期刊
POULTRY SCIENCE
卷 81, 期 6, 页码 877-886出版社
POULTRY SCIENCE ASSOC INC
DOI: 10.1093/ps/81.6.877
关键词
broiler; pulmonary hypertension; vascular occlusion; immunology; ascites
Experiments were conducted to determine whether intravenous injections of micro-particles, having a size suitable to be trapped by the pulmonary precapillary arterioles, could be used to increase the pulmonary vascular resistance and thereby trigger an acute increase in the pulmonary arterial pressure (pulmonary hypertension). Anesthetized male broilers injected intravenously with inorganic (silica gel, polystyrene) or organic (cellulose, Sephadex) micro-particles developed an immediate pulmonary hypertension in proportion to the cumulative quantities of micro-particles injected. Micro-particle occlusion of a portion of the pulmonary arterioles forced the cardiac output to flow at a higher rate through the remaining vascular channels, thereby exposing a diffusion limitation characterized by undersaturation of the systemic arterial blood with oxygen (hypoxemia). The concurrent onset of systemic hypotension (reduced systemic arterial blood pressure) was not due to a reduction in cardiac output but rather was attributed to hypoxemic vasodilation of the systemic vasculature (reduced total peripheral resistance). Preliminary histological evaluations revealed micro-particles lodged in inter- and intraparabronchial arterioles, surrounded by aggregates of thrombocytes and mononuclear leukocytes within 30 min post-injection. These observations infer that intravenously injected micro-particles are carried to the lungs by the returning venous blood, where trapping of the micro-particles by the pulmonary vasculature triggers acute responses (increased pulmonary vascular resistance, pulmonary hypertension, systemic hypoxemia, systemic hypotension) that mirror those previously observed following acute occlusion of one pulmonary artery. Additional studies will be required to determine the extent to which the focal immune response to trapped micro-particles promotes local vasoconstriction that amplifies the pulmonary hypertension attributable to direct physical obstruction of precapillary arterioles.
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