Isolated lobar arterio-portal liver perfusion in the experiment

The study is devoted to topographic, anatomical and experimental justification of isolated lobar arterio-portal perfusion, the material for which served as liver preparations (n=28), explanted from the corpses of adult men and women who died at the age of 48 to 78 years as a result of injuries and diseases not associated with liver lesions and its major vessels, the data of radiographs of liver preparations (n=10), injected with x-ray contrast solutions, as well as selective angiograms (n=24) obtained with celiac topographic and anatomical features of the main vessels of the left lobe of the liver in relation to the problems of its isolated lobar arterio-portal perfusion are clarified. Based on the analysis of selective angiograms, obtained by clickography shown the absence of functioning vascular anastomoses between lobes of the liver. While further studies conducted on liver preparations (n=8), an experimental model of isolated lobar arterio-portal perfusion of the left lobe of the liver was developed. The approbation of this model convincingly confirmed the results obtained during anatomical studies. The peculiarity of the arterial and portal blood flow of the left surgical lobe of the liver is its isolation from the vascular arterio-portal basins of the right lobe of the liver. The experiment shows the possibility of isolated perfusion of the left lobe of the liver. The developed experimental model demonstrated the validity of the idea of isolated lobar arterio-portal perfusion of the left lobe of the liver and created favorable conditions for further improvement of the concept of retrograde isolated liver perfusion and the possibility of improving its technical aspects for further clinical testing in the complex treatment of patients with multiple bilobar metastatic liver damage.

Role of estrogen receptor subtypes in estrogen-induced organ-specific vasorelaxation after trauma-hemorrhage

Although endothelin-1 (ET-1)-induced organ hypoperfusion after trauma-hemorrhage is improved by estrogen administration, it remains unclear whether estrogen receptor (ER) subtypes play any role in the attenuation of ET-1-induced vasoconstriction in any specific organ bed. To investigate this, isolated perfusion experiments in the heart, liver, small intestine, kidney, and lung were carried out in sham, at the time of maximum bleedout (MBO; i.e., 5-cm midline incision, with removal of 60% of circulating blood volume over 45 min to maintain a mean blood pressure of 40 mmHg), and 2 h after trauma-hemorrhage and resuscitation (T-H/R). Organ-specific ET-1-induced vasoconstriction was evaluated, and the effects of 17β-estradiol (E2) and ER-specific agonists propylpyrazole triol (PPT; ERα agonist) and diarylpropionitrile (DPN; ERβ agonist) were determined. ET-1 induced the greatest vasoconstriction in sham animals, with the strongest response in the kidneys, followed by the small intestine and liver. ET-1-induced responses were weakest in the heart and lungs. ET-1-induced vasoconstriction was evident at the time of MBO but was significantly decreased at 2 h after T-H/R. ERβ plays an important role in cardiac performance, as evidenced by improved heart performance (+dP/d t) in the presence of DPN. DPN also induced a greater effect than PPT in the reduction of ET-1-induced vasoconstriction in the kidneys and lungs. In contrast, PPT attenuated ET-1-induced vasoconstriction in the liver, whereas both DPN and PPT were equally effective in the small intestine. The increased +dP/d t values induced by E2, DPN, or PPT were evident at the time of MBO but were significantly decreased at 2 h after T-H/R. These data indicate that the effects of ET-1 on vasoconstriction and the role of ER subtypes in estrogen-induced vasorelaxation are organ specific and temporally specific after trauma-hemorrhage.