Venous blood pressure in broilers during acute inhalation of five percent carbon dioxide or unilateral pulmonary artery occlusion

Abstract

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.

Ascites and venous carbon dioxide tensions in juvenile chickens of highly selected genotypes and native strains

“…High mean paCO 2 (higher than 60 mm Hg) and low pH and paO 2 values in arterial blood of sire lines differed at wk 5 highly significant (P< 0.001) from values found in dam lines and in BC birds. Wideman et al (1999) demonstrated that even a short period of 5 minutes of a modest increase in partial pressure of CO 2 (up to 55 mm Hg) together with a reduced pH in arterial blood of broilers was sufficient to trigger a significant increase in pulmonary arterial pressure, predisposing the birds to ascites. Reeves et al (1990) discovered that at sea level, ascites susceptible chickens have impaired ventilatory drives and that they have relative hypoventilation at an early age.…”

“…A study by Wideman et al (1999) in broilers showed that a moderate increase in CO 2 concentrations of arterial blood (up to 55 mm Hg) in concert with a decreased pH, by inhalation of 5% CO 2 , clearly increased pulmonary arterial pressure. Birds with those increased arterial CO 2 values are apparently predisposed to ascites.…”

Ascites Syndrome in Broiler Chickens - A Physiological Syndrome Affected by Red Blood Cell

“…However, such an increase, if not coupled to plasma volume expansion would increase blood viscosity, followed by increased bloodflow resistance [90]. The back pressure in the veins causes venous congestion, dilation and prominent vessels [50]. The lack of O2 in the heart muscle results in hypoxic damage and, finally, right-ventricular hypertrophy.…”

“…Several significant alterations to the blood system in AS broilers were well documented: increased red blood cell numbers, through increased erythropoietin production [96,100,[150][151][152][153]; elevation of hematocrit values and blood viscosity [54,72,154], and central venous blood congestion [50,155]. These findings raised the question of the association between the plasma and the fluid that accumulated in the abdominal cavity, and whether the increase in hematocrit resulted from a decline in plasma volume caused by plasma leakage out of the blood vessels, or from increased erythropoiesis that occurred as a compensatory reaction to the lack of oxygen in the tissue.…”

“…In low, ventilation-induced ascites, the broilers had significant inflammation or osseous-nodule formation in the lungs [174,175], whereas in cold-stress-induced ascites, birds showed no inflammation [173]. Wideman et al [50] suggested that increases in pulmonary vascular resistance initiate increases in venous pressure by challenging the capacity of the right ventricle to thrust all the returning venous blood through the lungs. An acute reversal of systemic hypoxemia was reported to have no effect on pulmonary hypertension -a finding that discounted the influence of hypoxic pulmonary vasoconstriction [176].…”