Venous blood pressure in broilers during acute inhalation of five percent carbon dioxide or unilateral pulmonary artery occlusion.
We evaluated the hypothesis that venous congestion (increased venous volume), as reflected by venous hypertension (increased venous pressure), can arise when the right ventricle is unable to elevate the pulmonary arterial pressure sufficiently to propel the cardiac output through an anatomically inadequate or inappropriately constricted pulmonary vasculature. Changes in venous pressure were evaluated in clinically healthy broilers during modest increases in pulmonary vascular resistance induced by inhalation of 5% CO2 and during large increases in pulmonary vascular resistance accomplished by acutely tightening a snare around one pulmonary artery. Inhalation of 5% CO2 induced a pronounced respiratory acidosis, as reflected by increases the partial pressure of CO2 and the hydrogen ion concentration in arterial blood. Inhalation of 5% CO2 also increased pulmonary arterial pressure by approximately 3 mm Hg and increased venous pressure by approximately 1 mm Hg when compared with the pre-inhalation venous pressure. Tightening the pulmonary artery snare increased the pulmonary arterial pressure by approximately 10 mm Hg, and this degree of pulmonary hypertension was sustained until the snare was released. When compared with the pre- and post-snare intervals, tightening of the pulmonary artery snare induced a sustained increase in venous pressure of > or = 1 mm Hg. Veins have highly compliant walls that permit an approximate doubling in volume with only small (4 to 6 mm Hg) increases in central venous pressure. Presumably the apparently modest 1 mm Hg increase in venous pressure measured after CO2 inhalation or unilateral pulmonary artery occlusion reflects a large increase in venous volume and, thus, substantial venous congestion. These observations support the hypothesis that increases in pulmonary vascular resistance can initiate increases in venous pressure by challenging the capacity of the right ventricle to propel all of the returning venous blood through the lungs. Central venous congestion predisposes broilers to the onset of cirrhosis and ascites by impeding the outflow of hepatic venous blood and increasing the hydrostatic pressure within hepatic sinusoids.
Wideman
R F
RF
Department of Poultry Science, University of Arkansas, Fayetteville 72701, USA. rwideman@comp.uark.edu
Maynard
P
P
Bottje
W G
WG
D000142:Acidosis, Respiratory; D000280:Administration, Inhalation; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology / Q000662:veterinary; D001201:Ascites / Q000209:etiology / Q000662:veterinary; D001794:Blood Pressure / Q000187:drug effects*; D002245:Carbon Dioxide / Q000494:pharmacology; D002645:Chickens / Q000502:physiology*; D006976:Hypertension, Pulmonary / Q000503:physiopathology / Q000662:veterinary*; D008103:Liver Cirrhosis / Q000209:etiology / Q000662:veterinary; D008297:Male; D011651:Pulmonary Artery / Q000473:pathology; D014655:Vascular Resistance; D016278:Ventricular Function, Right / Q000502:physiology*
D002245:Carbon Dioxide