The significance of the intact pericardium for cardiac performance was examined in 18 open-chest dogs. Myocardial chord lengths (MCL) in the right and left ventricle were measured simultaneously by ultrasonic crystals implanted in the myocardium of the anterior walls. In 14 dogs, the ultrasonic elements were inserted into the myocardium through needle openings in the pericardium (intact pericardium). In four other dogs, the elements were inserted through 6-to 7-cm-long incisions in the pericardium which were sutured afterward (sutured pericardium). Stroke volume was calculated in each of seven dogs with an intact pericardium from electromagnetic measurement of flow in the superior and inferior venae cavae. After blood volume expansion to about 13 mm Hg, the pericardium was opened and the end-diastolic pressure-MCL relationships and stroke volumes before and after pericardiotomy were compared. By opening the intact pericardium, the right and left ventricular enddiastolic MCL rose by 2.7 ± 0.7% and by 3.7 ± 1.1%, respectively, and stroke volume increased by 13 ± 4%. However, by reopening the sutured pericardium, the increases in both right and left ventricular end-diastolic MCL were clearly greater (12.2 ± 5.6% and 9.9 ± 2.9%, respectively), and the restrictive effect of the pericardium was therefore overestimated when the pericardium was not left intact. Thus, after a moderate blood volume expansion, the intact pericardium exerts a certain, although moderate restrictive effect on cardiac performance.
The purpose of the present work was to study the tissue reaction to polypropylene mesh (Marlex®) implanted in three different layers of the abdominal wall, comparable to common clinical practices. The reaction to mesh was compared in terms of tissue oedema, blood flow, and histological appearance in rats. When mesh was placed between muscle layers, blood flow in the abdominal wall was high during the first 4 days after implantation but similar to flow in nonoperated rats 14 and 140 days after implantation. When mesh was placed under skin or on the peritoneum, there was no hyperaemia early after implantation, and flow rate was clearly lower than in non-operated controls 140 days after implantation. The operative procedure produced increased tissue water content, declining from the 1 st to the 14th day after operation. Mesh induced additional oedema in adjacent muscle tissue irrespective of localization of the implant (p < 0.01, vs. sham). Except when separated by peritoneum, mesh caused hyperaemia in muscle tissue in direct contact with mesh the 1st and the 4th day after implantation. After 14 and 140 days no mesh-induced hyperaemia was present. The inflammatory response to mesh was similar in the peritoneum and between muscles, less pronounced in the subcutis. It was characterized by the accumulation of macrophages and the formation of inflammatory granulation tissue in the subacute phase, later followed by the formation of fibrous tissue around mesh fibres. This study suggests that mesh implants should be placed in apposition to muscles in order to obtain well-vascularized healing.
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