Glutaraldehyde and 2,3-butanediol treatment of bovine pericardium for aortic valve bioprosthesis in sheep: a preliminary study.

BACKGROUND: Bovine pericardium can be used for cardiovascular repair surgeries, but challenges involving biocompatibility and durability remain. This study aimed to carry out pre-clinical testing of aortic valve replacement using an aortic valve prosthesis made of bovine pericardium modified with glutaraldehyde (GA) and 2,3-butanediol (BD). METHODS: The mechanical, plasma protein adsorption, platelet adhesion, collagenase digestion, and ninhydrin properties of the material (control vs. GA vs. GA + BD) were tested. All 3 tissues were implanted in rats and observed after 8 weeks under microscopy with alizarin red staining for calcification. Aortic valves made from the fully-treated material were implanted in sheep. A commercial bioprosthesis was used as control. Effectiveness and safety indicators were observed at 180 days after implantation. RESULTS: Compared with the control group, the GA + BD material showed higher elongation at breaking and tensile load (both P<0.05), lower plasma protein adsorption, lower platelet adhesion, lower collagenase digestion, lower ninhydrin value, and higher cross-linking (all P<0.05). After implantation in rat models, the GA + BD material showed little or no dissolution; there was no obvious calcification; and it was surrounded by a small amount of fibrosis, with peripheral capillary proliferation. After implantation in sheep models, the aortic valve leaflets of the experimental animals freely opened and closed, their surface was smooth, and no abnormal echo was observed. The echocardiographic results and hemodynamic were comparable between the two groups. All safety parameters were normal. CONCLUSIONS: Modification of bovine pericardium with GA and BD results in a biomaterial with favorable properties for use as an aortic valve prosthesis.

Antegrade cerebral perfusion during deep hypothermia circulatory arrest attenuates the apoptosis of neurons in porcine hippocampus.

BACKGROUND: Cerebral damage is a major problem after reconstructive surgery of the aortic arch and the descending aorta. Current protective strategies, including deep hypothermia and antegrade cerebral perfusion (ACP), are used to prolong the tolerated duration of circulatory arrest. The aim of the study was to observe the influence of deep hypothermic circulatory arrest (DHCA) and ACP on neuronal apoptosis in the hippocampus. To further elucidate the mechanisms of neurologic injury and protection, we assessed the expression of the antiapoptotic protein Bcl-2 and the proapoptotic protein Bax. METHODS: We randomly divided 18 pigs into 3 groups: The control group (n = 6) received normal-temperature cardiopulmonary bypass (CPB), the DHCA group (core temperature, 18 degrees C; n = 6) received DHCA for 90 minutes, and the third group (DHCA + ACP) (core temperature, 18 degrees C; ACP, flow rate of 30 mL/kg per minute at a pressure of 15-25 mm Hg; n = 6) received DHCA for 90 minutes. Hippocampal tissue was sampled 2 hours after CPB was finished. Bcl-2 and Bax expression was examined by immunohistochemistry. Morphologic changes in hippocampal tissue were measured with transmission electron microscopy. RESULTS: Bax protein levels were significantly higher in the DHCA group than in the other 2 groups (P < .05), whereas Bcl-2 protein levels were significantly higher in the DHCA + ACP group than in the other 2 groups (P < .05). Obvious neuronal apoptosis was observed in the DHCA group but not in the controls, and few apoptotic neurons were seen in the DHCA + ACP group. CONCLUSIONS: DHCA can induce neuronal apoptosis in the hippocampus. ACP during the DHCA period protects cerebral tissue by suppressing apoptosis through decreasing Bax expression and increasing Bcl-2 expression.