The effect of cerebrospinal fluid pressure on dural venous pressure in young rats

1989 ◽  
Vol 71 (1) ◽  
pp. 119-123 ◽  
Author(s):  
Hazel C. Jones ◽  
Julie A. Gratton
Keyword(s):  
Cerebrospinal Fluid ◽  
Venous Pressure ◽  
Venous Blood ◽  
Fluid Pressure ◽  
Positive Pressure ◽  
Cisterna Magna ◽  
Young Rats ◽  
Sinus Wall ◽  
Old Rats ◽  
Overall Resistance

✓ In order to study cerebrospinal fluid (CSF) absorption across the dural sinus wall, the effect of CSF pressure (recorded from the cisterna magna) on dural venous pressure (recorded from the transverse sinus) was investigated in groups of rats at 2, 10, 20, and 31 days after birth and in adulthood. At normal resting pressures there was no positive pressure gradient between the CSF and sinus venous blood in 2-, 10-, and 20-day-old rats, but in 31-day-old and adult rats there was a positive gradient of 16 and 12 mm H2O, respectively. A series of constant-rate infusions of artificial CSF was made into the cisterna magna, and subsequent plateaus in both CSF and venous blood were recorded. The gradient of a plot of plateau pressure against infusion rate gave the overall resistance to absorption of the CSF for each age group, which was higher in 2- and 10-day-old rats than at three older ages. The effect on dural venous pressure was age-related, with the largest increase at 2 days, the smallest at 20 days, and no effect at 31 days or in adults. The pressure difference between CSF and sinus blood has been used to calculate resistance to absorption across the sinus wall. This showed that the high overall resistance to drainage in young rats can be largely accounted for by the rise in sinus pressure. It is concluded that drainage of CSF into the sinuses is greatly restricted in young animals.

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.

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.

Cerebrospinal fluid pressures during hypercapnia and hypoxia in dogs

1960 ◽  
Vol 198 (4) ◽  
pp. 704-708 ◽  
Author(s):  
Harold S. Small ◽  
Stanley W. Weitzner ◽  
Gabriel G. Nahas
Keyword(s):  
Cerebrospinal Fluid ◽  
Similar Pattern ◽  
Fluid Pressure ◽  
Probable Mechanism ◽  
Cerebrospinal Fluid Pressure ◽  
Apneic Oxygenation ◽  
Cisterna Magna ◽  
Controlled Ventilation ◽  
Cerebral Vasodilatation

Cerebrospinal fluid pressure (CSFP) in the cisterna magna, intra-aortic and intrathoracic venous pressures were measured during apneic oxygenation (diffusion respiration) in dogs under light pentobarbital-succinylcholine anesthesia. CSFP doubled in 2 minutes and reached a peak 375% above control in 10 minutes. During this time there were no consistent changes in arterial or venous pressures. Dogs ventilated with 5, 10 and 15% CO2 showed a similar pattern. Cerebral vasodilatation caused by CO2 is the probable mechanism in both groups. A sustained elevation of CSFP was observed throughout CO2 administration for as long as 90 minutes. In all cases there was a prompt return to control levels on termination of the hypercapnia. Controlled ventilation with 8% O2 caused an average 84% rise in CSFP, with a plateau occurring after 4–5 minutes. This was accompanied by marked increases in arterial and venous pressures. Cerebral vasodilatation probably occurs here also. During 90 seconds of asphyxia the sharpest increase (175%) in CSFP occurred. This was accompanied by marked increases in arterial and venous pressures, and represents the effect of hypoxia and hypercapnia combined.

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