Dependence between Cerebral Metabolism and Blood Flow as Reflected in the Quantitative EEG

2015 ◽  
pp. 102-108 ◽  
Author(s):  
Ilmar A. Sulg ◽  
Kyosti A. Sotaniemi ◽  
Uolevi Tolonen ◽  
Eero Hokkanen
Keyword(s):  
Blood Flow ◽  
Cerebral Metabolism ◽  
Quantitative Eeg

Influence of endogenous norepinephrine on cerebral blood flow and metabolism

1976 ◽  
Vol 231 (2) ◽  
pp. 489-494 ◽  
Author(s):  
ET MacKenzie ◽  
J McCulloch ◽  
AM Harper
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Cerebral Circulation ◽  
Brain Metabolism ◽  
Cerebral Metabolism ◽  
Cerebral Oxygen ◽  
Brain Norepinephrine ◽  
Cerebral Oxygen Consumption

The influence of brain norepinephrine on cerebral metabolism and blood flow was examined because exogenous norepinephrine, administered in a way that the blood-brain barrier is bypassed, has been shown to effect pronounced changes in the cerebral circulation. Reserpine (40 mug/kg, by intracarotid infusion) was administered in order to release brain norepinephrine in five anesthetized baboons. Reserpine significantly increased cerebral oxygen consumption (23%) and cerebral blood flow (50%). This response lasted for approximately 60 min. In a further five animals, effects of central beta-adrenoreceptor blockade were studied. Pro pranolol (12 mug/kg-min) produced an immediate, significant reduction in both cerebral oxygen consumption (40%) and cerebral glucose uptake (39%). Cerebral blood flow was reduced minimally. However, the responsiveness of the cerebral circulation to induced hypercapnia was severely attenuated from a gradient of 3.22 before, to 1,11 after, administration. These experiments suggest that central norepinephrine can influence the cerebral circulation primarily through noradrenergic effects on brain metabolism.

Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

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

scholarly journals Coronary and cerebral metabolism-blood flow coupling and pulmonary alveolar ventilation-blood flow coupling may be disabled during acute carbon monoxide poisoning

2020 ◽  
Vol 129 (5) ◽  
pp. 1039-1050
Author(s):  
Ronald F. Coburn
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Regional Blood Flow ◽  
Cerebral Metabolism ◽  
Carbon Monoxide Poisoning ◽  
Alveolar Ventilation ◽  
Physiological Adaptation ◽  
Acute Carbon Monoxide Poisoning ◽  
Flow Coupling ◽  
Adaptation Mechanisms

This article introduces and supports a postulate that the tissue hypoxia component of carbon monoxide poisoning results in part from impairment of physiological adaptation mechanisms whereby tissues can match regional blood flow to O2 uptake, and the lung can match regional blood flow to alveolar ventilation.

Cerebral Blood Flow, Cerebral Metabolism and Cerebrospinal Fluid Biochemistry in Brain-Injured Patients after Exposure to Hyperbaric Oxygen

1976 ◽  
Vol 14 (5) ◽  
pp. 351-364 ◽  
Author(s):  
François Artru ◽  
Bernard Philippon ◽  
Françoise Gau ◽  
Michel Berger ◽  
Raymond Deleuze
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Hyperbaric Oxygen ◽  
Cerebral Metabolism ◽  
Brain Injured ◽  
Injured Patients

scholarly journals Effects of Indomethacin and Ibuprofen on Cerebral Metabolism and Blood Flow in Traumatized Brain

1983 ◽  
Vol 3 (4) ◽  
pp. 448-459 ◽  
Author(s):  
Hanna M. Pappius ◽  
Leonhard S. Wolfe
Keyword(s):  
Blood Flow ◽  
Considerable Increase ◽  
Glucose Utilization ◽  
Single Injection ◽  
Cerebral Metabolism ◽  
Local Cerebral Blood Flow ◽  
Lesion Area ◽  
Local Cerebral Glucose Utilization ◽  
Biphasic Effect ◽  
Prostaglandin System

Local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) were studied by autoradiographic techniques in indomethacin- and ibuprofen-treated rats with focal cortical freezing lesions. Widespread depression of LCGU, which developed with time after the lesion in untreated animals was significantly diminished by the prostaglandin synthetase inhibitors indomethacin (single injection 7.5 mg/kg) and ibuprofen (36 mg/kg/day). Both drugs were effective when given 6 h before or up to 24 h after the lesion was made. The effect of the drugs was most striking in cortical areas of the traumatized hemisphere, where the depression was most profound in untreated animals. Thus, 3 days afer the lesion, average LCGU in these regions was 46%, 86%, and 98% of normal in untreated, indomethacin-pretreated, and ibuprofen-pretreated rats, respectively. Prostaglandin formation was completely inhibited in the lesion area in the indomethacin-treated rats (PGF2α 1.8 ng/g, compared to 57.5 ng/g in untreated and 1.4 ng/g in nonlesioned animals). The results suggest that some components of the prostaglandin system are involved in mechanisms underlying a widespread depression in functional state of the rat brain that develops in response to injury. In control animals, indomethacin was shown to have a biphasic effect on LCBF, an early depression shown previously by others followed at 24 h by a considerable increase.

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