Disease relevance of Warm Ischemia

• Oxidative stress in fatty livers of obese Zucker rats: rapid amelioration and improved tolerance to warm ischemia with tocopherol [1].
• For investigating whether HO-1 and VEGF play a role in the adaptive response to ischemia-reperfusion injury after renal transplantation, kidney biopsies were analyzed from living (n = 45) and cadaveric (n = 16) donors, obtained at three time points: at the end of cold storage T(-1), after warm ischemia T(0), and after reperfusion T(+1) [2].
• Pretreatment with NAC helps maintain hepatic glutathione during warm ischemia; given after ischemia, NAC is effective in replenishing depleted glutathione stores [3].
• Cyclosporine A sensitizes the kidney to tubulointerstitial fibrosis induced by renal warm ischemia [4].
• CONCLUSIONS: These results demonstrated that chemical preconditioning by 3-nitropropionate administration immediately before cardiac arrest suppressed succinate-related oxidation during postmortem warm ischemia and reduced ischemia-reperfusion injury in cardiac arrested rat lungs [5].

Psychiatry related information on Warm Ischemia

• A 30-min period of warm ischemia did not impair the endocrine function of the pancreatic grafts, which was assessed by measuring the blood glucose levels and glucose decay constants (K), and a 60-min period of warm ischemia was considered to be the critical period for reversible tissue damage [6].

High impact information on Warm Ischemia

• Data from quantitative real-time RT-PCR analysis revealed that B7-1 and B7-2 mRNA levels were elevated in hepatic lobes after warm ischemia/reperfusion (5.13- and 52.9-fold increase, respectively), whereas ICAM-1 mRNA expression was rather constitutive but further enhanced by warm ischemia/reperfusion (4.24-fold increase) [7].
• Also, survival in treated Ob rats following a lethal 90 minutes of partial in vivo warm ischemia was examined [1].
• We have found that the DNA binding activity of AP-1 was dramatically increased following warm ischemia at 1 to 3 hours postreperfusion [8].
• Thus, both furosemide and bumetanide showed a clear benificial effect on rat livers subjected to warm ischemia [9].
• Also, after 120 minutes of warm ischemia, LDH and aspartate aminotransferase release were significantly decreased and bile flow increased by pretreatment with bumetanide [9].

Chemical compound and disease context of Warm Ischemia

• Confounding factors of renal function such as age, body weight, cold and warm ischemic time, cytomegaly virus status, methylprednisone and cyclosporine dosages, cyclosporine concentrations, as well as concomitant antihypertensive medication did not differ among the three groups [10].
• The 60 kidneys were selected from 70 non-heartbeating donors based on age younger than 50 years, warm ischemia less than 30 minutes, creatinine less than 200 micromol./l., and no hypertension or major histological lesions [11].
• For clinical use, however, it seems safer to commence with hypothermia after 60 min of inosine-protected warm ischemia [12].
• We investigated the effect of warm ischemia and reperfusion on sinusoidal microcirculation in rats with fatty livers from a choline-deficient diet [13].
• Furosemide infusion prior to ischemia is thought to protect the kidney from injury induced by 60 min of warm ischemia [14].

Biological context of Warm Ischemia

• OBJECTIVE: To study the effect of warm ischemia and reperfusion (I/R) on local perfusion and leukocyte-vessel wall interactions in vivo in all small bowel layers, and to quantify small bowel tissue injury histologically and by measuring intestinal fatty acid binding protein (I-FABP) release from the enterocytes [15].
• We utilized the measurement of exhaled breath ethane, a metabolic product unique to oxidant-mediated lipid peroxidation, as a noninvasive indicator of this process in swine liver subjected to warm ischemia/reperfusion [16].
• This study aimed to clarify the difference in the effects of sodium acetate and sodium lactate administration on hepatic energy metabolism during hepatic warm ischemia and reperfusion [17].
• It appeared that glucose transport, the pentose phosphate pathway, and gluconeogenesis were maintained during cold preservation and warm ischemia [18].
• Cathepsin B inactivation attenuates hepatocyte apoptosis and liver damage in steatotic livers after cold ischemia-warm reperfusion injury [19].

Anatomical context of Warm Ischemia

• The goal of the present study was to assess the renoprotective potential and safety of hepatocyte growth factor (HGF) gene transfer using a porcine kidney transplant warm ischemia injury model [20].
• Twenty-four-hour preservation of the pancreas graft subjected to 60-min warm ischemia was successful by the two-layer (EC with adenosine/PFC) method (4/5, 80%), but neither simple cold storage in EC (0/5, 0%), nor EC with adenosine (1/5, 20%), nor the two-layer (EC/PFC) method (0/3, 0%) was successful [21].
• As compared with vehicle + I/R group, administration of melatonin significantly enhanced arteriole diameter, improved capillary perfusion, and attenuated endothelial dysfunction in the microcirculation of skeletal muscle after 4 hr warm ischemia [22].
• We prefer the double vena cava technique for reconstructing middle hepatic vein tributaries with thick, short hepatic veins because the technique can reduce the warm ischemic time of the graft and make a wide anastomosis [23].
• Resveratrol protects against cold ischemia-warm reoxygenation-induced damages to mitochondria and cells in rat liver [24].

Associations of Warm Ischemia with chemical compounds

• Accordingly, the mortality index posttransplantation = 0.0084 donor age + 0.019 recipient age + 0.816 log creatinine + 0.0044 warm ischemia (in minutes) + 0.659 (if second transplant) + 0.10 log bilirubin + 0.0087 PT + 0.01 cold ischemia (in hours) [25].
• This study evaluated in the rat (1) the effect of CsA and CsG on blood flow and the function of the kidney subjected to 60 min of warm ischemia and (2) the protective effect of the calcium antagonist verapamil (VP) [26].
• Simultaneously significant factors for graft failure included log creatinine, log alanine transaminase, log aspartate transaminase, UNOS status, donor gender, and warm ischemia time [27].
• The present study evaluated and compared the effects of SRI 63-441, a potent platelet activating factor antagonist, superoxide dismutase (SOD), an oxygen free radical scavenger, and ibuprofen, a cyclooxygenase inhibitor on hepatic function after 90 minutes of warm ischemia [28].
• Improved renal function using adenosine triphosphate-magnesium chloride in preservation of canine kidneys subjected to warm ischemia [29].

Gene context of Warm Ischemia

• In this report, we first evaluated the expression of VEGF in a mouse model of liver warm ischemia [30].
• CYP3A, known to account for an average 30% of total P450 content in the human liver was the most susceptible to the warm ischemia [31].
• Using a 90-min lobar warm ischemia model, wild type (WT), TLR4 KO/mutant and TLR2 KO mice were first assessed for the severity of hepatocellular damage at 6 h postreperfusion [32].
• To test our hypothesis, we induced partial warm ischemia to the livers of Nramp1(+/+) and Nramp1(-/-) mice for 45 min of by clamping the hilum of the median and left lateral lobes, followed by 30 or 60 min of reperfusion [33].
• Impact of warm ischemic time on microsomal P450 isoforms in a porcine model of therapeutic liver resection [31].

Analytical, diagnostic and therapeutic context of Warm Ischemia

• RESULTS: Control livers (no warm ischemia) and livers exposed to 15 minutes of warm ischemia function normally after transplantation, whereas all livers submitted to 60 minutes of warm ischemia display primary nonfunction and cause recipient death [34].
• Hepatic preconditioning after prolonged warm ischemia by means of S-adenosyl-L-methionine administration in pig liver transplantation from non-heart-beating donors [35].
• The relation between adenine nucleotide liver concentrations and the viability of liver allografts after cold preservation and warm ischemia was studied [36].
• The effects of treatment with chlorpromazine (4 mg/kg) and phenoxybenzamine (1 and 5 mg/kg) on renal function and morphology after warm ischemia and contralateral nephrectomy were studied [37].
• Serum creatinine levels of the surviving rats after 120 min of warm ischemia was 9.98 +/- 0.19 mg/100 ml in the control group and 5.84 +/- 0.95 and 7.27 +/- 1.62 mg/100 ml, respectively, in alpha-tocopherol and CoQ10 administered group, when determined 2 days after the operation [38].

References