Zhang Li-li, Zhang Jing, Zhao Zi-gang, Zhang Yu-ping, Niu Chun-yu
Department of Pathophysiology, Hebei North University, Zhangjiakou 075029, Hebei, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2010 Dec;22(12):740-3.
To observe the intervention role of normal lymph plasma on renal and hepatic micro-regional blood perfusion in rats with endotoxic shock.
Thirty male Wistar rats were equally divided into control group, model group and lymph plasma group by random digits table. The latter two groups were injected intravenously with lipopolysaccharide (LPS, 15 mg/kg) to duplicate endotoxic shock model, and equal amount of normal saline was given in the control group instead of LPS. Fifteen minutes after the reproduction of model, normal lymph plasma in an amount of 1/15 of blood volume was infused in lymph plasma group. In control and model groups, normal saline was given instead of lymph plasma. Blood pressure was monitored continuously for 6 hours after LPS injection (or normal saline) in all groups, and the micro-regional blood perfusion of the kidney and liver was also observed at the same time with laser Doppler flowmetry. The survival time among groups was compared.
After injecting LPS, the blood pressure of both model and lymph plasma groups declined quickly, and in model group, it gradually descended after a brief elevation. The blood pressure of lymph plasma group although was lower than that of control group at early and later stage, but it was still higher than that of model group. After LPS injection, the micro-regional blood perfusion (PU) of kidney and liver in model group and lymph plasma group were also decreased significantly compared with the control group (kidney: 559.90±111.87, 577.50±91.49 vs. 672.60±50.81; liver: 160.50±54.17, 163.56±34.04 vs. 232.30±34.23, all P<0.05). The blood perfusion of kidney in two groups was increased markedly after 30 minutes compared with control group, and the high level was maintained in the lymph plasma group up to 75 minutes, then it maintained at the level of control group. However, in model group, the blood perfusion was significantly reduced at 120 minutes, and it was significantly lower than control group after 210 minutes. The renal micro-regional blood perfusion (PU) in lymph plasma group was significantly higher than that of model group at 270-360 minutes, especially after 330 minutes (330 minutes : 615.44±98.71 vs. 364.40±146.76, 360 minutes: 584.56±104.72 vs. 307.11±143.11, both P<0.05). The liver blood perfusion in both groups became normal at 30 minutes, and in model group it declined progressively at 270 minutes. In lymph plasma group the liver blood perfusion (PU) was markedly increased compared with model group, especially after 330 minutes (330 minutes : 224.67±20.65 vs. 172.90±46.74, 360 minutes: 218.56±20.40 vs. 158.52±44.71, both P<0.05 ). In model group, the onset of decrease in perfusion (minutes) in the kidney was significantly earlier than that of liver (123.00±68.85 vs. 282.00±96.90, P<0.01). Survival time (hours) was markedly prolonged in lymph plasma group than that of model group (11.80±2.67 vs. 7.21±1.33, P<0.01).
Normal lymph plasma may play a beneficial intervention role in kidney and liver tissue hypoperfusion, and it ameliorates hypotension and prolongs survival time in endotoxic shock.
观察正常淋巴血浆对内毒素休克大鼠肾和肝微循环区域血流灌注的干预作用。
将30只雄性Wistar大鼠通过随机数字表法等分为对照组、模型组和淋巴血浆组。后两组静脉注射脂多糖(LPS,15mg/kg)复制内毒素休克模型,对照组给予等量生理盐水代替LPS。造模15分钟后,给淋巴血浆组输注相当于血容量1/15的正常淋巴血浆。对照组和模型组给予生理盐水代替淋巴血浆。所有组在注射LPS(或生理盐水)后连续监测血压6小时,同时用激光多普勒血流仪观察肾和肝的微循环区域血流灌注。比较各组的生存时间。
注射LPS后,模型组和淋巴血浆组血压均迅速下降,模型组血压在短暂升高后逐渐下降。淋巴血浆组血压虽在早期和后期低于对照组,但仍高于模型组。注射LPS后,模型组和淋巴血浆组肾和肝的微循环区域血流灌注(PU)与对照组相比也显著降低(肾:559.90±111.87,577.50±91.49 vs. 672.60±50.81;肝:160.50±54.17,163.56±34.04 vs. 232.30±34.23,均P<0.05)。两组肾血流灌注在30分钟后与对照组相比显著增加,淋巴血浆组在75分钟内维持在高水平,然后维持在对照组水平。然而,模型组在120分钟时血流灌注显著降低,210分钟后显著低于对照组。淋巴血浆组在270 - 360分钟时肾微循环区域血流灌注(PU)显著高于模型组,尤其是330分钟后(330分钟:615.44±98.71 vs. 364.40±146.76,360分钟:584.56±104.72 vs. 307.11±143.11,均P<0.05)。两组肝血流灌注在30分钟时恢复正常,模型组在270分钟时逐渐下降。淋巴血浆组肝血流灌注(PU)与模型组相比显著增加,尤其是330分钟后(330分钟:224.67±20.65 vs. 172.90±46.74,360分钟:218.56±20.40 vs. 158.52±44.71,均P<0.05)。模型组肾灌注开始下降的时间(分钟)显著早于肝(123.00±68.85 vs. 282.00±96.90,P<0.01)。淋巴血浆组生存时间(小时)明显长于模型组(11.80±2.67 vs. 7.21±1.33,P<0.01)。
正常淋巴血浆可能对肾和肝组织低灌注起有益的干预作用,改善内毒素休克时的低血压并延长生存时间。