Cerebrovascular response to changes of cerebral venous pressure and cerebrospinal fluid pressure

1991 ◽  
Vol 109 (1-2) ◽  
pp. 52-56 ◽  
Author(s):  
R. Pucher ◽  
Y. Kato ◽  
M. Mokry ◽  
L. M. Auer
Keyword(s):  
Cerebrospinal Fluid ◽  
Venous Pressure ◽  
Fluid Pressure ◽  
Cerebrospinal Fluid Pressure ◽  
Cerebral Venous Pressure

CARDIOVASCULAR EFFECTS OF THE INSECTICIDE ENDRIN

1964 ◽  
Vol 42 (1) ◽  
pp. 41-51 ◽  
Author(s):  
T. E. Emerson Jr. ◽  
C. M. Brake ◽  
L. B. Hinshaw
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Venous Pressure ◽  
Fluid Pressure ◽  
Cardiovascular Effects ◽  
Acute Administration ◽  
Blood Ph ◽  
The Central Nervous System ◽  
Cerebral Venous Pressure

Little is known of the cardiovascular effects of endrin insecticide. Experiments to investigate these phenomena were carried out on dogs with a variety of preparations. Results show that acute administration of endrin produces bradycardia, hypertension, copious salivation, hyperexcitability, tonic–cionic convulsions, increased body temperature, leukocytosis, hemoconcentration, and decreased blood pH. Cerebral venous pressure and cerebrospinal fluid pressure elevations are also prominent features of endrin poisoning. Although most of these effects appear to be caused by endrin acting directly on the central nervous system some may result secondarily from altered cerebral hemodynamics.

Adrenal component to pulmonary hypertension induced by elevated cerebrospinal fluid pressure

1979 ◽  
Vol 47 (1) ◽  
pp. 153-160 ◽  
Author(s):  
M. B. Maron ◽  
C. A. Dawson
Keyword(s):  
Pulmonary Hypertension ◽  
Cerebrospinal Fluid ◽  
Intact Animal ◽  
Venous Pressure ◽  
Venous Blood ◽  
Fluid Pressure ◽  
Cerebrospinal Fluid Pressure ◽  
Mixed Venous Blood ◽  
Vasoactive Agent ◽  
Lung Lobe

In this study we investigated the possibility that a circulating vasoactive agent contributes to the pulmonary hypertension elicited by elevated cerebrospinal fluid pressure (PCSF) using a denervated canine left lower lung lobe (LLL) preparation that was pump perfused with mixed venous blood at constant flow and venous pressure. Raising the PCSF to an average 190 Torr resulted in a 34.3% increase in LLL inflow pressure. This response was eliminated by adrenal venous occlusion and also by alpha-blockade of the LLL. The results indicated that adrenal catecholamines were responsible for the LLL response. The passively induced elevation of left atrial pressure (Pla) that occurs in the intact animal during elevated PCSF was stimulated in the LLL by raising the outflow pressure. This maneuver attenuated the increase in LLL vascular resistance and suggested that the elevation in Pla seen in the intact animal could mask humorally mediated responses of the magnitude we observed.

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