Severe Acute Mountain Sickness and Suspected High Altitude Cerebral Edema Related to Nitroglycerin Use

Mazzuero, Giorgio; Mazzuero, A.; Pascariello, Adolfo

doi:10.1089/ham.2007.1074

Cited by 8 publications

(5 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…At low altitude NO plays a role in tension type headache and NO prodrugs are associated with headache and nausea 11. Nitroglycerin causes headache and exacerbates AMS12 as does sildenafil 13. Smoking impairs endothelial function, decreasing NO formation and increasing NO degradation14 and smokers expire less NO 15.…”

Section: Discussionmentioning

confidence: 99%

Smoking, acute mountain sickness and altitude acclimatisation: a cohort study

Ding²,

Liu³

et al. 2012

Thorax

View full text Add to dashboard Cite

RationaleThe relationship between cigarette smoking and acute mountain sickness (AMS) is not clear. Objective To assess AMS risk and altitude acclimatisation in relation to smoking. Methods 200 healthy non-smokers and 182 cigarette smokers were recruited from Han lowland workers. These were men without prior altitude exposure, matched for age, health status and occupation, who were transported to an altitude of 4525 masl. Measurements AMS, smoking habits, arterial saturation (SpO 2 ), haemoglobin (Hb), lung function and mean pulmonary artery pressure (PAPm) were assessed upon arrival and after 3 and 6 months. Main results Compared with non-smokers, smokers had a lower incidence of AMS and lower AMS scores than non-smokers upon arrival; higher Hb and PAPm associated with lower SpO 2 at 3 and 6 months at altitude; and lower forced expiratory volume in 1 s and maximal voluntary ventilation at 3 and 6 months. Conclusions Smoking slightly decreases the risk of AMS but impairs long-term altitude acclimatisation and lung function during a prolonged stay at high altitude.

show abstract

Section: Discussionmentioning

confidence: 99%

Smoking, acute mountain sickness and altitude acclimatisation: a cohort study

Ding²,

Liu³

et al. 2012

Thorax

View full text Add to dashboard Cite

show abstract

“…Nitroglycerin is a prodrug for NO (Olesen, 2008) and is well known for causing a classic headache after its use in normoxia. It also exacerbates AMS (Mazzuero et al, 2008), hence it could be hypothesized that hypoxia-induced NO formation has a greater effect on cerebral venous vessels.…”

Section: Increased Central Venous Pressuresmentioning

confidence: 99%

The Headache of High Altitude and Microgravity—Similarities with Clinical Syndromes of Cerebral Venous Hypertension

Imray

Hargens

2011

High Altitude Medicine & Biology

View full text Add to dashboard Cite

Syndromes thought to have cerebral venous hypertension as their core, such as idiopathic intracranial hypertension and jugular foramen outlet obstruction, classically result in headaches. Do they provide an insight into the cause of the headache that commonly occurs at altitude? The classic theory of the pathogenesis of high altitude headache has been that it results from increased intracranial pressure (ICP) secondary to hypoxemia in people who have less compliant intracranial volumes (Roach and Hackett, 2001). However, there does not appear to be a correlation between the headache of acute mountain sickness (AMS) and the presence of cerebral edema (Bailey et al, 2006; Wilson et al, 2009). Research has concentrated on arterial perfusion to the brain in hypoxia, but there has been little study of venous drainage. Hypoxia results in markedly increased cerebral blood flow; however, if it has been considered at all, venous outflow has to date been assumed to be of little consequence. Retinal venous distension and the increased venous blood demonstrated by near infra-red spectroscopy and more recently by MRI imply that, in hypoxia, a relative venous insufficiency may exist. Similarly, there is increasing evidence that manifestations of the fluid shift during microgravity is of similar nature to idiopathic intracranial hypertension, which is thought to be primarily a venous insufficiency condition. The unique anthropomorphic adaptations of large brained biped humans with cerebral venous systems that have to cope with large changes in hydrostatic pressure may predispose us to conditions of inflow/outflow mismatch. In addition, slight increases in central venous pressures (e.g., from hypoxia-induced pulmonary vasoconstriction) may further compromise venous outflow at altitude. A better understanding of cerebral venous physiology may enlighten us with regards the pathogenesis of headaches currently considered idiopathic. It may also enable us to trigger headaches for study and hence enable us to develop new treatment strategies.

show abstract

“…High-altitude induces hypoxemia, which when uncompensated (or only partially compensated) can lead to dizziness, nausea, headaches, and shortness of breath. Further development of AMS associates with the onset of high-altitude cerebral edema (HACE) and then, the neurological symptoms progress to loss of consciousness possibly leading to fatal ataxia (including the failure of motor control of breathing) (Dehnert and Bartsch, 2017;Kedzierewicz and Cabane, 2013;Mazzuero et al, 2008).…”

Section: Neurological Pathogenesis Of Covid-19 and Acute Mountain Sicknessmentioning

confidence: 99%

Coping with hypoxemia: Could erythropoietin (EPO) be an adjuvant treatment of COVID-19?

Soliz

Schneider‐Gasser

Arias‐Reyes

et al. 2020

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

A very recent epidemiological study provides preliminary evidence that living in habitats located at 2500 m above sea level (masl) might protect from the development of severe respiratory symptoms following infection with the novel SARS-CoV-2 virus. This epidemiological finding raises the question of whether physiological mechanisms underlying the acclimatization to high altitude identifies therapeutic targets for the effective treatment of severe acute respiratory syndrome pivotal to the reduction of global mortality during the COVID-19 pandemic. This article compares the symptoms of acute mountain sickness (AMS) with those of SARS-CoV-2 infection and explores overlapping patho-physiological mechanisms of the respiratory system including impaired oxygen transport, pulmonary gas exchange and brainstem circuits controlling respiration. In this context, we also discuss the potential impact of SARS-CoV-2 infection on oxygen sensing in the carotid body. Finally, since erythropoietin (EPO) is an effective prophylactic treatment for AMS, this article reviews the potential benefits of implementing FDA-approved erythropoietin-based (EPO) drug therapies to counteract a variety of acute respiratory and non-respiratory (e.g. excessive inflammation of vascular beds) symptoms of SARS-CoV-2 infection.

show abstract

Severe Acute Mountain Sickness and Suspected High Altitude Cerebral Edema Related to Nitroglycerin Use

Cited by 8 publications

References 10 publications

Smoking, acute mountain sickness and altitude acclimatisation: a cohort study

Smoking, acute mountain sickness and altitude acclimatisation: a cohort study

The Headache of High Altitude and Microgravity—Similarities with Clinical Syndromes of Cerebral Venous Hypertension

Coping with hypoxemia: Could erythropoietin (EPO) be an adjuvant treatment of COVID-19?

Contact Info

Product

Resources

About