Portal vein arterialization promotes liver regeneration after extended partial hepatectomy in a rat model

In the current study, we sought to establish a novel rat model of portal vein artefialization （PVA） and evaluate its impact on liver regeneration after extended partial hepatectomy （PH）. A total of 105 Sprague-Dawley rats were randomly assigned to three groups： 68% hepatectomy （the PH group）, portal arterialization after 68% hepatectomy （the PVA group）, and fight nephrectomy only （the control group）. Liver regeneration rate （LRR）, 5-bromo-2-deoxyuridine （BrdU） labeling index, and liver functions were assessed on postoperative day 2, 7, 14 and 28. The 28-day survival rates were compared among the three groups. The 28-day survival rates were similar in all groups （P = 0.331）, and the anastomotic patency was 100%. The LRR in the PVA group was significantly higher than that of the PH group within postoperative 14 days （P 〈 0.05）. The PVA and PH group had increased serum alanine aminotransferase levels （232 ±61 U/L and 212 ±53 U/L, respectively） compared with the control group （101 ±13 U/L） on postoperative day 2, whereas from postoperative day 7 to day 28 there were no differences among the three groups. Serum albumin values were higher after the PVA procedure within postoperative day 14, which gradually became comparable on postoperative day 28 among the three groups. The peaks of BrdU labeling index appeared on postoperative day 2 in all rats, and the PVA procedure was associated with increased BrdU labeling index from postoperative day 7 to 28. The 28-day survival of the PVA rats was comparable. Our findings demonstrate that the PVA procedure utilizing portal vein trunk-renal artery microvascular reconstruction promotes remnant liver regeneration and confers beneficial effects on maintaining and even optimizing liver function after extended partial hepatectomy in rats.

The current status of malignant hyperthermia

Malignant hyperthermia(MH) is a rare and life-threatening pharmacogenetic disorder triggered by volatile anesthetics, the depolarizing muscle relaxant succinylcholine, and rarely by strenuous exercise or environmental heat. The exact prevalence of MH is unknown, and it varies from 1:16 000 in Denmark to 1:100 000 in New York State. The underlying mechanism of MH is excessive calcium release from the sarcoplasmic reticulum(SR),leading to uncontrolled skeletal muscle hyper-metabolism. Genetic mutations in ryanodine receptor type 1(RYR1)and CACNA1 S have been identified in approximately 50% to 86% and 1% of MH-susceptible(MHS) individuals,respectively. Classic clinical symptoms of MH include hypercarbia, sinus tachycardia, masseter spasm,hyperthermia, acidosis, muscle rigidity, hyperkalemia, myoglobinuria, and etc. There are two types of testing for MH: a genetic test and a contracture test. Contracture testing is still being considered as the gold standard for MH diagnosis. Dantrolene is the only available drug approved for the treatment of MH through suppressing the calcium release from SR. Since clinical symptoms of MH are highly variable, it can be difficult to establish a diagnosis of MH. Nevertheless, prompt diagnosis and treatments are crucial to avoid a fatal outcome. Therefore, it is very important for anesthesiologists to raise awareness and understand the characteristics of MH. This review summarizes epidemiology, clinical symptoms, diagnosis and treatments of MH and any new developments.

Effect of Cholesterol Content in Diet on Atorvastatin(ATO)-induced Liver Injury in Golden Hamsters

[Objectives]The objective of this study was to investigate the effect of cholesterol content in high-fat diet on atorvastatin(ATO)-induced liver injury in golden hamsters and compare the degree of liver injury caused by two high-fat diets with different cholesterol proportions.[Methods]Male golden hamsters were randomly and evenly divided into different groups and given different high-fat diets for 14 consecutive days by gavage to establish hyperlipidemia models.From the 15th d on,the hamsters in the model groups were given ATO at a dose of 5 mg/kg,one a day,for 9 consecutive days.Blood was sampled from the orbital veins of the hamsters for the determination of biochemical indicators.Liver tissues of the hamsters were sampled,paraffin-embedded,sliced,stained by HE(hematoxylin-eosin)method and observed under an optical microscope.[Results]Compared with standard diet group,the body weight increased significantly(P<0.05),the serum TC,TG and LDL-C levels increased significantly(P<0.05),the serum HDL-C level declined significantly(P<0.05),and the ALT and AST levels increased significantly(P<0.05)in the high-fat diet groups.This trend was more obvious in the high-fat II group than the high-fat I group.After ATO intervention,the HDL-C,TBIL and TBA levels increased significantly(P<0.05),and the liver ALT and AST levels further increased(P<0.05)in the model groups.This trend was more obvious in the model II group than the model I group.The morphological inspection shows that the fat deposition in the liver tissues was severe;the hepatocytes in the model groups were obviously damaged;the liver injury in the hamsters fed high-fat diet containing 0.2%cholesterol and intervened with ATO was relatively mild but severer than the high-fat diet groups.[Conclusions]Hamster models of hyperlipidemia were successfully established in this study.High-fat diet could cause liver injury.While lowering blood lipid level,ATO aggravated liver injury.Among the high-fat diets with different proportions of cholesterol,the diet containing 0.2%cholesterol had little effect on ATO-induced liver injury.