Effect of Acetazolamide and Gingko Biloba on the Human Pulmonary Vascular Response to an Acute Altitude Ascent

Ke, Tao; Wang, Jiye; Swenson, Erik R.; Zhang, Xiangnan; Hu, Yunfeng; Chen, Yaoming; Liu, Mingchao; Zhang, Wenbin; Zhao, Feng; Shen, Xuefeng; Yang, Qun; Chen, Jingyuan; Luo, Wenjing

doi:10.1089/ham.2012.1099

Cited by 30 publications

(19 citation statements)

References 30 publications

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“…Previously, pre-treatment of acetazolamide has resulted in an almost negligible difference of PASP (~2mmHg; no statistical analyses were performed) 48hours after final drug treatment when compared to individuals that received placebo treatment 25 . Although unlikely to alter our findings, we were unable to rule out the possibility of persisting physiological sequelae secondary to acetazolamide treatment during our day two testing.…”

Section: Study Participants and Designmentioning

confidence: 99%

Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High Altitude

Hoiland

Foster

Donnelly

et al. 2015

Chest

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Abstract:The hypoxic ventilatory response (HVR) at sea level (SL) is moderately predictive of the change in pulmonary artery systolic pressure (PASP) to acute normobaric hypoxia. However, because of progressive changes in the chemoreflex control of breathing and acid-base balance at high altitude (HA), HVR at SL may not predict PASP at HA. We hypothesized that resting peripheral oxyhemoglobin saturation (SpO 2 ) at HA would correlate better than HVR at SL to PASP at HA. In 20 participants at SL, we measured normobaric, isocapnic HVR (L/min·-%SpO 2 -1 ) and resting PASP using echocardiography.Both resting SpO 2 and PASP measures were repeated on day 2 (n=10), days 4-8 (n=12), and 2-3 weeks (n=8) after arrival at 5050m. These data were also collected at 5050m on life-long HA residents (Sherpa; n=21

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Section: Study Participants and Designmentioning

confidence: 99%

Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High Altitude

Hoiland

Foster

Donnelly

et al. 2015

Chest

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“…Acetazolamide (AZ) has been used to stimulate ventilation in patients with chronic obstructive pulmonary disease, to correct metabolic alkalosis (Adamson & Swenson, ), to treat sleep‐disordered breathing (Edwards et al., ; Javaheri, Sands, & Edwards, ) and in the prophylaxis of acute mountain sickness (AMS; Kayser et al., ; Leaf & Goldfarb, ). Another property of AZ is its ability to reduce pulmonary vasoconstriction upon acute exposure to hypoxia (Ke et al., ; Teppema et al., ). The rationale for the use of AZ in chronic obstructive pulmonary disease patients and in correcting metabolic alkalosis, however, is limited and disputed (Adamson & Swenson, ).…”

Section: Introductionmentioning

confidence: 99%

Influence of methazolamide on the human control of breathing: A comparison to acetazolamide

Teppema

Boulet

Hackett

et al. 2019

Experimental Physiology

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Acetazolamide is used to prevent/treat acute mountain sickness and both central and obstructive sleep apnoea. Methazolamide, like acetazolamide, reduces hypoxic pulmonary vasoconstriction, but has fewer side-effects, including less impairment of skeletal muscle function. Given that the effects of methazolamide on respiratory control in humans are unknown, we compared the effects of oral methazolamide and acetazolamide on ventilatory control and determined the ventilationlog P O 2 relationship in humans. In a double-blind, placebo-controlled, randomized cross-over design, we studied the effects of acetazolamide (250 mg three times daily), methazolamide (100 mg twice daily) and placebo in 14 young male subjects who were exposed to 7 min of normoxic hypercapnia and to three levels of eucapnia and hypercapnic hypoxia. With placebo, methazolamide and acetazolamide, the CO 2 sensitivities were 2.39 ± 1.29, 3.27 ± 1.82 and 2.62 ± 1.79 l min −1 mmHg −1 (n.s.) and estimated apnoeic thresholds 32 ± 3, 28 ± 3 and 26 ± 3 mmHg, respectively (P < 0.001, placebo versus methazolamide and acetazolamide).The relationship between ventilation (V I ) and log P O 2 (using arterialized venous P O 2 in hypoxia) was linear, and neither agent influenced the relationship between hypoxic sensitivity (ΔV I ∕Δ log P O 2 ) and arterial [H + ]. Using ΔV I ∕Δ log P O 2 rather than ΔV I /Δ arterial oxyhaemoglobin saturation enables a more accurate estimation of oxygenation and ventilatory control in metabolic acidosis/alkalosis when right-or leftward shifts of the oxyhaemoglobin saturation curve occur. Given that acetazolamide and methazolamide have similar effects on ventilatory control, methazolamide might be preferred for indications requiring the use of a carbonic anhydrase inhibitor, avoiding some of the negative side-effects of acetazolamide. K E Y W O R D Saltitude sickness, carbonic anhydrase inhibitors, hypercapnia, hypoxia, respiration, ventilation

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“…2004) and humans (Teppema et al . 2007; Ke et al . 2013) by a mechanism unrelated to CA inhibition (Höhne et al .…”

Section: Introductionmentioning

confidence: 99%

Carbonic anhydrase is not a relevant nitrite reductase or nitrous anhydrase in the lung

Pickerodt

Kronfeldt

Ruß

et al. 2018

The Journal of Physiology

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The carbonic anhydrase (CA) inhibitors acetazolamide and its structurally similar analogue methazolamide prevent or reduce hypoxic pulmonary vasoconstriction (HPV) in dogs and humans in vivo, by a mechanism unrelated to CA inhibition. In rodent blood and isolated blood vessels, it has been reported that inhibition of CA leads to increased generation of nitric oxide (NO) from nitrite and vascular relaxation in vitro. We tested the physiological relevance of augmented NO generation by CA from nitrite with acetazolamide in anaesthetized pigs during alveolar hypoxia in vivo. We found that acetazolamide prevents HPV in anaesthetized pigs, as in other mammalian species. A single nebulization of sodium nitrite reduces HPV, but this action wanes in the succeeding 3 h of hypoxia as nitrite is metabolized and excreted. Pulmonary artery pressure reduction and NO formation as measured by exhaled gas concentration from inhaled sodium nitrite were not increased by acetazolamide during alveolar hypoxia. Thus, our data argue against a physiological role of carbonic anhydrase as a nitrous anhydrase or nitrite reductase as a mechanism for its inhibition of HPV in the lung and blood in vivo.

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Effect of Acetazolamide and Gingko Biloba on the Human Pulmonary Vascular Response to an Acute Altitude Ascent

Cited by 30 publications

References 30 publications

Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High Altitude

Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High Altitude

Influence of methazolamide on the human control of breathing: A comparison to acetazolamide

Carbonic anhydrase is not a relevant nitrite reductase or nitrous anhydrase in the lung

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