Cerebral Blood Flow Autoregulation, Cerebrospinal Fluid Acid-Base Parameters, and Profound Hypotension Induced by Sodium Nitroprusside and Deep Halothane Anesthesia

1975 ◽  
pp. 21-23 ◽  
Author(s):  
N. P. Keaney ◽  
D. G. McDowall ◽  
J. M. Turner ◽  
J. R. Lane ◽  
Y. Okuda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Sodium Nitroprusside ◽  
Halothane Anesthesia ◽  
Acid Base ◽  
Base Parameters ◽  
Profound Hypotension ◽  
Cerebral Blood Flow Autoregulation

scholarly journals Multiple Factors Involved in the Pathogenesis of White Matter Lesions

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Jing Lin ◽  
Dilong Wang ◽  
Linfang Lan ◽  
Yuhua Fan
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
White Matter ◽  
Genetic Factors ◽  
Subsequent Development ◽  
White Matter Lesions ◽  
Blood Brain Barrier Disruption ◽  
Fluid Attenuated Inversion Recovery ◽  
Cerebral Blood Flow Autoregulation ◽  
Brain Barrier Disruption

White matter lesions (WMLs), also known as leukoaraiosis (LA) or white matter hyperintensities (WMHs), are characterized mainly by hyperintensities on T2-weighted or fluid-attenuated inversion recovery (FLAIR) images. With the aging of the population and the development of imaging technology, the morbidity and diagnostic rates of WMLs are increasing annually. WMLs are not a benign process. They clinically manifest as cognitive decline and the subsequent development of dementia. Although WMLs are important, their pathogenesis is still unclear. This review elaborates on the advances in the understanding of the pathogenesis of WMLs, focusing on anatomy, cerebral blood flow autoregulation, venous collagenosis, blood brain barrier disruption, and genetic factors. In particular, the attribution of WMLs to chronic ischemia secondary to venous collagenosis and cerebral blood flow autoregulation disruption seems reasonable. With the development of gene technology, the effect of genetic factors on the pathogenesis of WMLs is gaining gradual attention.

Cerebral blood flow velocity and cerebrospinal fluid pressure after single bolus of propofol

1989 ◽  
Vol 11 (3) ◽  
pp. 150-151 ◽  
Author(s):  
A. Parma ◽  
R. Massei ◽  
A. Pesenti ◽  
C. Ferrari da Passano ◽  
G. Gran ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Fluid Pressure ◽  
Cerebrospinal Fluid Pressure ◽  
Single Bolus

Early Effects of Acid-Base Management during Hypothermia on Cerebral Infarct Volume, Edema, and Cerebral Blood Flow in Acute Focal Cerebral Ischemia in Rats

2002 ◽  
Vol 97 (4) ◽  
pp. 868-874 ◽  
Author(s):  
Rainer Kollmar ◽  
Thomas Frietsch ◽  
Dimitrios Georgiadis ◽  
Wolf-Rüdiger Schäbitz ◽  
Klaus F. Waschke ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Edema ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Cerebral Infarct ◽  
Moderate Hypothermia ◽  
Acid Base ◽  
Base Management ◽  
Ph Stat

Background Although the frequency for the use of moderate hypothermia in acute ischemic stroke is increasing, the optimal acid-base management during hypothermia remains unclear. This study investigates the effect of pH- and alpha-stat acid-base management on cerebral blood flow (CBF), infarct volume, and cerebral edema in a model of transient focal cerebral ischemia in rats. Methods Twenty Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion (MCAO) for 2 h during normothermic conditions followed by 5 h of reperfusion during hypothermia (33 degrees C). Animals were artificially ventilated with either alpha- (n = 10) or pH-stat management (n = 10). CBF was analyzed 7 h after induction of MCAO by iodo[(14)C]antipyrine autoradiography. Cerebral infarct volume and cerebral edema were measured by high-contrast silver infarct staining (SIS). Results Compared with the alpha-stat regimen, pH-stat management reduced cerebral infarct volume (98.3 +/- 33.2 mm(3) vs. 53.6 +/- 21.6 mm(3); P > or = 0.05 mean +/- SD) and cerebral edema (10.6 +/- 4.0% vs. 3.1 +/- 2.4%; P > or = 0.05). Global CBF during pH-stat management exceeded that of alpha-stat animals (69.5 +/- 12.3 ml x 100 g(-1) x min(-1) vs. 54.7 +/- 13.3 ml x 100 g(-1) x min; P > or = 0.05). The regional CBF of the ischemic hemisphere was 62.1 +/- 11.2 ml x 100 g(-1) x min(-1) in the pH-stat group versus 48.2 +/- 7.2 ml x 100 g(-1) x min(-1) in the alpha-stat group ( P> or = 0.05). Conclusions In the very early reperfusion period (5 h), pH-stat management significantly decreases cerebral infarct volume and edema as compared with alpha-stat during moderate hypothermia, probably by increasing CBF.

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