hemodynamics ◽

Pial Arteries ◽

Arterial Circulation ◽

Neurosurgical Patients

The relationships among cerebral blood flow, cerebral blood volume, intracranial pressure (ICP), and the action of cerebrovascular regulatory mechanisms (autoregulation and CO2 reactivity) were investigated by means of a mathematical model. The model incorporates the cerebrospinal fluid (CSF) circulation, the intracranial pressure-volume relationship, and cerebral hemodynamics. The latter is based on the following main assumptions: the middle cerebral arteries behave passively following transmural pressure changes; the pial arterial circulation includes two segments (large and small pial arteries) subject to different autoregulation mechanisms; and the venous cerebrovascular bed behaves as a Starling resistor. A new aspect of the model exists in the description of CO2 reactivity in the pial arterial circulation and in the analysis of its nonlinear interaction with autoregulation. Simulation results, obtained at constant ICP using various combinations of mean arterial pressure and CO2 pressure, substantially support data on cerebral blood flow and velocity reported in the physiological literature concerning both the separate effects of CO2 and autoregulation and their nonlinear interaction. Simulations performed in dynamic conditions with varying ICP underline the existence of a significant correlation between ICP dynamics and cerebral hemodynamics in response to CO2 changes. This correlation may significantly increase in pathological subjects with poor intracranial compliance and reduced CSF outflow. In perspective, the model can be used to study ICP and blood velocity time patterns in neurosurgical patients in order to gain a deeper insight into the pathophysiological mechanisms leading to intracranial hypertension and secondary brain damage.

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Effects of nitroglycerin on intracranial pressure and cerebral blood flow

Acta Anaesthesiologica Scandinavica ◽

10.1111/j.1399-6576.1992.tb03585.x ◽

1992 ◽

Vol 36 ◽

pp. 34-36 ◽

Cited By ~ 14

Author(s):

M. Lagerkranser

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Intracranial Pressure

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Suctioning and Cerebral Blood Flow

PEDIATRICS ◽

10.1542/peds.73.5.737a ◽

1984 ◽

Vol 73 (5) ◽

pp. 737-737

Author(s):

JEFFREY M. PERLMAN ◽

JOSEPH J. VOLPE

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Intracranial Pressure ◽

Flow Velocity ◽

Arterial Blood Pressure ◽

Blood Flow Velocity ◽

Cerebral Blood Flow Velocity ◽

Base Line ◽

Arterial Blood

In Reply.— Marshall misread a critical piece of information in the text. His interpretation of the data would be correct, if the intracranial pressure, arterial blood pressure, and cerebral blood flow velocity changes occurred simultaneously. However, as we stated in the text (see section on "Temporal Features of Changes with Suctioning"), the intracranial pressure fell to base-line values immediately following suctioning, whereas the changes in arterial blood pressure and cerebral blood flow velocity occurred more slowly over an approximately two-minute period.

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Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

10.2310/vasc.2401 ◽

2018 ◽

Author(s):

Ryan Martin ◽

Lara Zimmermann ◽

Marike Zwienenberg ◽

Kee D Kim ◽

Kiarash Shahlaie

Keyword(s):

Traumatic Brain Injury ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Injury ◽

Intracranial Pressure ◽

Cerebral Autoregulation ◽

Cerebral Metabolism ◽

Elevated Intracranial Pressure ◽

Metabolic Demand ◽

Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

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