Reduction of Ischemia/Reperfusion Injury With Bendavia, a Mitochondria-Targeting Cytoprotective Peptide

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First Millimeter-Wave Animal In Vivo Measurements of L-Glucose and D-Glucose: Further Steps Towards a Non-Invasive Glucometer

The authors present the first in vivo measurements of L-Glucose and D-Glucose concentrations using millimeter waves. Employing direct injection of solutions into the rat jugular vein, we have been able to correlate immediate changes in blood glucose readings with transmission loss through the ears of anesthetized rats at Ka band (27–40 GHz). The sensed changing D-glucose levels are shown to track blood values, but with a delay of approximately 10–15 minutes, which may be due to cellular glucose uptake. Surprisingly, levels of L-glucose, the non-bioactive enantiomer (L-isomer) are also tracked by millimeter-wave transmission through the ear, suggesting that we are looking at the direct chemical presence of glucose or products of its breakdown in the tissue, rather than metabolism. Both isomers of glucose are gradually removed from the bloodstream after injection of insulin, consistent with the observed changes in the millimeter-wave absorption. These results represent a major step towards the realization of a non-invasive glucose monitor based on millimeter-wave transceivers

Neointimal hyperplasia on a cell-seeded polytetrafluoroethylene graft is promoted by transfer of tissue plasminogen activator gene and inhibited by transfer of nitric oxide synthase gene

The objective of this study was to examine the effect of tissue plasminogen activator (tPA) and endothelial nitric oxide synthase (eNOS) on thrombosis and neointimal hyperplasia on a polytetrafluoroethylene (PTFE) graft seeded with smooth muscle cells (SMCs). SMCs retrovirally transduced with tPA and eNOS genes were seeded on PTFE grafts and then implanted into the infrarenal rabbit aorta. Thrombosis and neointimal hyperplasia on the grafts were examined after 30 and 100 days of implantation. At 30 days of implantation, thrombus was observed on the luminal surface of both unseeded and SMC seeded control grafts, whereas grafts seeded with SMCs secreting tPA were nearly free of thrombus. At 100 days, the neointima on grafts seeded with tPA transduced SMCs was significantly thicker (925 ± 150 μm, n = 5) than neointima on the other grafts (range, 132 to 374 μm; P < .001). Neointima thickness on grafts seeded with eNOS transduced SMCs (154 ± 27 μm) was similar to that of unseeded grafts (132 ± 16 μm, P > .05); both were thinner than those on grafts seeded with SMCs transduced with only lacZ gene (287 ± 35 μm). The ratio of seeded cells in the neointima was significantly higher on SMC/tPA grafts (46% ± 8%) than SMC/NOS grafts (21% ± 6%, P < .05), indicating tPA transduced cells proliferated more than eNOS transduced cells. Engineered tPA expression in seeded SMCs causes significantly more neointimal hyperplasia, despite the favorable inhibition of luminal thrombus. eNOS expression in the seeded cells inhibits neointimal hyperplasia. Vascular prosthetic grafts are vulnerable to thrombosis and restenosis resulting in high incidence of limb loss when autogenous vein is not available. Modification of vascular prosthetic grafts to more closely mimic natural conditions may protect against clot formation and may have an immediate and prolonged effect on vascular surgical results. This study examined the patency of a prosthetic vascular graft by seeding the grafts with genetically engineered cells to prevent thrombosis and restenosis

Acute administration of nicotine induces transient elevation of blood pressure and increases myocardial infarct size in rats.

AimsWe investigated the acute effects of nicotine on myocardial infarct size, no reflow, hemodynamics and cardiac function in an acute myocardial ischemia and reperfusion infarction rat model.Main methodsFemale Sprague-Dawley rats (n = 23/group) received an intravenous loading dose of nicotine at 2.0 μg/kg/min or saline control for 30 min before starting coronary artery occlusion, then followed by a maintenance dose 0.35 μg/kg/min of nicotine to the end of 30 min occlusion and 3 h reperfusion.Key findingsAt baseline, there was no difference in systolic blood pressure (BP in mmHg) (nicotine, 69.0 ± 2.7; control, 69.3 ± 4.4; p = NS) or diastolic BP (nicotine, 45.7 ± 3.2; control, 48.2 ± 4.2; p = NS) between groups. Nicotine administration initially increased systolic BP (nicotine, 97.0 ± 8.6; control, 69.2 ± 3.3, p &lt; 0.0001) and diastolic BP (nicotine, 65.6 ± 6.4; control, 47.4 ± 3.1, p = 0.0003) at 10 min after starting injection of the loading dose; BP dropped to control levels in both groups at 30 min. During occlusion and reperfusion, the BP and heart rate were not altered by nicotine. Nicotine significantly increased myocardial infarct size as a percentage of the ischemic risk zone compared to the controls (nicotine, 54.9 ± 1.9; control, 48.6 ± 2.7, p &lt; 0.05), but nicotine did not affect the no-reflow size and heart function.SignificanceWhile acute nicotine only transiently elevated blood pressure, it did not affect hemodynamic parameters during coronary artery occlusion. Nicotine increased myocardial infarct size, suggesting that the increase in infarct size was not simply due to an increase in oxygen demand due to altered afterload, heart rate, or contractility, but may have been due to a more direct effect on the myocardium