Surgical revascularization is the gold standard in most cases of complex coronary artery disease. For coronary artery bypass grafting, autologous grafts are state-of-the-art due to their long-term patency. A non-negligible amount of patients lack suitable bypass material as a result of concomitant diseases or previous interventions. As a promising alternative, tissue-engineered vascular grafts made of biomaterials such as bacterial cellulose (BC) are gaining more and more attention. However, the production of small-diameter grafts (inner diameter < 6 mm) of application-oriented length (> 5 cm) and their in vivo long-term patency remain challenging. In this study, grafts of 20 cm in length with an inner diameter of 3 mm were generated in a custom-made bioreactor. To potentially improve graft compliance and, therefore in vivo patency, BC was combined with an embedded cobalt–chromium mesh. The grafts were designed for in vivo endothelialization and specific surgical properties and implanted as an aortocoronary bypass in a left anterior descending occluded pig model (n = 8). Coronary angiography showed complete patency postoperatively at 4 weeks. Following 4 weeks in vivo, the grafts were explanted revealing a three-layered wall structure. Grafts were colonized by smooth muscle cells and a luminal layer of endothelial cells with early formation of vasa privata indicating functional remodeling. These encouraging findings in a large animal model reveal the great potential of small-diameter BC grafts for coronary and peripheral bypass grafting.

Ventilator-induced lung injury (VILI) is a major contributor to morbidity and mortality in critically ill patients. Mechanical damage to the lungs is potentially aggravated by the activation of the renin-angiotensin system (RAS). This article describes RAS activation profiles in VILI and discusses the effects of angiotensin (Ang) 1-7 supplementation or angiotensin-converting enzyme (ACE) inhibition with captopril as protective strategies.

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OBJECTIVES: This study investigated whether the novel St. Thomas’ Hospital polarizing cardioplegic solution (STH-POL) with esmolol/adenosine/magnesium offers improved myocardial protection by reducing demands for high-energy phosphates during cardiac arrest compared to the depolarizing St. Thomas’ Hospital cardioplegic solution No 2 (STH-2). METHODS: Twenty anaesthetised pigs on tepid cardiopulmonary bypass were randomized to cardiac arrest for 60 min with antegrade freshly mixed, repeated, cold, oxygenated STH-POL or STH-2 blood cardioplegia every 20 min. Haemodynamic variables were continuously recorded. Left ventricular biopsies, snap-frozen in liquid nitrogen or fixed in glutaraldehyde, were obtained at Baseline, 58 min after cross-clamp and 20 and 180 min after weaning from bypass. Adenine nucleotides were evaluated by high-performance liquid chromatography, myocardial ultrastructure with morphometry. RESULTS: With STH-POL myocardial creatine phosphate was increased compared to STH-2 at 58 min of cross-clamp [59.9 ± 6.4 (SEM) vs 44.5 ± 7.4 nmol/mg protein; P < 0.025], and at 20 min after reperfusion (61.0 ± 6.7 vs 49.0 ± 5.5 nmol/mg protein; P < 0.05), ATP levels were increased at 20 min of reperfusion with STH-POL (35.4 ± 1.1 vs 32.4 ± 1.2 nmol/mg protein; P < 0.05). Mitochondrial surface-to-volume ratio was decreased with polarizing compared to depolarizing cardioplegia 20 min after reperfusion (6.74 ± 0.14 vs 7.46 ± 0.13 µm2/µm3; P = 0.047). None of these differences were present at 180 min of reperfusion. From 150 min of reperfusion and onwards, cardiac index was increased with STH-POL; 4.8 ± 0.2 compared to 4.0 ± 0.2 l/min/m2 (P = 0.011) for STH-2 at 180 min. CONCLUSIONS: Polarizing STH-POL cardioplegia improved energy status compared to standard STH-2 depolarizing blood cardioplegia during cardioplegic arrest and early after reperfusion.