Effect of ischemia duration and nitric oxide on coronary vasoconstriction after ischemia–reperfusion

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

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Enhanced Endothelin-Mediated Coronary Vasoconstriction and Attenuated Basal Nitric Oxide Activity in Experimental Hypercholesterolemia

Circulation ◽

10.1161/01.cir.96.6.1930 ◽

1997 ◽

Vol 96 (6) ◽

pp. 1930-1936 ◽

Cited By ~ 57

Author(s):

Verghese Mathew ◽

Charles R. Cannan ◽

Virginia M. Miller ◽

Dustan A. Barber ◽

David Hasdai ◽

...

Keyword(s):

Nitric Oxide ◽

Coronary Vasoconstriction ◽

Experimental Hypercholesterolemia

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Role of nitric oxide in hepatic and pulmonary injury following ischemia-reperfusion of rat liver

Gastroenterology ◽

10.1016/s0016-5085(03)83633-8 ◽

2003 ◽

Vol 124 (4) ◽

pp. A719-A720

Author(s):

Yuji Takamatsu ◽

Kazuo Shimada ◽

Koji Yamaguchi ◽

Kazuo Chijiiwa ◽

Masao Tanaka

Keyword(s):

Nitric Oxide ◽

Rat Liver ◽

Ischemia Reperfusion ◽

Pulmonary Injury

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Role of TLR-4/IL-6/TNF-α, COX-II and eNOS/iNOS pathways in the impact of carvedilol against hepatic ischemia reperfusion injury

Human & Experimental Toxicology ◽

10.1177/0960327121999442 ◽

2021 ◽

pp. 096032712199944

Author(s):

Mohamed IA Hassan ◽

Fares EM Ali ◽

Abdel-Gawad S Shalkami

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Inducible Nitric Oxide Synthase ◽

Liver Enzymes ◽

Ischemia Reperfusion ◽

Hepatic Ischemia ◽

Hepatic Ischemia Reperfusion ◽

Oxide Synthase ◽

Inducible Nitric Oxide

Aim: Hepatic ischemia/reperfusion (I/R) injury is a syndrome involved in allograft dysfunction. This work aimed to elucidate carvedilol (CAR) role in hepatic I/R injury. Methods: Male rats were allocated to Sham group, CAR group, I/R group and CAR plus I/R group. Rats subjected to hepatic ischemia for 30 minutes then reperfused for 60 minutes. Oxidative stress markers, inflammatory cytokines and nitric oxide synthases were measured in hepatic tissues. Results: Hepatocyte injury following I/R was confirmed by a marked increase in liver enzymes. Also, hepatic I/R increased the contents of malondialdehyde however decreased glutathione contents and activities of antioxidant enzymes. Furthermore, hepatic I/R caused elevation of toll-like receptor-4 (TLR-4) expression and inflammatory mediators levels such as tumor necrosis factor-α, interleukin-6 and cyclooxygenase-II. Hepatic I/R caused down-regulation of endothelial nitric oxide synthase and upregulation of inducible nitric oxide synthase expressions. CAR treatment before hepatic I/R resulted in the restoration of liver enzymes. Administration of CAR caused a significant correction of oxidative stress and inflammation markers as well as modulates the expression of endothelial and inducible nitric oxide synthase. Conclusions: CAR protects liver from I/R injury through reduction of the oxidative stress and inflammation, and modulates endothelial and inducible nitric oxide synthase expressions.

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Hypoxia compared with normoxia alters the effects of nitric oxide in ischemia-reperfusion lung injury

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1997.273.3.l504 ◽

1997 ◽

Vol 273 (3) ◽

pp. L504-L512 ◽

Cited By ~ 2

Author(s):

Y. C. Huang ◽

P. W. Fisher ◽

E. Nozik-Grayck ◽

C. A. Piantadosi

Keyword(s):

Nitric Oxide ◽

Lung Injury ◽

Average Rate ◽

Ischemia Reperfusion ◽

Oxidant Stress ◽

No Production ◽

Protective Effects ◽

Lung Weight ◽

Edema Formation ◽

No Donors

Because both the biosynthesis of nitric oxide (NO.) and its metabolic fate are related to molecular O2, we hypothesized that hypoxia would alter the effects of NO. during ischemia-reperfusion (IR) in the lung. In this study, buffer-perfused lungs from rabbits underwent either normoxic IR (AI), in which lungs were ventilated with 21% O2 during ischemia and reperfusion, or hypoxic IR (NI), in which lungs were ventilated with 95% N2 during ischemia followed by reoxygenation with 21% O2. Lung weight gain (WG) and pulmonary artery pressure (Ppa) were monitored continuously, and microvascular pressure (Pmv) was measured after reperfusion to calculate pulmonary vascular resistance. We found that both AI and NI produced acute lung injury, as shown by increased WG and Ppa during reperfusion. In AI, where perfusate PO2 was > 100 mmHg, the administration of the NO. synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) before ischemia worsened WG and Ppa. Pmv also increased, suggesting a hydrostatic mechanism involved in edema formation. The effects of L-NAME could be attenuated by giving L-arginine and exogenous NO. donors before ischemia or before reperfusion. Partial protection was also provided by superoxide dismutase. In contrast, lung injury in NI at perfusate PO2 of 25-30 mmHg was attenuated by L-NAME; this effect could be reversed by L-arginine. Exogenous NO. donors given either before ischemia or before reperfusion, however, did not increase lung injury. NO. production was measured by quantifying the total nitrogen oxides (NOx) accumulating in the perfusate. The average rate of NOx accumulation was greater in AI than in NI. We conclude that hypoxia prevented the protective effects of NO on AI lung injury. The effects of hypoxia may be related to lower NO. production relative to oxidant stress during IR and/or altered metabolic fates of NO.-mediated production of peroxynitrite by hypoxic ischemia.

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