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摘要：
目的 探讨富氢水（hydrogen rich solution, HRS）对CPB大鼠心肌水通道蛋白（aquaporin, AQP）‑1和AQP‑4的影响。 方法 清洁级成年雄性SD大鼠30只，采用随机数字表法分为3组（每组10只）：假手术组（S组）、CPB组、CPB+HRS处理组（HRS组）。S组不进行CPB、CPB组行CPB 60 min、HRS组在CPB前30 min注射HRS 6 ml/kg。CPB后2 h处死大鼠，开胸从腔静脉抽血离心后保存血浆，ELISA法检测血浆心肌肌钙蛋白I（cardiac troponin I, cTnI）、心型脂肪酸结合蛋白（heart type‑fatty acid binding protein, hFABP）浓度。取心脏将左心室心肌切成4片，第1片心肌组织H‑E染色后光镜下观察；第2片心肌组织用分光光度法检测丙二醛（malondialdehyde, MDA）含量、髓过氧化物酶（myeloperoxidase, MPO）和超氧化物歧化酶（superoxide dismutase, SOD）活性；第3片心肌组织计算其心肌含水量；第4片心肌组织用Western blot法测定AQP‑1、AQP‑4水平。 结果 S组心肌细胞排列整齐有序，有清晰的边界和完整的细胞核；CPB组心肌细胞排列杂乱，没有明确的界限，有肌纤维断裂和核降解；HRS组心肌损伤形态改善。与S组比较，CPB组和HRS组大鼠血浆cTnI、hFABP浓度，心肌MDA含量、MPO活性及心肌含水量增加（P<0.05），心肌SOD活性降低（P<0.05）；与CPB组比较，HRS组大鼠血浆cTnI、hFABP浓度，心肌MDA含量、MPO活性及心肌含水量降低（P<0.05），心肌SOD活性增加（P<0.05）。与S组比较，CPB组大鼠心肌AQP‑1和AQP‑4水平增加（P<0.05）；与CPB组比较，HRS组大鼠心肌AQP‑1和AQP‑4水平降低（P<0.05）。 结论 HRS减轻CPB所致大鼠心肌损伤，其机制可能与降低AQP‑1和AQP‑4水平有关。
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Abstract: Objective To evaluate the effect of hydrogen rich solution (HPS) on myocardial aquaporin (AQP)‑1 and AQP‑4 in rats after cardiopulmonary bypass (CPB). Methods A total of 30 adult male SD rats were selected. According to the random number table method, they were divided into three groups (n=10): a sham operation group (group S), a CPB group, and a CPB+HPS treatment group (group HRS). Group S did not perform CPB, while Group CPB underwent CPB for 60 min. Group HRS was injected with 6 ml/kg HRS 30 min before CPB. The rats were sacrificed 2 h after CPB. Blood samples were collected from the vena cava before centrifugation to obtain serum samples. The plasma levels of cardiac troponin I (cTnI) and heart type fatty acid binding protein (hFABP) were detected by enzyme‑linked immunosorbent assay (ELISA). Then the heart was harvested and the myocardial tissue of the left ventricle was cut into four pieces. The first piece was stained with hematoxylin eosin (H‑E) and observed under a light microscope. The content of malondialdehyde (MDA), and the activity of myeloperoxidase (MPO) and superoxide dismutase (SOD) were detected by spectrophotometry in the second piece. The water content in the third piece of myocardial tissue was calculated, and the expression of AQP‑1 and AQP‑4 was determined by Western blot in the fourth piece. Results Cardiomyocytes in group S were orderly arranged with clear boundary and complete nucleus, but those in group CPB were disorderly arranged without clear boundary, with tearing of muscle fibers and nuclear degradation. The myocardial injury in group HRS was improved. Compared with group S, group CPB and group HRS presented significant increases in the plasma contents of cTnI and hFABP, myocardial MDA content, MPO activity and water content (P<0.05), and decreases in myocardial SOD activity (P<0.05). Compared with group CPB, group HRS showed remarkable decreases in the plasma contents of cTnI and hFABP, myocardial MDA content, MPO activity and water content (P<0.05), and increases in myocardial SOD activity (P<0.05). Compared with group S, the levels of AQP‑1 and AQP‑4 in group CPB increased (P<0.05). Compared with group CPB, the levels of AQP‑1 and AQP‑4 in group HRS decreased (P<0.05). Conclusions HRS can attenuate CPB induced myocardial injury in rats, which may be related to the decreased expression of AQP‑1 and AQP‑4.
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