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.

Pulmonary venoconstriction caused by elevated cerebrospinal fluid pressure in the dog

1980 ◽  
Vol 49 (1) ◽  
pp. 73-78 ◽  
Author(s):  
M. B. Maron ◽  
C. A. Dawson
Keyword(s):  
Cerebrospinal Fluid ◽  
Fluid Pressure ◽  
Cerebrospinal Fluid Pressure ◽  
Epinephrine Infusion ◽  
Pressure Drops ◽  
Lung Lobe ◽  
Pulmonary Vasoconstriction ◽  
Lower Lung ◽  
Occlusion Technique ◽  
Highly Correlated

Previously we found that raising cerebrospinal fluid pressure (PCSF) caused pulmonary vasoconstriction mediated by adrenal catecholamines. To localize the site of this vasoconstriction we used the outflow occlusion technique to divide changes in the pulmonary arteriovenous pressure gradient (Pa-v) into upstream and downstream pressure drops. Experiments were conducted in 10 dogs in which the animal's left lower lung lobe was denervated and perfused at constant flow and outflow pressure with blood pumped from the dog's pulmonary artery. Raising PCSF to 218 Torr caused Pa-v to rise from 9.0 to 12.5 Torr. Most (83%) of this increase resulted from an increase in the downstream pressure drop. Previous studies have indicated that changes in the upstream and downstream pressure drops, as measured by this technique, are highly correlated with changes in the resistance of the arterial and venous sides of the vascular bed. Thus, it appears that elevated PCSF caused primarily pulmonary venoconstriction. Similar results were obtained with norepinephrine and epinephrine infusion. This is consistent with previous studies, indicating that adrenal catecholamines are responsible for the increase in Pa-v in response to PCSF in this preparation.

Adrenal component to pulmonary hypertension caused by nicotine administration in the dog

1980 ◽  
Vol 49 (1) ◽  
pp. 66-72 ◽  
Author(s):  
M. B. Maron ◽  
D. A. Rickaby ◽  
C. A. Dawson
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Left Atrial ◽  
Venous Return ◽  
Venous Blood ◽  
Main Pulmonary Artery ◽  
Mixed Venous Blood ◽  
Lung Lobe ◽  
Nicotine Administration ◽  
Lower Lung

In this study, we investigated the possibility that the adrenal gland contributes to nicotine-induced pulmonary hypertension using a canine left lower lung lobe (LLL) preparation that was pump-perfused with mixed venous blood at constant flow and outflow pressure. Main pulmonary artery, left atrial, and LLL arterial pressures were monitored to assess the responses of the animal's intact right lung and isolated LLL. With the adrenal venous return intact, injection of 10-26 micrograms/kg nicotine into the left ventricle or ascending aorta resulted in a 42% increase in LLL arterial pressure and a 70% increase in the pulmonary arterial-left atrial pressure gradient (Ppa-Pla). When the adrenal venous return was interrupted, the increases in LLL arterial pressure and Ppa-Pla were reduced to 6 and 10%, respectively. The LLL response could be eliminated by alpha-adrenergic receptor blockade, suggesting that adrenal catecholamines may contribute to the pulmonary hypertension induced by nicotine infusion.

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.

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