Nitroglycerin application and coronary arteriogenesis

Abstract

BackgroundIn the presence of a coronary occlusion, pre-existing small collateral vessels (arterioles) develop into much larger arteries (biological bypasses) that have the potential to allow a certain level of perfusion distal to the blockage. Termed arteriogenesis, this phenomenon proceeds via a complex combination of events, with nitric oxide (NO) playing an essential role. The aim of this study was to investigate the effects of supplemental administration of NO donors, i.e., short-acting nitroglycerin (NTG) or slow-release pelleted isosorbide dinitrate (ISDN), on collateral development in a repetitive coronary artery occlusion model in rats.MethodsCoronary collateral growth was induced via a repetitive occlusion protocol (ROP) of the left anterior descending coronary artery (LAD) in rats. The primary endpoints were the histological evaluation of rat heart infarct size and ST-segment elevation (ECG-analysis) upon final permanent occlusion of the LAD (experimentally induced myocardial infarction). The effects of NTG or ISDN were also evaluated by administration during 5 days of ROP. We additionally investigated whether concomitant application of NTG can compensate for the anti-arteriogenic effect of acetylsalicylic acid (ASA).ResultsAfter 5 days of ROP, the mean infarct size and degree of ST-elevation were only slightly lower than those of the SHAM group; however, after 10 days of the protocol, the ROP group displayed significantly less severe infarct damage, indicating enhanced arteriogenesis. Intermittent NTG application greatly decreased the ST-elevation and infarct size. The ISDN also had a positive effect on arteriogenesis, but not to the same extent as the NTG. Administration of ASA increased the infarct severity; however, concomitant dosing with NTG somewhat attenuated this effect.ConclusionIntermittent treatment with the short-acting NTG decreased the size of an experimentally induced myocardial infarct by promoting coronary collateral development. These new insights are of great relevance for future clinical strategies for the treatment of occlusive vascular diseases.

Angiotensin‐converting enzyme inhibitors stimulate cerebral arteriogenesis

“…5,6 Blood supply to the brain is primarily redistributed by an extensive collateral circulatory system within the circle of Willis. 7 In cases of vascular occlusion, redistribution of cerebral flow via enlarged collateral arteries restores blood supply to the compromised ischaemic regions, 8 and collateral status is associated with reduced infarct volumes.…”

The Effects of Sildenafil and/or Nitroglycerin on Random-pattern Skin Flaps After Nicotine Application in Rats

“…Topical NTG can induce venous and arterial vessel dilation by smooth muscle relaxation of their walls 14 . Although NTG is bioactivated into NO, there are some suggestions that its vasodilator effect is due to a NO-independent mechanism, which is evidenced in recent experimental and clinical studies showing that NO alone cannot exert all of the vasodilatory effects, in turn suggesting that additional vasoactive mechanisms are involved 48,49 . NTG also can exert its vasodilatory action through the activation of endothelial cells to synthesize prostacyclin.…”

Blood Group Types O and Non-O Are Associated With Coronary Collateral Circulation Development

“…Good CCC is important because it has protective effects on ventricular function and infarct size, and reduces mortality and morbidity of CAD. [12][13][14] Therefore, factors affecting the coronary collateral development are of interest for clinical studies. Coronary collateral circulation formation is affected by many factors, such as severity and duration of coronary artery stenosis, shear stress, endothelial dysfunction, and endogenous mediators.…”