Evaluation of potential changes in liver and lung tissue of rats in an ischemia-reperfusion injury model (modified pringle maneuver)

Abstract

In surgical procedures involving the liver, such as transplantation, resection, and trauma, a temporary occlusion of hepatic vessels may be required. This study was designed to analyze the lesions promoted by ischemia and reperfusion injury of the hepatic pedicle, in the liver and lung, using histopathological and immunohistochemical techniques. In total, 39 Wistar rats were divided into four groups: control group (C n = 3) and ischemia groups subjected to 10, 20, and 30 minutes of hepatic pedicle clamping (I10, n = 12; I20, n = 12; I30, n = 12). Each ischemia group was subdivided into four subgroups of reperfusion (R15, n = 3; R30, n = 3; R60, n = 3; R120, n = 3), after 15, 30, 60, and 120 minutes of reperfusion, respectively. Significant differences were observed in the liver parenchyma (P < 0.05) between the values of microvesicles and hydropic degeneration at different times of ischemia and reperfusion. However, the values of vascular congestion, necrosis, and pyknotic nuclei showed no significant differences (P > 0.05). In the lung parenchyma, a significant difference was observed (P < 0.05) between the values of alveolar septal wall thickening and inflammatory infiltration at different times of ischemia and reperfusion. However, there was no significant difference (P < 0.05) between the values of vascular congestion, bronchial epithelial degeneration, interstitial edema, and hemorrhage. The positive immunoreactivity of caspase-3 protein in the liver parenchyma (indication of ongoing apoptosis), showed no significant differences (P > 0.05) at different times of ischemia and reperfusion. In the pulmonary parenchyma, the immunoreactivity was not specific, and was not quantified. This study demonstrated that the longer the duration of ischemia and reperfusion, the greater are the morphological lesions found in the hepatic and pulmonary parenchyma.

Establishment of an experimental model of small intestinal ischemia and reperfusion injuries in New Zealand rabbits

“…There are experimental studies described in literature for comprehension of the pathophysiology and the establishment of therapies for ischemia and reperfusion injuries (Yassin et al 1997, Camargo et al 2003, Chang et al 2005, Ribeiro & Yoshida 2005, Gonzalez et al 2015, Freitas et al 2017. However, when the pilot study of the present project was initiated, we found a discrepancy in results obtained from those described by authors using a similar methodology to the one employed.…”

“…Among the described experimental models, there are studies performed on rats, rabbits, dogs, cats, pigs and horses (Camargo et al 2003, Kostopanagiotou et al 2007, Avgerinos et al 2010, Yurdakan et al 2012, Freitas et al 2017). According to Ribeiro & Yoshida (2005), the most experimentally used test subjects are rodents, represented by about 73% of the studies, mainly for their ease to work with, adequateness to protocols, availability and low cost, as well as their anatomy being similar to humans.…”

“…Experimental studies on I/R injuries can be defined by two dissimilar phases: the ischemic phase, in which there is a vessel occlusion, or occlusion of the feeding vessels, or decreased circulating blood flow, such as in controlled hypovolemic shock; and a phase called reperfusion, characterized by unblocking of the previously occluded vessel, or shock correction, in a way that the tissue perfusion becomes proper again (Carden & Granger 2000, Camargo et al 2003, Ribeiro & Yoshida 2005, Freitas et al 2017).…”

What is the protective effect of metformin on rat ovary against ischemia‐reperfusion injury?

“…Initiator caspases induce and trigger the apoptotic cascade, while effector caspases carry out the cell death program. Caspase‐3 is generally known as a major effector caspase . Malondialdehyde (MDA) is an end‐product of lipid peroxidation, representing a well‐known example of oxidative damage in cell membranes brought about by ROS in the ischemia‐reperfusion period…”

Liver ischemia and reperfusion injury. Pathophysiology and new horizons in preconditioning and therapy

“…However, the maintenance of oxidative stress differs between both types of ischemia. Concerning to metabolism and molecular pathways, warm ischemia is more damaging, because, in hypothermic ischemia, cellular metabolism and ATP consumption are significantly lower [1][2]4 .It is apparently paradoxical that in steatotic livers, the I/R lesion tends to be even worse, depending on the degree of steatosis; the worst results are obtained in the moderate and severe cases of microvesicular steatosis. Thus, in steatosis, worsening of graft and receptor survival is observed in the case of transplants, with the increased histological lesion and hepatic functional derangement 5-6 .The pathophysiology of liver ischemia and reperfusion injury are always evolutionary justifying, as clear rationale, the constant update to discuss new horizons in preconditioning and therapy.…”