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“Objective: Effects of ventricular restraint on the left ventricle are well documented, but effects on the right ventricle are not. We hypothesized that restraint affects the
right and left ventricles differently.
Methods: We studied acute effects of restraint on left and right ventricular mechanics in healthy sheep (n = 14) with our previously described technique of adjustable and measurable restraint. Transmural pressure, myocardial oxygen consumption indices, diastolic compliance, and end-systolic elastance were assessed at 4 restraint levels for both ventricles. We then studied long-term effects of restraint for 4 months in an ovine model of ischemic dilated cardiomyopathy (n = 6). Heart failure was induced by coronary artery ligation, and polypropylene selleck chemicals mesh was wrapped around the heart to simulate clinical restraint therapy. All subjects were followed
up with serial cardiac magnetic resonance imaging to assess left and right ventricular volumes and function.
Results: Restraint decreased left ventricular transmural pressure (P < .03) and myocardial oxygen consumption indices (P < selleck kinase inhibitor .05) but not left ventricular diastolic compliance (P = .52). Restraint had no effect on right ventricular transmural pressure (P = .82) or myocardial oxygen consumption indices (P = .72) but reduced right ventricular diastolic compliance (P < .01). In long-term studies, restraint led to reverse left ventricular Taselisib mouse remodeling with decreased left ventricular end-diastolic volume (P < .006) but did not affect right ventricular end-diastolic volume (P = .82).
Conclusions: Ventricular restraint affects the left and right ventricles differently. Benefits of restraint for right ventricular function
are unclear. The left ventricle can tolerate more restraint than the right ventricle. With current devices, the right ventricle may limit overall therapeutic efficacy. (J Thorac Cardiovasc Surg 2010;139:1012-8)”
“Amaranth seed proteins have a better balance of essential amino acids than cereals and legumes. In addition, the tryptic hydrolysis of amaranth proteins generates, among other peptides, angiotensin converting enzyme (ACE) inhibitory (ACEi) peptides. ACE converts angiotensin I (Ang I) into Ang II. but is also responsible for the degradation of bradykinin (BK). In contrast to Ang II, BK stimulates vasodilation modulated through endothelial nitric oxide (NO) production. The aim of the present study was to characterize the ACEi activity of amaranth trypsin-digested glutelins (TDGs) and their ability to induce endothelial NO production. An IC(50) value of 200 mu g ml(-1) was measured for TDG inhibition of ACE. TDGs stimulated endothelial NO production in coronary endothelial cells (CEC) by 52% compared to control.