Jim Irwin in the eighties enroute by "ambulance" at 3 M.P.H. (orbited Moon at 25,000 M.P.H.)
to the hospital in Turkey, after suffering a fall while searching for the remains of Noah's Ark on Mt. Ararat.
The Apollo 15 Space Syndrome CIRCULATION 1998; 97:119-120
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 lrwin and Scott both experienced severe pain and edema of the fingertips. 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. Twenty-one months later, Irwin experienced a myocardial infarction. 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. 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). This dehydration would have intensified the potential for microgravity-related renin-angiotensin elevations and catecholamine elevations, with the latter aggravated by pain-provoked sleep deprivation as well.
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). This conceivably could predispose to the serious arrhythmias and potassium deficits, 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 there is a loss of protection from increased free radicals (superoxide anions) which inactivate nitric oxide conducive to endothelial injuries and in turn to vasospasm.
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 silent) might also exist, predisposing ultimately to a myocardial infarction with[4,6] or without 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 elevations and potential imbalance with nitric oxide reductions and more frequent magnesium ion deficits), portending serious endothelial dysfunction. Since young women retain magnesium better on marginal magnesium intakes than young men, and estrogens have been shown to have several cardiovascular protective effects, it is tempting to speculate that young female astronauts are far less likely to experience this syndrome.
William J. Rowe, MD
Former Assistant Clinical Professor of Medicine
Medical College of Ohio at Toledo
1. lrwinJD. 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.
4. Hennig B. Toborek M, McClain CJ. Diana JN. Nuiritional implications in vascular endothelial cell metabolism. J Am Coll Nutr. 1996:15:345-358.
5. Gutteridge JMC. Biological origin of free radicals, and mechanisms of antioxidant protection. Chem Biol Interact. 1994:91:133-140.
6. Gibbons GH. Endothelial function as a determinant of vascular function and structure: a new therapeutic target. Am J Cardiol. 1997:79:3—8.
7. Corn BN, Trock BJ. Goodman RL. Irradiation-related ischemic heart disease.J Clin Oncol. 1990:8:741-750.
8. Alkov OY. Bednenko VS. Hypokmesia 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. MagHCS Res. 1990:3: 197-215.
10. Kauser K, Rubany GM. Vasculoprotection by estrogen contributes to gender differences in cardiovascular diseases: potential mechanism and role of endothclium. In: Rubany GM, Dzau VJ. eds. The Endothelium in Clinical Practice. New York, NY: Marcel Dekker: 1997:439-467.