From the Departments of Emergency Medicine.
Intensive Care Medicine, Sapporo Medical University, Sapporo, Japan.
Pancreas. 2021 Feb 1;50(2):235-242. doi: 10.1097/MPA.0000000000001738.
The mechanisms underlying hypothermia-induced pancreatic injury are unclear. Thus, we investigated the pathophysiology of hypothermia-induced pancreatic injury.
We created a normal circulatory model with body surface cooling in rats. We divided the rats into control (36°C-38°C), mild hypothermia (33°C-35°C), moderate hypothermia (30°C-32°C), and severe hypothermia (27°C-29°C) (n = 5 per group) groups. Then, we induced circulatory failure with a cooling model using high-dose inhalation anesthesia and divided the rats into control (36°C-38°C) and severe hypothermia (27°C-29°C) (n = 5 per group) groups. Serum samples were collected before the introduction of hypothermia. Serum and pancreatic tissue were collected after maintaining the target body temperature for 1 hour.
Hematoxylin and eosin staining of the pancreas revealed vacuoles and edema in the hypothermia group. Serum amylase (P = 0.056), lactic acid (P < 0.05), interleukin 1β (P < 0.05), interleukin 6 (P < 0.05), and tumor necrosis factor α (P = 0.13) levels were suppressed by hypothermia. The circulatory failure model exhibited pancreatic injury.
Hypothermia induced bilateral effects on the pancreas. Morphologically, hypothermia induced pancreatic injury based on characteristic pathology typified by vacuoles. Serologically, hypothermia induced protective effects on the pancreas by suppressing amylase and inflammatory cytokine levels.
低温诱导胰腺损伤的机制尚不清楚。因此，我们研究了低温诱导胰腺损伤的病理生理学。
我们在大鼠中创建了一个具有体表冷却的正常循环模型。我们将大鼠分为对照组（36°C-38°C）、轻度低温组（33°C-35°C）、中度低温组（30°C-32°C）和重度低温组（27°C-29°C）（每组 5 只）。然后，我们使用高剂量吸入麻醉诱导循环衰竭，并将大鼠分为对照组（36°C-38°C）和重度低温组（27°C-29°C）（每组 5 只）。在引入低温前采集血清样本。维持目标体温 1 小时后采集血清和胰腺组织。
胰腺苏木精-伊红染色显示低温组有空泡和水肿。血清淀粉酶（P = 0.056）、乳酸（P < 0.05）、白细胞介素 1β（P < 0.05）、白细胞介素 6（P < 0.05）和肿瘤坏死因子 α（P = 0.13）水平受低温抑制。循环衰竭模型表现出胰腺损伤。
低温对胰腺产生双向影响。形态上，低温诱导以空泡为特征的典型病理学胰腺损伤。血清学上，低温通过抑制淀粉酶和炎症细胞因子水平对胰腺产生保护作用。
