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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experimental model, based on Pringle's scheme of acute warm hepatic ischemia in normothermia was employed in order to study the hepatoprotective properties of prolactin (PRL). In the proposed model one liver lobe was maintained in the portal circulation and the remaining lobes were perfused with HTK solution for 2 hours. The experiment was carried out on female rabbits of the Chinchilla race. In the control group (n= 10) the liver was perfused with HTK solution. In the examined group (n=10), 3 microg of PRL per g of liver per hour was added to HTK solution. Additionally, the animals in the PRL-treated group were intravenously administered a dose of 600 microg of PRL / kg body weight. 1 h before the surgical treatment. The activities of alanine aminotransferase (ALT), alkaline phosphatase (ALP). gamma-glutamyl transferase (GGT) and the lactate concentration were determined in the eluate obtained from the perfused part of the liver. It was found that administration of prolactin during 2 h of perfusion led to a significant decrease of ALT, ALP and lactate concentrations in the eluate. In addition, increase of calcium concentration in the liver was significantly lower with the prolactin group. The observed results let us to draw the conclusion that administration of PRL shows signs of protective effects on hepatocytes in normothermic acute ischemia.
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PMID:The influence of prolactin on the chosen biochemical parameters of the rabbit liver in ischemia. 1579 42

Ischemic preconditioning (IPC) and intermittent vascular control (IVC) have been shown to reduce the number of ischemia/reperfusion injuries during liver resections with the Pringle maneuver. Our study aimed to compare the beneficial effect of these two modalities in relation to the duration of normothermic liver ischemia. A group of 24 Landrace pigs with a mean body weight of 25 to 30 kg were subjected to extended liver resection of more than 65%. Although, 12 animals underwent IPC (10 minutes of ischemia and 10 minutes of reperfusion), and subsequently the Pringle maneuver was applied for 90 minutes (n= 6) or 120 minutes (n= 6). Another 12 animals underwent liver resection by IVC (20 minutes of ischemia alternated with 5 minutes of reperfusion) for 60 minutes (n = 6) or 120 minutes (n = 6) of inflow vascular control. At 90 minutes of liver ischemia, the IPC group demonstrated lower levels of asportate aminotransferase (AST) (173 +/- 53 vs. 265 +/- 106 IU; p =0.089) and malondialdehyde (MDA) (2.60 +/- 1.03 vs. 5.33 +/- 2.25 micromol/L; p =0.022) and higher liver tissue cAMP (200 +/- 42 vs. 146 +/- 40 pmol/g wet wt, p = 0.04) compared to the IVC group. However, no pathologic differences were observed between the two groups. By contrast, at 120 minutes of liver ischemia, IVC proved to be more beneficial, reflected by lower levels of AST (448 +/- 135 vs. 857 +/- 268 IU; p = 0.006) and MDA (8.33 +/- 1.75 vs. 12.7 +/- 4.31 micromol/L; (p = 0.045), a higher cAMP level (127 +/- 10 vs. 97 +/- 31 pmol/g wet wt p = 0.045), and eventually less cellular necrosis (necrosis score 1.66 +/- 0.51 vs. 2.85 +/- 1.16; p = 0.04) compared to the IPC group. It appears that IPC should be employed when liver ischemia is anticipated to last less than 90 minutes, followed by IVC when the liver ischemia is expected to last 120 minutes.
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PMID:Ischemic preconditioning versus intermittent vascular inflow control during major liver resection in pigs. 1595 43

Temporary portal triad clamping (Pringle maneuver) during liver resection reduces intraoperative blood loss. A normal liver can safely tolerate normothermic ischemia for up to 60 min. However, its safety in patients with surgical obstructive jaundice (SOJ) is not known. Therefore, we investigated the effect of hepatic ischemia in an experimental rat model of SOJ created by ligating the bile duct. Four groups of rats were created: Group I (sham operation, 10 days later, liver resection); Group II (sham operation, 10 days later, liver resection with 5 min of hepatic ischemia); Group III (bile duct ligation, 10 days later, liver resection); and Group IV (bile duct ligation, 10 days later, liver resection with 5 min of hepatic ischemia). The ischemic injury was assessed by the survival of rats, liver tissue malondialdehyde and total glutathione (markers of free radical injury), serum alanine aminotransferase, aspartate aminotransferase, and liver histology. The results showed decreased survival (47.6% vs. 90% [p = .046]), increased liver tissue malondialdehyde (161 +/- 35 vs. 129 +/- 33 microg/gm liver tissue [p = .05]), and decreased liver tissue total glutathione (565 +/- 169 vs. 1075 +/- 276 nmol/gm liver tissue [p = .05]) in rats with SOJ subjected to hepatic ischemia when compared to nonjaundiced rats. The changes in serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase showed an increasing trend in the SOJ group but were not statistically significant. Ischemic changes in liver histology were seen more often in the SOJ group but were not statistically significant. These data suggest that temporary portal triad clamping in an experimental model of SOJ is detrimental to the outcome of liver resection.
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PMID:Evaluation of Pringle maneuver during liver resection in a rat model of surgical obstructive jaundice. 1603 81

Ischemia reperfusion (IR) of the liver is a multifactorial process that, at least in part, is responsible for the morbidity associated with major liver surgery under occlusion of the portal triad with the Pringle maneuver, total vascular exclusion or after liver transplantation. Surgeons are confronted with IR injury (IRI) more often than they anticipate. Although the human body has its own defense system, understanding the pathophysiology of IRI is essential for the surgeon in preventing and/or treating the reperfusion injury in common clinical practice. Several endogenous mechanisms exist to overcome IRI and a large number of pharmacological agents have also been found to confer protection against ischemic injury in the liver. They either blocked the injurious pathways directly or they subjected the liver to preconditioning. Prostaglandins (PGs) are a group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase (COX) pathway. They are short-lived, hormone-like chemicals that regulate cellular activities on a moment-to-moment basis and are produced in most tissues of the body, although the liver has emerged as the major organ participating in the synthesis, degradation and elimination of arachidonate products of systemic origin. PGs are released through the prostaglandin transporter on the cell's plasma membrane. During the last decade intensive work on the cytoprotective effects of PGs on livers suffering from IRI have been well documented. Prostaglandins confer their protective effects on IR-injured livers mainly by inhibiting the generation of reactive oxygen species, preventing leukocyte migration, reducing the synthesis or production of membrane degradation products, improving hepatic insulin and lipid metabolism, and regulating the production of inflammatory cytokines and cell adhesion molecules. Production of PGs have been found essential also soon after partial hepatectomy for hepatocyte proliferation.
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PMID:The role of prostaglandins in liver ischemia-reperfusion injury. 1691 23

Control of bleeding from the transected liver basically consists of vascular inflow occlusion and control of hepatic venous backflow from the caval vein. Central venous pressure determines the pressure in the hepatic veins and is an extremely important factor in controlling blood loss through venous backflow. Vascular inflow occlusion (Pringle maneuver) involves clamping of the portal vein and the hepatic artery in the hepatic pedicle and gives rise to postischemic, reperfusion injury. Several strategies have been devised to reduce reperfusion injury (pharmacological interventions) or to increase ischemic tolerance of the liver (ischemic preconditioning). Intermittent clamping is recommended in complex liver resections or in patients with diseased livers. The combination of occlusion of vascular inflow and outflow of the liver results in total hepatic vascular exclusion (THVE) and is mainly used in tumors invading the caval vein. During THVE the liver can be cooled by hypothermic perfusion allowing for extended ischemia times. Selective THVE entails clamping of the main hepatic veins in their extrahepatic course, thus preserving caval flow. Safe liver surgery requires knowledge of the regular techniques of vascular occlusion for 'on demand' use when necessitated to reduce blood loss.
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PMID:Vascular occlusion techniques during liver resection. 1765 52

Pringle described a new technique to reduce blood loss during liver surgery. Adult Wistar rats were subjected to 1 h of partial liver ischemia and followed by 3 h reperfusion. Eighteen Wistar rats were divided into sham-operated control group (I) (n=6), ischemia and reperfusion (I/R) group (II) (n=6), L-arginine treated group (100 mg/kg body weight/daily by oral route for 7 d before induced ischemia reperfusion maneuver) (III) (n=6). Ischemic and reperfusion hepatocellular injury occurred as indicated by increased-alanine transaminase (ALT), aspartate transaminase (AST). Pre-treatment with L-arginine significantly decreased serum-ALT, AST after 1 h ischemia followed by 3 h of reperfusion. Nitric oxide production, in hepatocytes was increased 2 fold and MDA levels significantly decreased by L-arginine treatment as compared to I/R rat. Histopathology and TEM studies showed markedly diminished hepatocellular injury in L-arginine pretreated rats during the hepatic I/R, which reached a level comparable to saline-treated rat of sham operated group. Thus, findings it may be concluded that L-arginine afforded significant protection from hepatobiliary function from I/R injury by nitric oxide production.
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PMID:L-arginine protects from pringle manoeuvere of ischemia-reperfusion induced liver injury. 1845 13

The child's brain is more malleable or plastic than that of adults and this accounts for the ability of children to learn new skills quickly or recovery from brain injuries. Several mechanisms contribute to this ability including overproduction and deletion of neurons and synapses, and activity-dependent stabilization of synapses. The molecular mechanisms for activity-dependent synaptic plasticity are being discovered and this is leading to a better understanding of the pathogenesis of several disorders including neurofibromatosis, tuberous sclerosis, Fragile X syndrome and Rett syndrome. Many of the same pathways involved in synaptic plasticity, such as glutamate-mediated excitation, can also mediate brain injury when the brain is exposed to stress or energy failure such as hypoxia-ischemia. Recent evidence indicates that cell death pathways activated by injury differ between males and females. This new information about the molecular pathways involved in brain plasticity and injury are leading to insights that will provide better therapies for pediatric neurological disorders.
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PMID:Plasticity and injury in the developing brain. 1849 Jan 22

Surgical treatment of hepatocellular carcinoma (HCC) has made great progress in recent ten years, although the appropriate selection of treatment methods remains controversial. Surgical resection of HCC is still widely recognized as the first choice, which has been remarkably improved by effectively controlling intra-operative bleeding. However, the ischemia/reperfusion injury and long-term recurrence still proposes challenges to Pringle's maneuver. The indications of liver transplantation also expand in recent years, and many centers have used marginal donor liver and living donor liver. Remission of the shortage of donors, local ablation of small HCC, and surgical resection still lack the support of randomized controlled trials. In summary, the surgical treatment of HCC should strictly based on the indications of various therapies, which should be prudently verified by randomized controlled trials.
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PMID:[Recent advances and controversies in surgical management of hepatocellular carcinoma of hepatocellular carcinoma]. 1879 5

In liver resection operations the Pringle (Baron) maneuver can be used for temporary ischemia by clamping the hepatoduodenal ligament intermittently. In this beagle canine model we investigated whether hemorheological parameters may alter in systemic, portal and hepatic venous blood and in arterial samples during-after Pringle maneuvers. In Pringle Group unilateral femoral artery and external jugular vein were cannulated. From median laparotomy the hepatoduodenal ligament was exposed. The portal venous system was catheterized via a mesenteric vein and through the inferior caval vein a catheter was led to the hepatic veins. After stabilization, a 15-minute Pringle maneuver was carried out three times with 5-minute interpolated reperfusion periods. In Control Group Pringle maneuvers were not made. Before and after Pringle maneuvers parallel blood samples were taken from the cannulated vessels for determining hematological parameters and erythrocyte aggregation. Following Pringle maneuvers erythrocyte deformability, blood and plasma viscosity were also tested. The results showed that besides systemic hemorheological effects of the intermittent Pringle maneuver local leukocyte count, hematocrit and erythrocyte aggregation index altered mainly in portal venous blood, depending on the repeating number of the maneuvers. Thus, investigations of hemorheological parameters might be useful to determine the optimal duration of the Pringle maneuver.
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PMID:Hemorheological changes caused by intermittent Pringle (Baron) maneuver in beagle canine model. 1902 43

Curative hepatectomy is still the best therapeutic strategy for liver cancer treatment up to now. The Pringle manoeuvre has been commonly used to avoid massive blood loss during operation since its advent, which greatly accelerates the advance of liver surgery and oncological surgery. In the past century, more attentions have been paid to different effects of ischemia-reperfusion injury elicited by Pringle manoeuvre. Theses include its impacts on complex metabolic, immunological, and microvascular changes, which altogether might contribute to hepatocellular damage and dysfunction, and contribute to haemodynamic instability. Despite these adverse impacts, the short-term outcome of affected patients under hepatectomy was greatly improved with the advances of surgical techniques and perioperative management in recent years. While the long-term prognosis remains unsatisfactory due to a high incidence of intra/extrahepatic recurrence. The reason for it was not totally elucidated. Furthermore, the effect of the Pringle manoeuvre on the prognosis of oncologic patients and behavior of the tumor cell was not deliberately mentioned. This point was put forward to the front-desk by the specific phenomenon from recent animal studies. It is showed that ischemia-reperfusion injury of the liver remnant may be a significant factor to promote the tumor recurrence and metastasis. If it is a truth in human, there must be a big challenge to the Pringle manoeuvre. So we hypothesized that the long-term prognosis of cancer patients could be worsened by the ischemia-reperfusion injury elicited by Pringle manoeuvre during the hepatectomy and it should be revised, or even, avoided in future hepatectomy for oncologic patients. The less surgical stress including ischemia-reperfusion injury in the hepatic resection without Pringle manoeuvre might contribute to a better prognosis. To get a deeper understanding, prospective randomized clinical trials need to be done. It is surely supposed to provide more important information about the long-term effects of the Pringle manoeuvre, and to our hypothesis.
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PMID:The Pringle manoeuvre should be avoided in hepatectomy for cancer patients due to its side effects on tumor recurrence and worse prognosis. 1914 72


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