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.
Highlights
In liver lesions and transplants, temporary blockage of hepatic blood flow is sometimes necessary to facilitate surgical maneuvers [1,2]
The animals were randomly distributed to four experimental groups: Control group (C, n = 3), animals with no clamped hepatic pedicle; Ischemia group 10 (I10, n = 12) hepatic pedicle subjected to 10 minutes clamping; Ischemia group 20 (I20, n = 12) hepatic pedicle subjected to 20 minutes clamping, and Ischemia group 30 (I30, n = 12) hepatic pedicle subjected to 30 minutes clamping
No significant differences were found in the mean values of vascular congestion, necrosis, and pyknotic nuclei at different times of ischemia
Summary
In liver lesions and transplants, temporary blockage of hepatic blood flow is sometimes necessary to facilitate surgical maneuvers [1,2]. Since 1908, Pringle proposed full clamping of the hepatic pedicle (hepatic artery, portal vein, and the common bile duct) to restrain hepatic hemorrhages [3] This procedure results in splenic congestion and poor blood perfusion in the liver, stomach, small intestine, anterior part of the large intestine, pancreas, and spleen [4,5,6,7,8]. The ischemic event begins with an inflammatory response perpetuated after blood reperfusion due to production of reactive oxygen species (ROS) This phenomenon is known as ischemia-reperfusion injury and involves complex pathophysiological mechanisms and metabolic pathways, which are not well understood; the end result is organ failure and patient death [8,9,10]
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