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(Circulation. 1998;97:119-120.)
© 1998 American Heart Association, Inc.

Correspondence

The Apollo 15 Space Syndrome

William J. Rowe, MD

Former Assistant Clinical Professor of Medicine, Medical College of Ohio at Toledo

To the Editor:

With the permanent space station planned for the near future and with the recent surge of interest regarding manned missions to Mars, the potential for life-threatening risks looms dead ahead. In 1971 on the Apollo 15 lunar mission, astronauts Irwin and Scott both experienced severe pain and edema of the fingertips.¹ In addition, the mission was considered an "anomaly" since it was the first during any space mission distinguished by significant arrhythmias, more severe in Irwin's case with a brief loss of consciousness during an episode of bigeminy after return to the command module.² Twenty-one months later, Irwin experienced a myocardial infarction.² It is conceivable that Irwin's infarct was not coincidental but was at least partially triggered by endothelial injuries resulting from the Apollo 15 mission.

In the presence of microgravity, there is invariably a shift of fluid to the upper part of the body. But in addition on the Apollo 15 mission, there was a malfunction of the Insuit water devices, resulting in water deprivation, particularly in Irwin's case during the three extravehicular activities (EVAs) of up to 7 hours each, whereas Scott's Insuit apparatus functioned partially.² Irwin, sweating profusely and extremely thirsty during the EVAs, lost 5% of his weight compared with his mean preflight weight (from 74.3 to 70.8 kg), whereas Scott lost about half that much (from 81.1 to 78.9 kg).² This dehydration would have intensified the potential for microgravity-related renin-angiotensin elevations² and catecholamine elevations,³ with the latter aggravated by pain-provoked sleep deprivation as well.¹

Before the Apollo 15 mission, there was a predisposition for a significant magnesium ion deficit, which may persist for several months, since training occurred "in intense summer heat."^{2 3} This deficit would be compounded by a magnesium deficit secondary to skeletal muscle atrophy resulting from even this brief space mission (12 days).² This conceivably could predispose to the serious arrhythmias and potassium deficits,² potential catecholamine elevations with enhanced thrombus formation, and potential endothelial injuries of both peripheral and coronary vessels.^{3 4}

With a water deficit, in addition to compensatory renin-angiotensin elevations,² there is a loss of protection from increased free radicals (superoxide anions),⁵ which inactivate nitric oxide⁶ conducive to endothelial injuries and in turn to vasospasm.³

The Apollo 15 space syndrome, characterized by extremely painful swollen fingertips possibly secondary to peripheral vasospasm and compression by fluid, trapped distally, could serve as a warning that coronary vasospasm (possibly silent³ ) might also exist, predisposing ultimately to a myocardial infarction with^{4 6} or without³ an associated atherosclerotic plaque rupture, even without radiation effects playing a role.^{2 7}

Finally, this syndrome may be ultimately more common on longer space missions (with invariable angiotensin elevations⁸ and potential imbalance⁶ with nitric oxide reductions and more frequent magnesium ion deficits⁸ ), portending serious endothelial dysfunction.³ Since young women retain magnesium better on marginal magnesium intakes than young men,⁹ and estrogens have been shown to have several cardiovascular protective effects,¹⁰ it is tempting to speculate that young female astronauts are far less likely to experience this syndrome.

References

1. Irwin JB. To Rule the Night: The Discovery Voyage of Astronaut Jim Irwin. Philadelphia, Pa: Holman; 1973:73–74.

2. Johnston RS, Dietlein LF, Berry CA, eds. Biomedical Results of Apollo. Washington, DC: National Aeronautics and Space Administration; 1975:227–264,573–579,581–592. NASA SP-368.

3. Rowe WJ. Extraordinary unremitting endurance exercise and permanent injury to normal heart. Lancet. 1992;340:712–714.[Medline] [Order article via Infotrieve]

4. Hennig B, Toborek M, McClain CJ, Diana JN. Nutritional implications in vascular endothelial cell metabolism. J Am Coll Nutr. 1996;15:345–358.[Abstract]

5. Gutteridge JMC. Biological origin of free radicals, and mechanisms of antioxidant protection. Chem Biol Interact. 1994;91:133–140.[Medline] [Order article via Infotrieve]

6. Gibbons GH. Endothelial function as a determinant of vascular function and structure: a new therapeutic target. Am J Cardiol. 1997;79:3–8.[Medline] [Order article via Infotrieve]

7. Corn BN, Trock BJ, Goodman RL. Irradiation-related ischemic heart disease. J Clin Oncol. 1990;8:741–750.[Abstract]

8. Atkov OY, Bednenko VS. Hypokinesia and Weightlessness: Clinical and Physiologic Aspects. Madison, Wis: International Universities Press; 1992:10–11.

9. Seelig, MS. Increased need for magnesium with the use of combined oestrogen and calcium for osteoporosis treatment. Magnes Res. 1990;3:197–215.[Medline] [Order article via Infotrieve]

10. Kauser K, Rubany GM. Vasculoprotection by estrogen contributes to gender differences in cardiovascular diseases: potential mechanism and role of endothelium. In: Rubany GM, Dzau VJ, eds. The Endothelium in Clinical Practice. New York, NY: Marcel Dekker; 1997:439–467.

This article has been cited by other articles:

				W. J. Rowe The Case for a Subcutaneous Magnesium Product and Delivery Device for Space Missions J. Am. Coll. Nutr., October 1, 2004; 23(5): 525S - 528S. [Abstract] [Full Text] [PDF]

				A. Paskovaty and E. A. O'Rangers Health Consequences of Spaceflight Journal of Pharmacy Practice, April 1, 2003; 16(2): 101 - 106. [Abstract] [PDF]

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