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Rat hepatic ischemia-reperfusion on liver regeneration

Author: ZuoQiang
Tutor: DongJiaHong；ChenPing
School: Third Military Medical University
Course: Surgery
Keywords: Rats Liver Ischemia-reperfusion injury Liver regeneration Pathology ~ 3H-TdR incorporation RT-PCR CyclinD1 EGFR TNF-α IL-6
CLC: R657.3
Type: Master's thesis
Year: 2000
Downloads: 107
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Abstract

The purpose of liver surgery massive blood loss induced liver failure and even death. Clinical hepatic inflow occlusion method to reduce blood loss in itself will cause hepatic ischemia-reperfusion injury is limited. Another a long time at home and abroad on liver regeneration mechanism has been studied extensively, liver cell death or missing will quickly start of liver regeneration. It is noteworthy that the damage degree of liver function after ischemia-reperfusion recovery is closely related liver regeneration functions improve the recovery of liver function is also important, however, rarely ischemia-reperfusion injury on liver regeneration have been reported. With ischemia-reperfusion-depth research is bound to consider ischemia-reperfusion injury and liver regeneration relationship. Head of ischemia-reperfusion liver injury research is to increase the protection of the remnant liver cells, but less established for the promotion of liver regeneration thought against liver injury. Currently considered under the normal temperature of normal human liver can tolerate more than 60min ischemia, recent studies have found that hepatic inflow occlusion tolerated safety time limit in the portal vein bypass normal rat room temperature for up to 90min. This study intends to pre-reserved portal vein bypass lobe of the liver (approximately 70%) of the whole liver, blocking part of the lobe of the liver (approximately 30%) of the total hepatic blood supply, blood for the perfusion of ischemic lobe to the predetermined observation after the end of the new open resection of the portal vein bypass lobe of the liver (70% hepatectomy) of this model to analyze the rat hepatic ischemia-reperfusion liver regeneration function. Method 1. Animal models: the use of rat liver anatomical characteristics, by temporarily blocking the right lobe, caudate lobe (accounting for about 30% of the whole liver) hepatic pedicle, resulting in 30% of the lobe of the liver ischemia, retain the left lobe of the liver, the mid (about liver 70%) of the blood supply as a portal venous drainage channels to prevent portal congestion. Restore the right hepatic caudate lobe blood supply to a predetermined end points after the first, and then left hepatic resection, the mid (70% hepatectomy) to induce liver regeneration. 2111 / more than eleven back woo gas Tuen fly \\ the II group SO: - omln lschemla groupN-knife H. Mouth min lschemla group 30'PH ll -. 30min ischemia sroup 60'PH-60min ischcmia glOOp 90'Pll WW 90Olll ISChCml3 two after ischemia-reperfusion injury and liver regeneration: With Bu described model by ischemic reperfusion process, hepatic resistance gross morphological tissue disease survival pharmacology and ultrastructure, rat 7 to 10 days and the whole liver / body weight than the recovery of postoperative complications. TdR incorporation eve CyClinLDI mRNA and protein expression, EGFR expression h marsh TNF, IL-6 concentration keynote pay, respectively, to reflect and evaluate the degree of liver injury in the animal model, and again the main function of liver cells liver sewing cell. Lobe ischemia Chuan% hepatectomy results I of the animal model combines reliable ischemia emblem first glance feasible and easy to repeat the results are stable. 2 NPH, 30PH, 60'PH, 90'PHfl rats 48h after Cun Fen will were 100%, 100%, 70%, 60%, and 7 days after the deposit if rates were Chuan%, 100%, 600 / 6,40 Q / 6. 10 days after the same survival rate after day survival. Shows that rats exposed to ischemic C irrigation muddy and 70% hepatectomy injury deaths occurred in less than 48h. 3 normal Wistar rat liver / body weight ratio of about 418%; N-PH 30'Pll, 60'PH 90TH rats after 4 Tianquan liver / body weight ratios were 252%, 2500/0, 2320 / 0,189%; Tianquan liver after leaching heavy than 5 mao%, 3%, 365%, 347%: 10 Guinness after liver / body weight ratios were 415%, 422%, 437%, 443 %. m 4. The pathological changes of the liver with ischemic time and aggravation. The pathological changes of ischemia during cloudy swelling of the liver cells; reperfusion nearest 0 ~ 12h liver sinusoidal congestion, punctate dissolved necrosis; 12 ~ 24h reperfusion pathological changes gradually transition to a large number of neutrophils, lymphatic cell infiltration and diffuse necrosis of the liver cells mainly; performance as there are still a large number of neutrophils in 7 to 10 days. Lymphocytic infiltration of the necrotic tissue and fibrous tissue hyperplasia tightly wrapped, mild fibroplasia liver tissue outside the parcel. The hepatocyte proliferation change liver mitotic phase is characterized by the reduced ischemic time. Normal 70% hepatectomy induced mitotic phase in 24 ~ 48h gradually increased and reached the peak at 48h. NIH, 30'PH 60'FH 90'IH rats 48h after mitotic count were 43.6 f4.9 door high power field the Bu-fold X44 l on 3,4 eight high-power field (40X10 times), 22.7 ± 27 door high power field (40X10 times), 194 ± 3.4 door high power field (40.10 times). 5 rat postoperative 24h3H1dR of incorporation was significantly reduced ischemia time. 6 rats postoperative 12h CyclinD of; mRNA and subsequent protein expression levels as ischemia time was significantly reduced. 7, the rats within 12h after EGFR protein expression levels as ischemia time was significantly reduced. 8. TNF concentration in rats after 6h elevated to varying degrees, the longer ischemic time group increased more significantly and 24h sustained at a relatively high, the downward trend is not obvious. 9 rats in each group after 6h IL seven concentration were elevated to varying degrees, the longer ischemic time group increased less significant and sustained at a relatively low within 24h obvious increasing trend. Conclusion: l This study uses a 30% lobe withstand ischemia-reperfusion injury in rats, the removal of an animal model and then at the same time 70% of the lobe bypass, both analog portal vein congestion pure lobe ischemia-reperfusion 70% hepatectomy combined classical pathway induced liver regeneration is to study the impact on liver regeneration function better model ischemia and reperfusion. 2. Rat liver ischemia 30ndn?

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