Independent and Simultaneous Unilateral Occlusion of the Pulmonary Artery and Extra-Pulmonary Primary Bronchus in Broilers

Abstract

Acutely tightening a snare around one pulmonary artery previously was shown to trigger a reversible ventilation-perfusion (V/Q) mismatch in broilers, as reflected by decreases in the partial pressure of oxygen in arterial blood (hypoxemia), accompanied by increases in the hydrogen ion concentration (acidosis) and partial pressure of carbon dioxide (hypercapnia). In the present study, snares were loosely implanted around the right pulmonary artery and the right extrapulmonary primary bronchus in anesthetized male broilers. These snares were tightened and released independently and then simultaneously to evaluate the possibility that directing the entire respiratory minute volume toward the left lung might attenuate the V/Q mismatch caused by forcing the entire cardiac output (CO) through the left lung. Fully reversible arterial blood hypoxemia, acidosis, and hypercapnia occurred when either snare was tightened independently. Presumably, tightening the bronchial snare restricted ventilation but not blood flow to the right lung, thereby permitting blood to perfuse poorly ventilated gas exchange surfaces. Simultaneously tightening both snares triggered arterial blood hypoxemia, acidosis, and hypercapnia similar to or greater in magnitude than the responses obtained by tightening the pulmonary artery snare independently. Tightening either snare independently or both snares simultaneously caused pulmonary arterial pressure to increase (pulmonary hypertension), and permanent obstruction of one bronchus in a separate experiment caused an increase in the right:total ventricular weight ratio, which is indicative of chronic pulmonary hypertension. The mean systemic arterial pressure decreased when the pulmonary artery snare was tightened independently or in combination with the bronchial snare, but not when the bronchial snare was tightened independently. The respiratory rate increased and the heart rate decreased when the pulmonary artery snare was tightened independently, but not when the bronchial snare was tightened independently or in combination with the pulmonary artery snare. These results demonstrate that the V/Q mismatch caused by forcing all the CO to perfuse one lung cannot be attenuated by simultaneously directing the entire respiratory minute volume toward the same lung.

The effect of dietary l‐carnitine supplementation on pulmonary hypertension syndrome mortality in broilers exposed to low temperatures

“…Pulmonary hypertension syndrome (PHS, also known as ascites syndrome) is a costly metabolic disorder in fast‐growing broilers. Pulmonary hypertension is primarily caused by inherent insufficiency of pulmonary vascular capacity to cope with relatively small increase in cardiac output resulting from high oxygen requirement due to rapid growth (Wideman et al., 1996; Julian, 2000). Factors, such as high altitude (low oxygen supply; Olander et al., 1967; Cueva et al., 1974), cool temperature or high‐energy diets (high oxygen consumption; Da Silva et al., 1988; Julian et al., 1989) may enhance the oxygen requirement, leading to an increase in PHS incidence.…”

Pulmonary arterial hypertension (ascites syndrome) in broilers: A review

“…Intravenous AA infusions trigger rapid increases in the pulmonary vascular resistance and pulmonary arterial pressure in broilers, and these responses are blocked by inhibiting cyclooxygenases (Wideman et al, 2005a(Wideman et al, , 2009. Thromboxane A 2 , whether administered intravenously as the TxA 2 mimetic U44069 or produced by activated thrombocytes, consistently causes pulmonary vasoconstriction and pulmonary hypertension in broilers (Wideman et al, 1996b(Wideman et al, , 1998a(Wideman et al, , 1999a(Wideman et al, , 2005a(Wideman et al, , 2009Villamor et al, 2002;Chapman and Wideman, 2006b). The precise contribution of TxA 2 to the progression of pulmonary hypertension in PAHsusceptible broilers remains to be determined.…”

“…In the systemic circulation, hypoxemia elicits widespread arteriolar dilation to increase blood flow and restore adequate O 2 delivery to the organs and tissues (Wideman et al, 1996bWideman, 2000;. Systemic arteriolar vasodilation (reduced total peripheral resistance) allows blood to exit the large arteries more rapidly (increased tissue blood flow), leading to reductions in the mean systemic arterial pressure (systemic hypotension) accompanied by increases in the rate at which venous blood returns to the right ventricle.…”

Idiopathic pulmonary arterial hypertension: An avian model for plexogenic arteriopathy and serotonergic vasoconstriction

“…Rapid growth incurs corresponding increments in cardiac output that must be propelled through lungs that remain essentially isovolumetric throughout the respiratory cycle, and that are constrained in volume by the dimensions of the dorsal thoracic rib cage (Wideman, 1999, 2000, 2001). The pulmonary vasculature of broilers exhibits low compliance and is fully engorged with blood at a normal (resting) cardiac output, unlike the situation in mammals in which the pulmonary vasculature is compliant and recruitable when cardiac output increases (Peacock et al, 1989; Wideman and Kirby, 1995a,b; Wideman et al, 1996a,b; Wideman, 2000). Total lung volume also is poorly correlated with body mass in broilers, creating an incipient pulmonary hemodynamic insufficiency that continues to be further exacerbated by ongoing genetic selection for rapid muscle accretion and thus increased metabolic demand for O 2 (Julian, 1989; Peacock et al, 1989, 1990; Owen et al, 1995a,b; Silversides et al, 1997; Wideman, 1999).…”

“…Minimally invasive methods such as electrocardiography and pulse oximetry can be used to identify subclinical/intermediate stages of PAH, including the onset of right ventricular hypertrophy (electrocardiography) and systemic arterial hypoxemia (pulse oximetry and hematocrit) (Wideman, 2000, 2001). Mortality attributable to IPAH can exceed 20% of the broilers subjected to experimental conditions designed to excessively increase the cardiac output or pulmonary vascular resistance, including exposure to sustained sub- or supra-thermoneutral environmental temperatures, chronic hypoxia, respiratory disease, poor air quality, hyperthyroidism, or partial occlusion of the pulmonary vasculature (Cueva et al, 1974; Sillau and Montalvo, 1982; Huchzermeyer and DeRuyck, 1986; Hernandez, 1987; Julian, 1988, 1993; Peacock et al, 1989, 1990; Wideman and Kirby, 1995a,b; Wideman, 1999, 2000, 2001; Wideman et al, 1996a,b, 1997, 2000, 2007). …”