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Tissue engineering holds the promise of providing new solutions for heart transplant shortages and pediatric heart transplantation. The aim of this study was to evaluate the ability of a peritoneal-generated, tissue-engineered cardiac patch to replace damaged myocardium in a heterotopic heart transplant model. Fetal cardiac cells (1 × 106/scaffold) from syngeneic Lewis rats were seeded into highly porous alginate scaffolds. The cell constructs were cultured in vitro for 4 days and then they were implanted into the rat peritoneal cavity for 1 week. During this time the peritoneal-implanted patches were vascularized and populated with myofibroblasts. They were harvested and their performance in an infrarenal heterotopic abdominal heart transplantation model was examined ( n = 15). After transplantation and before reperfusion of the donor heart, a 5-mm left ( n = 6) or right ( n = 9) ventriculotomy was performed and the patch was sutured onto the donor heart to repair the defect. Echocardiographical studies carried out 1–2 weeks after transplantation showed normal LV function in seven of the eight hearts studied. After 1 month, visual examination of the grafted patch revealed no aneurysmal dilatation. Microscopic examination revealed, in most of the cardiac patches, a complete disappearance of the scaffold and its replacement by a consistent tissue composed of myofibroblasts embedded in collagen bundles. The cardiac patch was enriched with a relatively large number of infiltrating blood vessels. In conclusion, cardiac patches generated in the peritoneum were developed into consistent tissue patches with properties to seal and correct myocardial defects. Our study also offers a viable rat model for screening and evaluating new concepts in cardiac reconstruction and engineering.

We present a pilot study on the long term effects of irreversible electroporation (IRE) on a large blood vessel. The study was motivated by the anticipated use of IRE for treatment of cancer tumors abutting large blood vessels. A sequence of 10 direct current IRE pulses of 3800 V/cm, 100μs each, at a frequency of 10 pulses per second, were applied directly to the carotid artery in six rats. Measuring tissue conductivity during the procedure showed, as predicted, an increase in conductivity during the application of the pulse, which suggests that this measurement can be used to control the application of IRE. All the animals survived the procedure and showed no side effects. Histology performed 28 days after the procedure showed that the connective matrix of the blood vessels remained intact and the number of vascular smooth muscle cells (VSMC) in the arterial wall decreased with no evidence of aneurysm, thrombus formation or necrosis. Average VSMC density was significantly lower following IRE ablation compared with control (24 ± 11 vs. 139 ± 14, P

Captopril, a sulfhydryl-containing angiotensin-converting enzyme inhibitor, has been suggested as possessing antiischemic and antiinflammatory properties. To test the hypothesis that captopril may prevent neutrophil-induced myocardial injury during acute myocardial infarction (AMI), the authors subjected rats to coronary occlusion for thirty minutes and reperfusion for twenty-four hours (MI) or to sham operation (sham MI). Oral captopril (100 mg/kg) or vehicle was administered thirty minutes before coronary occlusion. The effect of captopril on mean arterial blood pressure was assessed in separate group of animals (n=8). Infarct size and neutrophil accumulation in myocardium were determined by measuring creatine phosphokinase depletion and myeloperoxidase (MPO) activity, respectively, in the left ventricular free wall (LVFW). Animals treated with 100 mg/kg of captopril exhibited significant reduction in mean arterial blood pressure compared with vehicle-treated animals (P < 0.01). Compared with vehicle-treated animals, administra tion of 100 mg/kg of captopril to MI animals attenuated neither twenty-four-hour (continued on next page) mortality (56% vs 52%, respectively), nor infarct size (36 ± 7% vs 34% ± 7% respec tively), nor MPO activity (1.0 ±0.17 vs 1.26 ±0.19). Thus, in the present experiment captopril did not reduce neutrophil-induced myocar dial damage following coronary occlusion and reperfusion. These findings may be partly explained by the negative effect of captopril on arterial blood pressure during AMI.