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G P DeSola

Publications and source records attributed to G P DeSola.

2 recordsLinked to original sources

Blood clearance of 99mTc-trimethyl-Br-IDA discriminates between different degrees of severe liver ischaemia--reperfusion injury in the rat.

The kinetics of 99mTc-Trimethyl-Br-IDA blood clearance was analysed in the rat 24 h after warm ischaemia and reperfusion of the liver. There were changes in the elimination of 99mTc-Trimethyl-Br-IDA depending on the length of the ischaemic period and the dose given. Statistically significant differences were found between the various periods of ischaemia when higher doses of the radionuclide were utilised. At lower doses, the clearance was not capable to discriminate between control rats and rats submitted to 45 min of ischaemia, but it did discriminate more severe degrees of ischaemic liver injury. Instead, galactose elimination capacity discriminated between ischaemic and control rats, but not between 45 and 90 min or between 90 and 120 min of ischaemia. Alanine aminotransferase was able to discriminate between control and ischaemic rats and between 45 and 90 min of ischaemia, but not between 90 and 120 min of ischaemia. The response of 99mTc-Trimethyl-Br-IDA clearance under extreme conditions of ischaemia and reperfusion is consistent and opens a possible window for the application of this test in the quantification of liver function in severely damaged livers and in decision making and prognosis in liver disease.

Alanine Transaminase↗

Regulation of the complement cascade by soluble complement receptor type 1. Protective effect in experimental liver ischemia and reperfusion.

The complement cascade was inactivated in a model of rat liver ischemia with the purpose of studying the role of complement in tissue injury after ischemia and reperfusion. Soluble human complement receptor type 1 (sCR1) was administered either in a single dose of 25 mg/kg or in 2 doses of 50 mg/kg i.v. over 24 hr after vascular occlusion. Sham-operated rats, nontreated rats submitted to liver ischemia, and rats pretreated with cobra venom factor and submitted to liver ischemia were used as controls. This experiment consists of the temporary interruption of arterial and portal blood flow to the left lateral and medial lobes of the liver for 45 min, followed by a 24-hr period of follow-up after reperfusion. Liver blood flow and hemoglobin saturation were recorded for 1 hr after declamping, with statistically significant differences between the experimental groups and the untreated control group, which received liver ischemia (P < 0.001). At 24 hr, galactose elimination was assayed as a liver function test; it was significantly better in the sCR1-treated rats when compared with control rats submitted to ischemia (P < 0.01). Alanine aminotransferase levels were also significantly lower in the sCR1-treated rats at 6 and 24 hr (P < 0.05). Complement activity was reduced to 25% and 12.5% of normal rats with the respective doses of sCR1. Immunoperoxidase stainings for C3 and C9 were performed on liver sections; they showed endothelial deposits of C3 and C9 in the control group subjected to ischemia. Few C3 deposits were present in the sCR1 (25 mg/kg)-treated rats, but not in the cobra venom factor or sCR1 (50 mg/kg) groups. These results confirm that complement is inactivated by sCR1 with amelioration of reperfusion injury in the rat liver.

Animals↗