Wideman R F, Kirby Y K, Owen R L, French H
Department of Poultry Science, University of Arkansas, Fayetteville 72701, USA.
Poult Sci. 1997 Feb;76(2):400-4. doi: 10.1093/ps/76.2.400.
Previously, it was demonstrated that acute (4 min) and chronic (12 d) occlusion of an extrapulmonary primary bronchus triggers pulmonary hypertension but not pulmonary hypertension syndrome (PHS, ascites) in broilers. The present study was conducted to determine whether a more prolonged period of bronchus occlusion causes PHS similar to that induced by clamping one pulmonary artery. Male and female broiler chicks, 14 to 18 d old, were anesthetized, the thoracic inlet was opened, and a silver clip was positioned to fully obstruct the left extrapulmonary primary bronchus (BRONCHUS CLAMP group) or the left pulmonary artery (PA-CLAMP group). Sham-operated chicks were anesthetized and the thoracic inlet was opened; however, neither the pulmonary artery nor the bronchus was clamped (SHAM group). An electrocardiogram (ECG) was obtained whenever clinical ascites became apparent in individual broilers, or prior to the final necropsy for broilers surviving to the end (Day 36) of the experiment. The right:total ventricular weight ratio (RV:TV) was evaluated as an index of pulmonary arterial pressure. Early post-surgical mortality (up to 21 d of age) was higher in the PA-CLAMP group (27% for males and females combined) than in the BRONCHUS CLAMP (10%) and SHAM (2%) groups. Cumulative ascites mortality (Days 22 to 36) also was higher in the PA-CLAMP group (86% for males, 77% for females) than in the BRONCHUS CLAMP (69% for males, 41% for females) and SHAM (23% for males, 0% for females) groups. Ascitic birds in all treatment groups had higher RV:TV ratios and more negative ECG Lead II S-wave amplitudes than nonascitic birds, reflecting the right ventricular hypertrophy and generalized ventricular dilation typically associated with PHS. These results demonstrate that unilateral bronchus occlusion is an effective experimental model for triggering ascites at a lower incidence than that obtained by occluding one pulmonary artery. Following the onset of pulmonary hypertension, the pathophysiological progression leading to ascites appears to be similar for broilers with either unilateral bronchus or pulmonary artery occlusion.
先前的研究表明,肺外主支气管急性(4分钟)和慢性(12天)闭塞会引发肉鸡肺动脉高压,但不会引发肺动脉高压综合征(PHS,腹水)。本研究旨在确定更长时间的支气管闭塞是否会导致与夹闭一条肺动脉所诱发的类似PHS。对14至18日龄的雄性和雌性肉鸡进行麻醉,打开胸廓入口,并放置一个银夹以完全阻塞左肺外主支气管(支气管夹闭组)或左肺动脉(肺动脉夹闭组)。对假手术的雏鸡进行麻醉并打开胸廓入口;然而,既不夹闭肺动脉也不夹闭支气管(假手术组)。每当个体肉鸡出现明显临床腹水时,或在实验结束(第36天)存活至最后的肉鸡进行最终尸检之前,获取心电图(ECG)。将右心室与总心室重量比(RV:TV)作为肺动脉压的指标进行评估。术后早期死亡率(至21日龄)在肺动脉夹闭组(雄性和雌性合计为27%)高于支气管夹闭组(10%)和假手术组(2%)。累积腹水死亡率(第22至36天)在肺动脉夹闭组(雄性为86%,雌性为77%)也高于支气管夹闭组(雄性为69%,雌性为41%)和假手术组(雄性为23%,雌性为0%)。所有治疗组中的腹水鸡比无腹水鸡具有更高的RV:TV比值和更负的心电图II导联S波振幅,这反映了通常与PHS相关的右心室肥大和全身性心室扩张。这些结果表明,单侧支气管闭塞是一种有效的实验模型,用于引发腹水,其发生率低于通过夹闭一条肺动脉所获得的发生率。在肺动脉高压发作后,对于单侧支气管或肺动脉闭塞的肉鸡,导致腹水的病理生理进展似乎相似。