Platelet count, platelet aggregation and fibrinogen levels following acute induction to high altitude (3200 and 3771 metres)

Chatterji, J. C.; Ohri, V C; Das, Bismay; Chadha, K. S.; Akhtar, Marjahan; Bhatacharji, P.; Tewari, Sujata; Behl, Ajay S.

doi:10.1016/0049-3848(82)90138-4

Cited by 29 publications

(14 citation statements)

References 8 publications

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“…The literature contains conflicting results about the effects of acute hypoxic exposure on platelet function. SHARMA [172] reported increased platelet counts following ascent above 3,000 m while other studies reported either a decrease [173][174][175] or no change in these levels [176]. Similar conflicting results have been demonstrated for bleeding times [177,178].…”

Section: Pulmonary Thromboembolic Diseasementioning

confidence: 52%

Travel to high altitude with pre-existing lung disease

Luks

Swenson²

2007

Eur Respir J

107

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The pathophysiology of high-altitude illnesses has been well studied in normal individuals, but little is known about the risks of high-altitude travel in patients with pre-existing lung disease. Although it would seem self-evident that any patient with lung disease might not do well at high altitude, the type and severity of disease will determine the likelihood of difficulty in a high-altitude environment. The present review examines whether these individuals are at risk of developing one of the main forms of acute or chronic high-altitude illness and whether the underlying lung disease itself will get worse at high elevations. Several groups of pulmonary disorders are considered, including obstructive, restrictive, vascular, control of ventilation, pleural and neuromuscular diseases. Attempts will be made to classify the risks faced by each of these groups at high altitude and to provide recommendations regarding evaluation prior to high-altitude travel, advice for or against taking such excursions, and effective prophylactic measures.

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Section: Pulmonary Thromboembolic Diseasementioning

confidence: 52%

Travel to high altitude with pre-existing lung disease

Luks

Swenson²

2007

Eur Respir J

107

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“…An additional 8 days at that altitude produced an increase to 7% below control levels. Similarly Chatterji et al (1982) found a 12%-26% fall in platelet counts after 48-72 h at 3200 m and 3771 m. Conversely Singh and Chohan (1972a) showed a significant rise in platelet numbers in 32 Indian soldiers ascending to between 3600 m and 5200 m. Sharma (1986) failed to demonstrate a significant difference in platelet numbers when 50 soldiers were moved from low altitude to 3650 m. However, in an earlier study he had reported a slight but significant increase in platelet numbers in well subjects, the reverse being seen in those with symptoms suggestive of acute mountain sickness (AMS) (Sharma 1980). All these studies used manual methods for platelet enumeration.…”

Section: Introductionmentioning

confidence: 96%

The effect of high altitude on platelet counts, thrombopoietin and erythropoietin levels in young Bolivian airmen visiting the Andes

Hudson

Bowen

Navia

et al. 1999

International Journal of Biometeorology

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Recognition of thrombosis as a complication of exposure to high altitude has stimulated interest in rheological changes resulting from hypobaric hypoxia. Previous studies of platelet counts at high altitude have yielded conflicting results and have not been studied in conjunction with potential mediating cytokines. We studied the effects of high-altitude exposure on platelet numbers, thrombopoietin (tpo) and erythropoietin (epo) levels in man. A group of 28 volunteers from the Bolivian Airforce stationed at Santa Cruz (600 m altitude) were studied 48 h and 1 week after their ascent to La Paz (3600 m). In addition 105 volunteers based at Santa Cruz for at least 1 year were compared with 175 age- and sex-matched residents at El Alto (4200 m). Platelet counts were measured immediately after sampling and serum samples assayed for tpo and epo. In the ascending group, mean platelet counts were 251 x 10(9), 367 x 10(9) and 398 x10 (9)/l at 600 m and following 48 h and 1 week at 3600 m respectively. Mean tpo levels were 132.5, 76 and 92 pg/ml with epo values of 2.98, 11.6 and 7.9 mIU/ml respectively. In the resident populations mean platelet counts were 271 x 10(9)/l in the low- and 471 x 10(9)/l in the high-altitude groups. Mean tpo and epo levels measured 69.3 pg/ml and 4.5 mIU/ml respectively at 600 m and 58.5 pg/ml and 5.1 mIU/ml at 4200 m. In conclusion we have demonstrated a significant and sustained elevation in platelet numbers within 48 h of ascent to high altitude. Our findings do not support a role for tpo as a mediator of the increased platelet count. However, these data do not discount epo as a potential candidate.

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“…A hypercoaguable state has also been demonstrated in animal models of chronic continuous hypoxia in dogs [87], rats [88] and mice [89]. In humans, platelet aggregation was found to be either increased, decreased or unchanged by exposure to altitude [90,91] but was increased in chronic respiratory disease [92,93]. Platelet aggregation was also increased in animal models of chronic continuous hypoxia in rats [88] and mice [89].…”

Section: Coaguabilitymentioning

confidence: 83%

The Pathophysiology of Sleep Apnoea: What We have Learned from Animal Models of Chronic Intermittent Hypoxia

O’Halloran¹,

Bradford²

2007

CRMR

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Sleep apnoea is a common condition associated with significant morbidity and mortality. The English bulldog is the only animal known to have sleep apnoea. In recent years, a number of animal models have been developed which have contributed greatly to our knowledge of the condition. These models develop a number of pathophysiological changes similar to human sleep apnoea such as systemic and pulmonary hypertension, increased haematocrit, and effects on blood coaguability, cardiac rhythmogenesis and central nervous system and upper airway muscle function. This review will describe what has been learned from these models concerning the pathophysiology of sleep apnoea with special emphasis on the role played by intermittent hypoxia.

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Platelet count, platelet aggregation and fibrinogen levels following acute induction to high altitude (3200 and 3771 metres)

Cited by 29 publications

References 8 publications

Travel to high altitude with pre-existing lung disease

Travel to high altitude with pre-existing lung disease

The effect of high altitude on platelet counts, thrombopoietin and erythropoietin levels in young Bolivian airmen visiting the Andes

The Pathophysiology of Sleep Apnoea: What We have Learned from Animal Models of Chronic Intermittent Hypoxia

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