Schertel E R, Pratt J W, Schaefer S L, Valentine A K, McCreary M R, Myerowitz P D
Department of Surgery, Ohio State University, Columbus, USA.
Surgery. 1996 Jan;119(1):81-8. doi: 10.1016/s0039-6060(96)80218-2.
Acid aspiration-induced acute lung injury (AALI) leads to myocardial leukosequestration and edema in rats and hemodynamic depression in dogs, but the effects of AALI on left ventricular (LV) function have not been carefully studied.
We examined the effects of 0.1 N HCl administration into the lung on LV function, leukosequestration, and edema in pentobarbital-anesthetized, atropinized (n = 8), or autonomically blocked (n = 7) dogs. Saline solution was administered into the lungs of a control group of autonomically blocked dogs (n = 6). LV contractility was assessed by end-systolic elastance (EES) and preload recruitable stroke work (PRSW). Active relaxation was assessed by the time constant of LV pressure decline (tau).
AALI resulted in significant (p < 0.05) decreases in mean arterial pressure and cardiac output and increases in pulmonary artery pressure and systemic vascular resistance in atropinized and autonomically blocked dogs but not in saline control group. In atropinized dogs tau did not change after injury, but EES and PRSW were increased significantly at 2 and 3 hours after injury, despite significant myeloperoxidase activity and extravascular fluid wet-dry weight ratios. EES, PRSW, and tau did not change in the autonomically blocked dogs in response to AALI or in the saline control group.
We concluded that AALI results in a baroreflex mediated enhancement of LV contractility in dogs, despite mild myocardial leukosequestration and edema formation.
酸误吸诱导的急性肺损伤（AALI）可导致大鼠心肌白细胞滞留和水肿，以及犬的血流动力学抑制，但AALI对左心室（LV）功能的影响尚未得到仔细研究。
我们研究了向戊巴比妥麻醉、已用阿托品处理（n = 8）或自主神经阻断（n = 7）的犬肺内注入0.1 N盐酸对LV功能、白细胞滞留和水肿的影响。向自主神经阻断的犬对照组（n = 6）的肺内注入生理盐水。通过收缩末期弹性（EES）和预负荷可募集搏功（PRSW）评估LV收缩性。通过LV压力下降时间常数（tau）评估主动舒张功能。
AALI导致已用阿托品处理和自主神经阻断的犬平均动脉压和心输出量显著降低（p < 0.05），肺动脉压和全身血管阻力升高，但生理盐水对照组未出现此情况。在已用阿托品处理的犬中，损伤后tau未改变，但损伤后2小时和3小时EES和PRSW显著增加，尽管髓过氧化物酶活性和血管外液湿重与干重比值显著升高。自主神经阻断的犬对AALI的反应以及生理盐水对照组中，EES、PRSW和tau均未改变。
我们得出结论，尽管存在轻度心肌白细胞滞留和水肿形成，但AALI可导致犬压力反射介导的LV收缩性增强。
