Xu Jin, Wang Zheng, Ma Gang, Sagawa Motoyasu, Shimazaki Miyako, Ueda Yoshimichi, Sakuma Tsutomu
Thoracic Surgery, Kanazawa Medical University, Uchinada, Ishikawa, Japan.
Respirology. 2009 Mar;14(2):195-202. doi: 10.1111/j.1440-1843.2008.01453.x. Epub 2008 Dec 11.
Acute pancreatitis causes pulmonary oedema with the accumulation of fluid in the alveolar spaces, possibly due to reduced clearance. This study tested the hypothesis that acute pancreatitis decreases alveolar fluid clearance in a rat model of pulmonary oedema during acute pancreatitis.
Acute pancreatitis was induced by a retrograde injection of 5% taurocholate sodium (0.2 mL) into the common bile duct. The lungs were isolated 4, 24 and 48 h after the induction of acute pancreatitis and alveolar fluid clearance was measured in the absence of pulmonary perfusion.
Alveolar fluid clearance increased to 31.0 +/- 3.5% of instilled volume/h in rats with acute pancreatitis for 4 h compared with 17.3 +/- 1.0% of instilled volume/h in sham rats (P < 0.01), then returned to the control level 48 h after acute pancreatitis (16.0 +/- 4.1% of instilled volume/h). In contrast, the lung water to dry lung weight ratio decreased maximally 24 h after acute pancreatitis (P < 0.01), then returned to the control level 48 h after acute pancreatitis. The plasma epinephrine levels increased to 25-fold higher in rats with acute pancreatitis for 4 h than in sham rats without acute pancreatitis. Prazosin (an alpha(1)-adrenergic antagonist, 10(-4) mol/L), yohimbine (an alpha(2)-adrenergic antagonist, 10(-4) mol/L) or a bilateral adrenalectomy inhibited the increase in part, a combination of prazosin (10(-4) mol/L) and yohimbine (10(-4) mol/L) completely inhibited the increase in alveolar fluid clearance in rats after acute pancreatitis for 4 h, whereas propranolol (a beta-adrenergic antagonist, 10(-4) mol/L) had no effect.
Endogenous catecholamine stimulates alpha-adrenoceptors and increases alveolar fluid clearance in rats with acute pancreatitis.
急性胰腺炎可导致肺水肿，肺泡间隙出现液体蓄积，这可能是由于清除功能降低所致。本研究检验了如下假说：在急性胰腺炎所致肺水肿的大鼠模型中，急性胰腺炎会降低肺泡液体清除率。
通过向胆总管逆行注射5%牛磺胆酸钠（0.2 mL）诱导急性胰腺炎。在诱导急性胰腺炎后4、24和48小时分离肺脏，并在无肺灌注的情况下测量肺泡液体清除率。
急性胰腺炎4小时的大鼠肺泡液体清除率增加至每小时注入量的31.0±3.5%，而假手术大鼠为每小时注入量的17.3±1.0%（P<0.01），急性胰腺炎48小时后恢复至对照水平（每小时注入量的16.0±4.1%）。相比之下，肺水与干肺重量比在急性胰腺炎24小时后降至最低（P<0.01），急性胰腺炎48小时后恢复至对照水平。急性胰腺炎4小时的大鼠血浆肾上腺素水平比无急性胰腺炎的假手术大鼠高出25倍。哌唑嗪（一种α1肾上腺素能拮抗剂，10-4mol/L）、育亨宾（一种α2肾上腺素能拮抗剂，10-4mol/L）或双侧肾上腺切除术可部分抑制这种升高，哌唑嗪（10-4mol/L）和育亨宾（10-4mol/L）联合使用可完全抑制急性胰腺炎4小时后大鼠肺泡液体清除率的升高，而普萘洛尔（一种β肾上腺素能拮抗剂，10-4mol/L）则无作用。
内源性儿茶酚胺刺激α肾上腺素能受体并增加急性胰腺炎大鼠的肺泡液体清除率。
