Pronounced effect of minor changes in body temperature  on ischemia and reperfusion injury in rat liver

Heijnen, Bob H. M.; Veen, Suzanne Q. van; Straatsburg, Irene H.; Gulik, Thomas M. van

doi:10.1152/jappl.2001.91.1.265

Cited by 29 publications

(24 citation statements)

References 14 publications

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“…The importance of maintaining a constant temperature is not always recognized, leading to discrepancies in results. A deviation of even a single degree celsius in liver temperature can have a substantial effect on ischaemia-reperfusion injury (Heijnen et al 2001 temperature-controlled conditions allowing more than 11 variation (Sahin & Rowland 1998) will lead to distorted results. Measurement of temperature is, in our opinion, preferred at the inflow site of the liver, precluding damage of the liver parenchyma by the probe, which might cause microvasculatory disturbances or oxygen leakage.…”

Section: Perfusion Temperaturementioning

confidence: 99%

The isolated perfused rat liver: standardization of a time-honoured model

Hart²,

et al. 2006

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SummaryFor many years, the isolated perfused rat liver (IPRL) model has been used to investigate the physiology and pathophysiology of the rat liver. This in vitro model provides the opportunity to assess cellular injury and liver function in an isolated setting. This review offers an update of recent developments regarding the IPRL set-up as well as the viability parameters that are used, with regards to liver preservation and ischaemia and reperfusion mechanisms.A review of the literature was performed into studies regarding liver preservation or liver ischaemia and reperfusion. An overview of the literature is given with particular emphasis on perfusate type and volume, reperfusion pressure, flow, temperature, duration of perfusion, oxygenation and on applicable viability parameters (liver damage and function).The choice of IPRL set-up depends on the question examined and on the parameters of interest. A standard technique is cannulation of the portal vein, bile duct and caval vein with pressure-controlled perfusion at 20 cm H 2 O (15 mmHg) to reach a perfusion flow of approximately 3 mL/min/g liver weight. The preferred perfusion solution is Krebs-Henseleit buffer, without albumin. The usual volume is 150-300 cm 3 , oxygenated to a pO 2 of more than 500 mmHg. The temperature of the perfusate is maintained at 371C. Standardized markers should be used to allow comparison with other experiments.Keywords Isolated perfused rat liver (IPRL); liver preservation; parameters; liver function; liver damage For many years, the isolated perfused rat liver (IPRL) model has been used to investigate the physiology and pathophysiology of the rat liver. This in vitro model provides the opportunity to assess cellular injury and liver function in an isolated setting.The IPRL model was first reported by Claude Bernard in 1855 (Gores et al. 1986).In the review about the IPRL written by Gores et al. in 1986, the authors stated that the model remained a valuable reperfusion model, although other methods such as the assessment of liver slices, cell cultures, cell suspensions and isolated organelles had emerged. To date, the IPRL provides valuable data in studies regarding liver physiology using new techniques in the field of molecular biology and genetics.In the field of liver preservation, the IPRL model has been used for, among others, assessment of ischaemia-reperfusion injury, metabolism of perfusate compounds, metabolism of ammonium and amino acids (Haussinger 1987), endothelial function using hyaluronic acid uptake (Reinders et al. 1996), oxygen consumption (Dahn et al.

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Section: Perfusion Temperaturementioning

confidence: 99%

The isolated perfused rat liver: standardization of a time-honoured model

Hart²,

et al. 2006

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“…Arterial blood pressure was maintained at approximately pre-operative levels by adjustment of the isoflurane levels. The animals were kept in supine position on a heating pad and rectal temperature was controlled at 37 ° C with the use of a heating lamp [33].…”

Section: Anaesthesiamentioning

confidence: 99%

Inhibition of classical complement activation attenuates liver ischaemia and reperfusion injury in a rat model

Heijnen¹,

Straatsburg²,

Padilla

et al. 2005

Clinical and Experimental Immunology

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SummaryActivation of the complement system contributes to the pathogenesis of ischaemia/reperfusion (I/R) injury. We evaluated inhibition of the classical pathway of complement using C1-inhibitor (C1-inh) in a model of 70% partial liver I/R injury in male Wistar rats ( n = = = = 35). C1-inh was administered at 100, 200 or 400 IU/kg bodyweight, 5 min before 60 min ischaemia (pre-I) or 5 min before 24 h reperfusion (end-I). One hundred IU/kg bodyweight significantly reduced the increase of plasma levels of activated C4 as compared to albumin-treated control rats and attenuated the increase of alanine aminotransferase (ALT). These effects were not better with higher doses of C1-inh. Administration of C1-inh pre-I resulted in lower ALT levels and higher bile secretion after 24 h of reperfusion than administration at end-I. Immunohistochemical assessment indicated that activated C3, the membrane attack complex C5b9 and C-reactive protein (CRP) colocalized in hepatocytes within midzonal areas, suggesting CRP is a mediator of I/R-induced, classical complement activation in rats. Pre-ischaemic administration of C1-inh is an effective pharmacological intervention to protect against liver I/R injury.

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“…14,15 In addition, hypothermia affects hemodynamic stability and also reduces I/R-induced injury. 16 Therefore, we established a highly standardized murine model of partial hepatic I/R by blood flow occlusion in which special attention was paid to anesthetic management, hemodynamic stability, and body temperature. Before studying the effects of hepatic I/R on the outgrowth of micrometastases, the model was validated by measuring parameters of oxidative stress and hepatocellular damage.…”

mentioning

confidence: 99%

Ischemia/reperfusion accelerates the outgrowth of hepatic micrometastases in a highly standardized murine model

Bilt¹,

Kranenburg²,

Nijkamp³

et al. 2005

Hepatology

156

131

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Mortality in colorectal cancer is associated with the development of liver metastases. Surgical removal of these tumors is the only hope for cure, but recurrence is common. During liver surgery, ischemia/reperfusion (I/R) often occurs as a result of hemorrhage or vascular clamping. Although the adverse effects of I/R on postoperative liver function are well documented, the influence of I/R on the outgrowth of residual micrometastases is unknown. We used a highly standardized mouse model of partial hepatic I/R to study the effects of I/R on the outgrowth of preestablished colorectal micrometastases. Five days following intrasplenic injection of C26 colon carcinoma cells, the vascular structures of the left lobe were clamped for 45 minutes under hemodynamically stable conditions. Tissue glutathione, plasma liver enzymes, hepatocellular necrosis, and tumor growth were assessed over time. I/R caused oxidative stress and early liver tissue damage. The outgrowth of micrometastases in occluded liver lobes was accelerated five-to sixfold compared with nonoccluded lobes and was associated with areas of necrotic liver tissue surrounded by inflammatory cells and apoptotic hepatocytes. Accelerated tumor growth and tissue necrosis were completely prevented by occluding blood flow intermittently. In contrast, ischemic preconditioning or treatment with the antioxidants ␣-tocopherol or ascorbic acid failed to protect against late tissue necrosis and tumor growth, although early hepatocellular damage was largely prevented by these methods. In conclusion, I/R is a strong stimulus of recurrent intrahepatic tumor growth. Measures to prevent I/R-induced late tissue necrosis cross-protect against this phenomenon. (HEPATOLOGY 2005;42:165-175.)

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Pronounced effect of minor changes in body temperature on ischemia and reperfusion injury in rat liver

Cited by 29 publications

References 14 publications

The isolated perfused rat liver: standardization of a time-honoured model

The isolated perfused rat liver: standardization of a time-honoured model

Inhibition of classical complement activation attenuates liver ischaemia and reperfusion injury in a rat model

Ischemia/reperfusion accelerates the outgrowth of hepatic micrometastases in a highly standardized murine model

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