571
Short Communications Horm. Metab. Res. 10 (1978) 571
Release of Vasopressin in Man at Altitude P.H. Hackett' , Mary L. Forsling 2 , J. Milledge 3 and D. Rennie 4 'P.o. Box 283, Katmandu, Nepal, 2 The Middlesex Hospital Medical School, London, W, P 60B, 3Northwick Park Hospital, Harrow, Middl8sex, U.K., 4Rush Medical Center, Chicago, IIlinois, U.S.A.
While Fors/ing and Miliedge (1977) found that 4 h. exposure to 10.5% oxygen (equivalent to 5490 m altitude) had little effect on vasopressin release in man, the resul t of prolonged exposure is not deal. Excessive fluid retention and hence possibly vasopressin could contribute to the various forms of oedema seen at altitude. These indude pulmonary, cerebral and peripheral oedema as defined previously (Hackett, Rennie and Levine 1976). The purpose of the present study was to investigate the release of vasopressin in the human at altitude with a view to a greater understanding of the pathophysiology of acute mountain sickness (AMS) and altitude oedema.
A
Methods
o
The observations were performed at Pheriche, Nepal (altitude. 4243 m) in the Himalayas on 14 subjects. These inciuded 7 control subjects (5 female) who showed no symptoms, 2 subjects with AMS (both femalel and 4 .subjects additionally with high altitude pulmonary oedema (2 female). On sampling, the blood was immediately centrifuged, the plasma separated and maintained in liquid nitrogen until analysed in London. Hormone determination was performed on extracted plasma as described by Chard and Fors/ing (1976).
H
A grant from the Wellcome Trust is gratefully acknowledged and Grant No. 47053 from the Rush Medical Center.
Received: 20 Jan. 1978
Accepted: 26 June 1978
0018-5043/78
• 05.00
•
4
•
~
•
3
2
• !o!••
units Im I)
(IJ
•
• •
~
-0-
••
ascent descent Na Mt. sickness
acute Mt. AMS + sickness pul. oedema
Fig. 1 Concentration of vasopressin (ADH) in plasma of control subjects and subjects with acute mountain sickness: _ peripheral oedema • no peripheral oedema.
References
Chard, T, M.L. Forsling: 'Hormones in Bood'. Ed. H.N. Antoniades, Harvard University Press, Cambridge (Mass.) pp. 485-516 (1976) Fors/ing, M.L., J.S. Milledge: J. Physiol. 207: 52-53 P (1977) Hackett, P.H., D. Rennie, H.D. Levine: Lancet (11): 11491154 (1976) Singh,l., M.S. Malhotra, P.K. Khanna, R.D. Nanda, T. Purshottam, TN. Upadhyay, U. Radhakrishnan, H.D. Drahmachari: In J. Biometeorol. 18: 21l-22l (1974) Requests for reprints should be addressed to: Dr. M.L. Forsling, Physiology Department, The Middlesex Hosiptal Medical School, London, WIP 6DB. (United Kingdom)
© 1978 Georg Thieme Publishers
Downloaded by: NYU. Copyrighted material.
•
o
Results and Discussion The resuits are summarised in the figure. The plasma vasopressin in the control group was 1.1 ± 0.15 JiU/ml (± SEM, n = 7) as compared with 0.7 ± 0.17 JiU/ml (n = 10) in a previous study at sea level and there was no difference in vasopressin concentration between the ascent and the descent from 5.300 m. Thus altitude alone did not appear to affect the release of vasopressin. The resul ts were similar to those seen with acute hypoxia, when a value of l.1 JiU/ml was recorded (Forsfing and Miliedge 1977). Plasma vasopressin was significantly elevated in those subjects with AMS to a me an concentration of 2.2 ± 0.5 (n = 7, P < 0.01). The results of Singh, Ma/hotra, Khanna, Nanda,PurshaUam, Upadhyay, Radhakrishnan and Brahmachari (1974) suggest a similar trend. I! was also noted that five of the ciimbers with AMS also suffered with peripheral oedema as indicated in the figure. The present studies do not indicate whether the increased vasopressin secretion was a primary change and a major factor in the pathophysiology of AMS or secondary to a shift in fluid from the vascular bed or indeed to stress. The concen trations recorded would have been sufficient to cause a degree of water retention provided that the renal sensitivity to vasopressin was unchanged.
1132-0571
5
Short Communications Horm. Metab. Res. 10 (1978) 571
Release of Vasopressin in Man at Altitude P.H. Hackett' , Mary L. Forsling 2 , J. Milledge 3 and D. Rennie 4 'P.o. Box 283, Katmandu, Nepal, 2 The Middlesex Hospital Medical School, London, W, P 60B, 3Northwick Park Hospital, Harrow, Middl8sex, U.K., 4Rush Medical Center, Chicago, IIlinois, U.S.A.
While Fors/ing and Miliedge (1977) found that 4 h. exposure to 10.5% oxygen (equivalent to 5490 m altitude) had little effect on vasopressin release in man, the resul t of prolonged exposure is not deal. Excessive fluid retention and hence possibly vasopressin could contribute to the various forms of oedema seen at altitude. These indude pulmonary, cerebral and peripheral oedema as defined previously (Hackett, Rennie and Levine 1976). The purpose of the present study was to investigate the release of vasopressin in the human at altitude with a view to a greater understanding of the pathophysiology of acute mountain sickness (AMS) and altitude oedema.
A
Methods
o
The observations were performed at Pheriche, Nepal (altitude. 4243 m) in the Himalayas on 14 subjects. These inciuded 7 control subjects (5 female) who showed no symptoms, 2 subjects with AMS (both femalel and 4 .subjects additionally with high altitude pulmonary oedema (2 female). On sampling, the blood was immediately centrifuged, the plasma separated and maintained in liquid nitrogen until analysed in London. Hormone determination was performed on extracted plasma as described by Chard and Fors/ing (1976).
H
A grant from the Wellcome Trust is gratefully acknowledged and Grant No. 47053 from the Rush Medical Center.
Received: 20 Jan. 1978
Accepted: 26 June 1978
0018-5043/78
• 05.00
•
4
•
~
•
3
2
• !o!••
units Im I)
(IJ
•
• •
~
-0-
••
ascent descent Na Mt. sickness
acute Mt. AMS + sickness pul. oedema
Fig. 1 Concentration of vasopressin (ADH) in plasma of control subjects and subjects with acute mountain sickness: _ peripheral oedema • no peripheral oedema.
References
Chard, T, M.L. Forsling: 'Hormones in Bood'. Ed. H.N. Antoniades, Harvard University Press, Cambridge (Mass.) pp. 485-516 (1976) Fors/ing, M.L., J.S. Milledge: J. Physiol. 207: 52-53 P (1977) Hackett, P.H., D. Rennie, H.D. Levine: Lancet (11): 11491154 (1976) Singh,l., M.S. Malhotra, P.K. Khanna, R.D. Nanda, T. Purshottam, TN. Upadhyay, U. Radhakrishnan, H.D. Drahmachari: In J. Biometeorol. 18: 21l-22l (1974) Requests for reprints should be addressed to: Dr. M.L. Forsling, Physiology Department, The Middlesex Hosiptal Medical School, London, WIP 6DB. (United Kingdom)
© 1978 Georg Thieme Publishers
Downloaded by: NYU. Copyrighted material.
•
o
Results and Discussion The resuits are summarised in the figure. The plasma vasopressin in the control group was 1.1 ± 0.15 JiU/ml (± SEM, n = 7) as compared with 0.7 ± 0.17 JiU/ml (n = 10) in a previous study at sea level and there was no difference in vasopressin concentration between the ascent and the descent from 5.300 m. Thus altitude alone did not appear to affect the release of vasopressin. The resul ts were similar to those seen with acute hypoxia, when a value of l.1 JiU/ml was recorded (Forsfing and Miliedge 1977). Plasma vasopressin was significantly elevated in those subjects with AMS to a me an concentration of 2.2 ± 0.5 (n = 7, P < 0.01). The results of Singh, Ma/hotra, Khanna, Nanda,PurshaUam, Upadhyay, Radhakrishnan and Brahmachari (1974) suggest a similar trend. I! was also noted that five of the ciimbers with AMS also suffered with peripheral oedema as indicated in the figure. The present studies do not indicate whether the increased vasopressin secretion was a primary change and a major factor in the pathophysiology of AMS or secondary to a shift in fluid from the vascular bed or indeed to stress. The concen trations recorded would have been sufficient to cause a degree of water retention provided that the renal sensitivity to vasopressin was unchanged.
1132-0571
5
