The Sydnonimine C87–3754 Evokes Endothelium-Independent Relaxations and Prevents Endothelium-Dependent Contractions in Blood Vessels of the Dog

Schini, Valérie B.; Bond, Richard A.; Gao, Yuangsheng; Illiano, Stéphane; Junquéro, Didier; Mombouli, Jean-Vivien; Nagao, Toshiyasu; Smart, Frank W.; Vanhoutte, PM

doi:10.1097/00005344-199300221-00004

Cited by 4 publications

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“…135 Intravenous administration of CAS 754 (l 0-1 00 fJ-g/kg) elicited a long-lasting, dose-dependent increase in coronary artery diameter in conscious dogs. After the endothelium was removed by limited angioplasty, the vasodilator effects of acetylcholine and reactive hyperemia were significantly diminished; however, CAS 754 continued to produce effective vasodilation.!"…”

Section: New Developments In Nitrosovasodilator Therapy 197mentioning

confidence: 97%

New Developments in Nitrosovasodilator Therapy

Leopold

Loscalzo

1997

Vasc Med

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Under basal conditions, nitric oxide (NO) modulates vascular tone, serves as an antithrombotic agent, and inhibits vascular smooth muscle cell proliferation. NO deficiency has been implicated in the pathophysiology of several vascular disorders, including hypertension, atherosclerosis, and restenosis, and provides a plausible biologic basis for the use of NO replacement therapy in these conditions. Treatment with conventional nitrate preparations is limited by a short therapeutic half-life, systemic absorption with potentially adverse hemodynamic effects, and drug tolerance. To overcome these limitations, novel delivery systems and novel NO donors have been developed that offer selective effects, a prolonged half-life, and a reduced incidence of tolerance.

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Section: New Developments In Nitrosovasodilator Therapy 197mentioning

confidence: 97%

New Developments in Nitrosovasodilator Therapy

Leopold

Loscalzo

1997

Vasc Med

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The role of nitric oxide in cardiac surgery

Nonami

1997

Surg Today

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The release of nitric oxide (NO) from coronary endothelial cells is impaired following reperfusion; however, several experimental studies have found that it exerts a cardioprotective effect during myocardial ischemia-reperfusion. Thus, attempts have been made to supplement NO production exogenously during reperfusion when endogenous NO release may be diminished. Conversely, other studies suggest that NO exacerbates reperfusion injury by inducing the production of peroxynitrite. NO has also been reported to provide beneficial effects as a selective pulmonary vasodilator to relieve pulmonary hypertension. A loss of NO-mediated relaxation caused by the dysfunction of endothelial cells is characteristic of intimal hyperplasia, and nitrosovasodilators have proven efficient against atherosclerotic coronary heart disease, which may be attributable to their antiplatelet effects as well as to vasodilation. Furthermore, protamine sulfate, which is rich in L-arginine, is thought to augment NO production by supplying exogenous L-arginine, or to act on endothelial cell receptors to stimulate the production of NO. This review summarizes the current role of NO in cardiac surgery.

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Effects of CAS 754, a New Nitric Oxide Donor, on Regional Cerebral Blood Flow in Focal Cerebral Ischemia

Wei

Weiss

1995

Anesthesia & Analgesia

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Nitric oxide (NO) plays an important role in regulating regional cerebral blood flow (rCBF). This study was performed to compare the effects of the NO donor, CAS 754, a sydnonimine derivative, and sodium nitroprusside (SNP) on rCBF in ischemic and nonischemic brain regions. Twenty-eight rats were anesthetized with 1.4% isoflurane and were mechanically ventilated. A middle cerebral artery (MCA) was occluded in each animal. In the CAS 754 group (n = 7), 40 min after MCA occlusion, 4-6 mg/kg of CAS 754 was administered intravenously (i.v.) to decrease the mean arterial blood pressure (MAP) to 55-60 mm Hg. In the SNP group (n = 7), an infusion of SNP was started to decrease the MAP to the same level as that of the CAS group. In the CAS-Ph group (n = 7), phenylephrine was infused after CAS754 had been administered in order to maintain the MAP at the control level (95-100 mm Hg). The remaining seven rats were used as a control group. rCBF was measured using 14C-iodoantipyrine in all four groups of animals 1 h after MCA occlusion (20 min after the start of drug administration). The average rCBF of the nonischemic brain regions (121 +/- 15 mL.min-1.100 g-1) was increased by 34% with CAS 754 (162 +/- 39 mL.min-1.100 g-1). However, SNP did not significantly change the average rCBF of the nonischemic brain regions (114 +/- 5 mL.min-1.100 g-1). Neither CAS 754 nor SNP significantly affected the rCBF of the ischemic cortex (control 51 +/- 7, CAS 61 +/- 13, SNP 53 +/- 18 mL.min-1.100 g-1). Phenylephrine infusion in the CAS 754-treated animals did not significantly affect the rCBF of the ischemic or nonischemic brain regions. In conclusion, our study demonstrated that CAS 754 was a more effective cerebral vasodilator than nitroprusside when administered systemically. In the ischemic cortex, neither CAS 754 nor nitroprusside improved rCBF Failure of CAS 754 to improve the rCBF of the ischemic cortex does not appear to be due to hypotension induced by CAS 754.

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The Sydnonimine C87–3754 Evokes Endothelium-Independent Relaxations and Prevents Endothelium-Dependent Contractions in Blood Vessels of the Dog

Cited by 4 publications

References 0 publications

New Developments in Nitrosovasodilator Therapy

New Developments in Nitrosovasodilator Therapy

The role of nitric oxide in cardiac surgery

Effects of CAS 754, a New Nitric Oxide Donor, on Regional Cerebral Blood Flow in Focal Cerebral Ischemia

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