Effects of profound hypothermia and circulatory arrest on cerebral oxygen metabolism and cerebrospinal fluid electrolyte composition in dogs

1974 ◽  
Vol 40 (2) ◽  
pp. 199-205 ◽  
Author(s):  
Edgar A. Bering
Keyword(s):  
Brain Temperature ◽  
Circulatory Arrest ◽  
Oxygen Metabolism ◽  
Cerebral Oxygen ◽  
Profound Hypothermia ◽  
Content Type ◽  
Cerebral Oxygen Metabolism ◽  
Natural Logarithm ◽  
K Concentration ◽  
Fine Print

✓ Cerebral oxygen metabolism was studied in the dog at brain temperatures ranging from 37° to 8°C. As brain temperature decreased, the cerebral oxygen metabolism (CMRO2) decreased following the Arrhenius equation. The natural logarithm of the CMRO2 was a linear function of the reciprocal of the absolute (K) brain temperature. Oxygen metabolism, although much decreased, continued at very low brain temperatures. The CSF composition was unchanged after 1 hour at brain temperatures down to 10°C. Circulatory arrest for tolerable periods and longer caused changes only in the CSF potassium concentration. The interval between the onset of circulatory arrest and the beginning of the CSF K concentration increased with decreasing temperature and the rate of CSF K increase was increasingly slower at lower temperatures. At all temperatures the rate of CSF K changed gradually increased with time. The interval before the CSF K started to increase was dependent upon the amount of O2 available in the brain and the length of this interval was inversely proportional to the CMRO2. The amount of CSF K concentration was not clearly related to the tolerable periods of circulatory arrest, but at normal temperatures an obviously increased CSF K following a period of acute cerebral anoxia without CSF hemorrhage may indicate brain damage.

Cerebral Oxygen Metabolism Measured During Hypothermic Circulatory Arrest

1991 ◽  
Vol 3 (4) ◽  
pp. 302-307 ◽  
Author(s):  
Patrick W. McCormick ◽  
Guruswamy Balakrishnan ◽  
Melville Stewart ◽  
Gary Lewis ◽  
James I. Ausman
Keyword(s):  
Circulatory Arrest ◽  
Oxygen Metabolism ◽  
Hypothermic Circulatory Arrest ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism

Cerebral oxygen metabolism during hypothermic circulatory arrest in humans

1993 ◽  
Vol 79 (6) ◽  
pp. 810-815 ◽  
Author(s):  
James I. Ausman ◽  
Patrick W. McCormick ◽  
Melville Stewart ◽  
Gary Lewis ◽  
Manuel Dujovny ◽  
...  
Keyword(s):  
Oxygen Saturation ◽  
Circulatory Arrest ◽  
Oxygen Metabolism ◽  
Cerebral Oximetry ◽  
Neurological Injury ◽  
Profound Hypothermia ◽  
Content Type ◽  
Hypoxic Injury ◽  
Hemoglobin Saturation ◽  
Negative Linear Correlation

✓ Profound hypothermia with circulatory arrest is an important surgical adjuvant that allows protected cessation of cerebral blood flow for a brief period. In seven patients undergoing this procedure, continuous spectroscopic measurement of cerebral hemoglobin oxygen saturation was performed. Circulatory arrest at 18°C was associated with a significant progressive desaturation (p < 0.01) of residual cerebral hemoglobin. Arrest time varied based on operative complexity (range 10 to 65 minutes), and a negative linear correlation between arrest time (y) and oxygen saturation (x) was noted (y = −0.87x + 64). Five patients whose saturation remained above 35% had no neurological injury attributable to hypoxia. One patient (Hunt and Hess Grade 0) whose saturation fell below 35% had evidence of a global hypoxic injury at postmortem examination. Spectroscopically measured cerebral hemoglobin saturation (cerebral oximetry) may be used to monitor metabolic activity during circulatory arrest. Although the clinical utility of such monitoring cannot be established at this time, the potential may exist to prolong the safe duration of induced circulatory arrest for cerebral protection.

scholarly journals Effect of supplemental dexmedetomidine in interventional embolism on cerebral oxygen metabolism in patients with intracranial aneurysms

2021 ◽  
Vol 49 (4) ◽  
pp. 030006052110029
Author(s):  
Zhang Guo ◽  
Weiwei Wang ◽  
Dahua Xie ◽  
Ruisheng Lin
Keyword(s):  
Intracranial Aneurysms ◽  
Jugular Vein ◽  
Oxygen Metabolism ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism ◽  
Time Points ◽  
Venous Oxygen Saturation ◽  
Group A ◽  
Group B ◽  
Oxygen Difference

Objective To investigate the effect of supplemental dexmedetomidine in interventional embolism on cerebral oxygen metabolism in patients with intracranial aneurysms. Methods Ninety patients who underwent interventional embolism of intracranial aneurysms were equally divided into Group A and Group B. In Group A, dexmedetomidine was injected intravenously 10 minutes before inducing anesthesia, with a loading dose of 0.6 µg/kg followed by 0.4 µg/kg/hour. Group B received the same amount of normal saline by the same injection method. Heart rate (HR), mean arterial pressure (MAP), arterial–jugular venous oxygen difference [D(a-jv) (O2)], cerebral oxygen extraction [CE (O2)], and intraoperative propofol use were recorded before inducing anesthesia (T0) and at five time points thereafter. Results The amount of propofol in Group A was lower vs Group B. At all five time points after T0, HR, MAP, D(a-jv) (O2), and CE (O2) in Group A were significantly lower vs Group B, with significant differences for jugular venous oxygen saturation (SjvO2) and the oxygen content of the internal jugular vein (CjvO2) between the groups. Conclusion Dexmedetomidine resulted in less intraoperative propofol, lower D(a-jv) (O2) and CE (O2), and improved cerebral oxygen metabolism.

scholarly journals Effect of Chlorpromazine on Cerebral Hemodynamics and Cerebral Oxygen Metabolism in Man

Circulation ◽  
1956 ◽  
Vol 14 (3) ◽  
pp. 380-385 ◽  
Author(s):  
JOHN H. MOYER ◽  
GEORGE MORRIS ◽  
ROBERT PONTIUS ◽  
ROBERT HERSHBERGER ◽  
C. Polk Smith
Keyword(s):  
Oxygen Metabolism ◽  
Cerebral Hemodynamics ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism

scholarly journals Effect of Comprehensive Cerebral Protection Program on Cerebral Oxygen Metabolism and Vascular Endothelial Function in Elderly Patients with Acute Cerebral Infarction

2019 ◽  
Author(s):  
Meihong ZHOU ◽  
Zhaojun HUANG
Keyword(s):  
Elderly Patients ◽  
Cerebral Infarction ◽  
Endothelial Function ◽  
Oxygen Metabolism ◽  
Acute Cerebral Infarction ◽  
Control Group ◽  
Cerebral Oxygen ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Cerebral Oxygen Metabolism

Background: We aimed to explore the effect of comprehensive cerebral protection on cerebral oxygen metabolism and vascular endothelial function in elderly patients with acute cerebral infarction. Methods: A total of 168 elderly patients with acute cerebral infarction treated in The First Affiliated Hospital of Nanchang University, China from January 2016 to January 2018 were selected. The patients were divided into a control group and an observation group using random number method, n=84. Patients in the observation group were given comprehensive cerebral protection treatment, and patients in the control group were treated with conventional standardized treatments. The changes of cerebral oxygen metabolism, hemorheology and vascular endothelial function before and after treatment were compared between the two groups. Results: After treatment, oxygen content in arteries and internal jugular veins (Da-vO2), ofoxygen uptake fraction (OEF), Oxygen saturation (SpO2), nitric oxide (NO) were increased in both groups in comparison to before treatment, jugular venous oxygen saturation (SjvO2), brain oxygen uptake rate (ERO2), endothelin (ET), intracranial pressure (ICP), whole blood viscosity, plasma viscosity, reduced viscosity of whole blood, and hematocrit were decreased. However, the changes in the observation group were larger than those in the control group, the difference was statistically significant (P<0.05). Conclusion: The treatment of cerebral infarction in elderly patients with acute cerebral infarction can effectively improve the cerebral oxygen metabolism and vascular endothelial function and improve the blood rheology, which has important clinical value.

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