Bovine Polymerized Hemoglobin Increases Cardiac Oxygen Consumption and Alters Myocardial Substrate Metabolism in Conscious Dogs: Role of Nitric Oxide

2000 ◽  
Vol 35 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Kit E. Loke ◽  
Paul R. Forfia ◽  
Fabio A. Recchia ◽  
Xiaobin Xu ◽  
Juan Carlos Osorio ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Conscious Dogs ◽  
Substrate Metabolism ◽  
Myocardial Substrate ◽  
Polymerized Hemoglobin

scholarly journals Role of nitric oxide in the regulation of oxygen consumption in conscious dogs.

1994 ◽  
Vol 75 (6) ◽  
pp. 1086-1095 ◽  
Author(s):  
W Shen ◽  
X Xu ◽  
M Ochoa ◽  
G Zhao ◽  
M S Wolin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Conscious Dogs

Nitric oxide modulates oxygen consumption by arteriolar walls in rat skeletal muscle

2005 ◽  
Vol 289 (6) ◽  
pp. H2673-H2679 ◽  
Author(s):  
Masahiro Shibata ◽  
Shigeru Ichioka ◽  
Akira Kamiya
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Oxygen Consumption Rate ◽  
Consumption Rate ◽  
Phosphorescence Quenching ◽  
Arterial Blood ◽  
No Release ◽  
Vessel Walls

To study the role of nitric oxide (NO) in regulating oxygen consumption by vessel walls, the oxygen consumption rate of arteriolar walls in rat cremaster muscle was measured in vivo during flow-induced vasodilation and after inhibiting NO synthesis. The oxygen consumption rate of arteriolar walls was calculated based on the intra- and perivascular Po2 values measured by phosphorescence quenching laser microscopy. The perivascular Po2 value of the arterioles during vasodilation was significantly higher than under control conditions, although the intravascular Po2 values under both conditions were approximately the same. Inhibition of NO synthesis, on the other hand, caused a significant increase in arterial blood pressure and a significant decrease in arteriolar diameter. Inhibition of NO synthesis also caused a significant decrease in both the intra- and perivascular Po2 values of the arterioles. Inhibition of NO synthesis increased the oxygen consumption rate of the vessel walls by 42%, whereas enhancement of flow-induced NO release decreased it by 34%. These results suggest that NO plays an important role not only as a regulator of peripheral vascular tone but also as a modulator of tissue oxygenation by reducing oxygen consumption by vessel walls. In addition, enhancement of NO release during exercise may facilitate efficient oxygen supply to the surrounding high metabolic tissue.

A544 ROLE OF NITRIC OXIDE ON HEMODYNAMIC CHANGES INDUCED BY PROTAMINE IN NON-HEPARINIZED CONSCIOUS DOGS

1997 ◽  
Vol 87 (Supplement) ◽  
pp. 544A
Author(s):  
T. Oguchi ◽  
M.-F. Doursout ◽  
J.E. Chelly
Keyword(s):  
Nitric Oxide ◽  
Conscious Dogs ◽  
Hemodynamic Changes

scholarly journals Role of Nitric Oxide in the Control of Cardiac Oxygen Consumption in B2-Kinin Receptor Knockout Mice

Hypertension ◽  
1999 ◽  
Vol 34 (4) ◽  
pp. 563-567 ◽  
Author(s):  
Kit E. Loke ◽  
Christine M. L. Curran ◽  
Eric J. Messina ◽  
Sarra K. Laycock ◽  
Edward G. Shesely ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Knockout Mice ◽  
Kinin Receptor

scholarly journals Role of Nitric Oxide in Regulating Cerebrocortical Oxygen Consumption and Blood Flow during Hypercapnia

1994 ◽  
Vol 14 (3) ◽  
pp. 503-509 ◽  
Author(s):  
Ildiko Horvath ◽  
Norbert T. Sandor ◽  
Zoltan Ruttner ◽  
Alan C. McLaughlin
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Methyl Ester ◽  
Superior Sagittal Sinus ◽  
No Synthase ◽  
Sagittal Sinus ◽  
No Synthase Inhibitor ◽  
Synthase Inhibitor

The effect of the nitric oxide (NO) synthase inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) on the response of cerebrocortical oxygen consumption (CMRO2) and blood flow (CBF) to two levels of hypercapnia (Paco2 ∼ 60 mm Hg and Paco2 ∼ 90 mm Hg) was investigated in ketamine-anesthetized rats. CBF was calculated using the Kety–Schmidt approach and CMRO2 was calculated from the product of CBF and the arteriovenous (superior sagittal sinus) difference for oxygen. l-NAME treatment did not have a significant effect on either CMRO2 or CBE under normocapnic conditions but inhibited the hypercapnic increase of CMRO2 and the hypercapnic increase in CBF. These results suggest that NO plays a role in the response of CMRO2 and CBF during hypercapnia and are consistent with the suggestion that at least part of the increase in CBF observed during hypercapnia is coupled to an increase in CMRO2.

scholarly journals Role of Nitric Oxide in the Control of Renal Oxygen Consumption and the Regulation of Chemical Work in the Kidney

1998 ◽  
Vol 82 (12) ◽  
pp. 1263-1271 ◽  
Author(s):  
Sarra K. Laycock ◽  
Traci Vogel ◽  
Paul R. Forfia ◽  
Joshua Tuzman ◽  
Xiaobin Xu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Chemical Work ◽  
Renal Oxygen Consumption ◽  
Renal Oxygen

scholarly journals Reduced coronary vasodilator responses to amlodipine in pacing-induced heart failure in conscious dogs: role of nitric oxide

2002 ◽  
Vol 136 (2) ◽  
pp. 264-270 ◽  
Author(s):  
Stéphane Champagne ◽  
Luc Hittinger ◽  
François Héloire ◽  
Yukio Suto ◽  
Lucien Sambin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Conscious Dogs ◽  
Coronary Vasodilator

gp91phox-containing NAD(P)H oxidase mediates attenuation of nitric oxide-dependent control of myocardial oxygen consumption by ANG II

2005 ◽  
Vol 289 (2) ◽  
pp. H862-H867 ◽  
Author(s):  
Shintaro Kinugawa ◽  
Juhua Zhang ◽  
Eric Messina ◽  
Erin Walsh ◽  
Harer Huang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Inflammatory Cells ◽  
Oxygen Electrode ◽  
No Production ◽  
Ang Ii ◽  
Wild Type ◽  
Stimulation Of

We have previously reported that ANG II stimulation increased superoxide anion (O2−) through the activation of NAD(P)H oxidase and inhibited nitric oxide (NO)-dependent control of myocardial oxygen consumption (MV̇o2) by scavenging NO. Our objective was to investigate the role of NAD(P)H oxidase, especially the gp91phox subunit, in the NO-dependent control of MV̇o2. MV̇o2 in mice with defects in the expression of gp91phox [gp91phox(−/−)] was measured with a Clark-type oxygen electrode. Baseline MV̇o2 was not significantly different between wild-type (WT) and gp91phox(−/−) mice. Stimulation of NO production by bradykinin (BK) induced significant decreases in MV̇o2 in WT mice. BK-induced reduction in MV̇o2 was enhanced in gp91phox(−/−) mice. BK-induced reduction in MV̇o2 in WT mice was attenuated by 10−8 mol/l ANG II, which was restored by coincubation with Tiron or apocynin. In contrast to WT mice, BK-induced reduction in MV̇o2 in gp91phox(−/−) mice was not altered by ANG II. There was a decrease in lucigenin (5 × 10−6 mol/l)-detectable O2− in gp91phox(−/−) mice compared with WT mice. ANG II resulted in significant increases in O2− production in WT mice, which was inhibited by coincubation with Tiron or apocynin. However, ANG II had no effect on O2− production in gp91phox(−/−) mice. Histological examination showed that the development of abscesses and/or the invasion of inflammatory cells occurred in lungs and livers but not in hearts and kidneys from gp91phox(−/−) mice. These results indicate that the gp91phox subunit of NAD(P)H oxidase mediates O2− production through the activation of NAD(P)H oxidase and attenuation of NO-dependent control of MV̇o2 by ANG II.

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