Nitric oxide contributes to cerebrovascular shear‐mediated dilation but not steady‐state cerebrovascular reactivity to carbon dioxide

2021 ◽  
Author(s):  
Ryan L. Hoiland ◽  
Hannah G. Caldwell ◽  
Jay M.J.R. Carr ◽  
Connor A. Howe ◽  
Benjamin S. Stacey ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Carbon Dioxide ◽  
Steady State ◽  
Cerebrovascular Reactivity

scholarly journals Steady-state nitric oxide concentrations during denitrification.

1990 ◽  
Vol 265 (20) ◽  
pp. 11535-11538 ◽  
Author(s):  
J Goretski ◽  
O C Zafiriou ◽  
T C Hollocher
Keyword(s):  
Nitric Oxide ◽  
Steady State

Biological elimination of nitric oxide and carbon dioxide from flue gas by marine microalga NOA-113 cultivated in a long tubular photobioreactor

1996 ◽  
Vol 82 (4) ◽  
pp. 351-354 ◽  
Author(s):  
Ken-Ichi Yoshihara ◽  
Hiroyasu Nagase ◽  
Kaoru Eguchi ◽  
Kazumasa Hirata ◽  
Kazuhisa Miyamoto
Keyword(s):  
Nitric Oxide ◽  
Carbon Dioxide ◽  
Flue Gas ◽  
Tubular Photobioreactor ◽  
Marine Microalga

scholarly journals Contribution of adenosine to compensatory dilation in hypoperfused contracting human muscles is independent of nitric oxide

2011 ◽  
Vol 110 (5) ◽  
pp. 1181-1189 ◽  
Author(s):  
Darren P. Casey ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Steady State ◽  
Arterial Pressure ◽  
Brachial Artery ◽  
Adenosine Receptor ◽  
Receptor Blockade ◽  
Independent Manner ◽  
Control Value ◽  
Percent Recovery

We previously demonstrated that nitric oxide (NO) contributes to compensatory vasodilation in the contracting human forearm subjected to acute hypoperfusion. We examined the potential role of an adenosine-NO interaction to this response in 17 male subjects (25 ± 2 yr). In separate protocols subjects performed rhythmic forearm exercise (20% of maximum) while hypoperfusion was evoked by balloon inflation in the brachial artery above the elbow. Each trial included exercise before inflation, exercise with inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound) and local [brachial artery catheter pressure (BAP)] and systemic [mean arterial pressure (MAP); Finometer] arterial pressure were measured. In protocol 1 ( n = 10), exercise was repeated during nitric oxide synthase inhibition [ NG-monomethyl-l-arginine (l-NMMA)] alone and during l-NMMA-aminophylline (adenosine receptor blockade) administration. In protocol 2, exercise was repeated during aminophylline alone and during aminophylline-l-NMMA. Forearm vascular conductance (FVC; ml·min−1·100 mmHg−1) was calculated from blood flow (ml/min) and BAP (mmHg). Percent recovery in FVC during inflation was calculated as (steady-state inflation + exercise value − nadir)/[steady-state exercise (control) value − nadir]. In protocol 1, percent recovery in FVC was 108 ± 8% during the control (no drug) trial. Percent recovery in FVC was attenuated with inhibition of NO formation alone (78 ± 9%; P < 0.01 vs. control) and was attenuated further with combined inhibition of NO and adenosine (58 ± 9%; P < 0.01 vs. l-NMMA). In protocol 2, percent recovery was reduced with adenosine receptor blockade (74 ± 11% vs. 113 ± 6%, P < 0.01) compared with control drug trials. Percent recovery in FVC was attenuated further with combined inhibition of adenosine and NO (48 ± 11%; P < 0.05 vs. aminophylline). Our data indicate that adenosine contributes to compensatory vasodilation in an NO-independent manner during exercise with acute hypoperfusion.

Respiration in man during metabolic alkalosis

1962 ◽  
Vol 17 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Daniel J. Stone
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Lung Function ◽  
Gas Exchange ◽  
Metabolic Alkalosis ◽  
Time Lag ◽  
Respiratory Compensation ◽  
Arterial Ph ◽  
Oral Sodium ◽  
Ventilation Response

A steady state metabolic alkalosis was induced in two subjects over a period of several days utilizing oral sodium bicarbonate in dosages of 50 g/day. The purpose of inducing steady state metabolic alkalosis was to study the effects of such a state on the respiratory center responses to inspired gas mixtures, containing carbon dioxide, and to contrast these results with the control studies. The experiment was so designed that the arterial pH in both subjects tended to return toward normal in the presence of significant increases in blood bicarbonate. Repeated study of ventilation responses with room air and 4% and 6% carbon dioxide in inspired air revealed a definite and significant decrease in ventilation response to carbon dioxide during the periods of steady state alkalosis as compared to the control periods. Normal responses returned after some time lag. A consistent rise in paCOCO2 occurred with alkalosis, thus demonstrating respiratory compensation. In neither subject was total lung function or gas exchange affected by the alkalosis. The experiment was confirmed on several occasions with reproducible results. Note: (With the Research Assistance of Mary Di Lieto) Submitted on May 22, 1961

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