[Comparison of lung protection for hydrochloric acid or oleic acid induced rat acute respiratory distress syndrome models pretreated with penehyclidine].

OBJECTIVE

To compare the lung protection roles of intraperitoneal pre-injection with penehyclidine for two kinds of rat models with pulmonary and extrapulmonary acute respiratory distress syndrome (ARDSp and ARDSexp).

METHODS

Forty healthy adult Sprague-Dawley (SD) rats were randomly divided into five groups (each n = 8): the rats in sham group received only tracheotomy; the ARDS rat models were reproduced by intratracheal inhalation of 0.1 mol/L hydrochloric acid (HCl) 2 mL/kg to simulate ARDSexp (HCl group) and 0.15 mL/kg oleic acid (OA) intravenous injection to simulate ARDSp (OA group) after tracheotomy; and the rats in two intervention groups were intraperitoneal injected with penehyclidine 0.5 mg/kg. All rats were received mechanical ventilation immediately after model reproduction. Carotid arterial blood was collected 4 hours after model reproduction for determining the arterial partial pressure of oxygen (PaO), and oxygenation index (PaO/FiO) was calculated. Carotid venous blood and lung tissues were harvested, and the levels of myeloperoxidase (MPO), interleukin-8 (IL-8) and nuclear factor-κB (NF-κB) in serum and lung tissue were determined by enzyme linked immunosorbent assay (ELISA). Pulmonary pathology was observed under optical microscope, and pathological score of Smith was calculated.

RESULTS

Under optical microscope, a large number of inflammatory cells infiltration in lung tissue, obvious alveolar collapse, fibrous exudation in alveolar and alveolar hyaline were found in HCl group. In OA group, however, microvascular congestion and interstitial pulmonary edema were the main pathological changes, with alveolar structure being kept relatively intact. Compared with sham group, pathological score of Smith in HCl and OA groups were increased, oxygenation was lowered, and inflammatory factors levels in serum and lung tissue were increased with levels in lung tissue being higher than those in serum, without significant difference between the two models. When pretreated with penehyclidine, however, pathological injury induced by HCl or OA was alleviated, and pathological score of Smith was also decreased as compared with that of corresponding model groups (5.48±1.76 vs. 9.69±2.02, 3.97±2.14 vs. 8.71±2.18, both P < 0.05), PaO/FiO was raised significantly [mmHg (1 mmHg = 0.133 kPa): 323±55 vs. 211±27, 307±56 vs. 207±31, both P < 0.05], the inflammatory factors levels in serum and lung tissue were obviously decreased [MPO (μg/L): 11.91±1.55 vs. 14.82±1.25, 12.75±1.16 vs. 16.97±2.06 in serum, 25.80±3.36 vs. 35.18±4.01, 24.23±1.24 vs. 33.94±1.43 in lung tissue; IL-8 (ng/L): 358±30 vs. 459±25, 377±38 vs. 427±34 in serum, 736±53 vs. 866±51, 701±53 vs. 809±39 in lung tissue; NF-κB (ng/L): 483±68 vs. 632±73, 514±83 vs. 685±78 in serum, 984±75 vs. 1 217±123, 944±90 vs. 1 163±105 in lung tissue; all P < 0.05]. But all parameters above were similar between the two pretreatment groups (all P > 0.05).

CONCLUSIONS

Inflammatory cell infiltration and alveolar collapse mainly happened in HCl induced ARDSp, while pulmonary interstitial edema and hemorrhage was mostly seen in ARDSexp rats induced by OA intravenous injection. There was no significant difference in oxygenation and inflammatory response between the two models of rats. Pre-intraperitoneal injection of penehyclidine equally improved oxygenation state, inhibited lung inflammation response, and reduced lung injury in the two kinds of ARDS, but there was no difference in protective role between two models pretreated with penehyclidine.