Abstract
Humans are destined to explore space, yet critical illness and injury may be catastrophically limiting for extraterrestrial travel. Humans are superorganisms living in symbiosis with their microbiomes, whose genetic diversity dwarfs that of humans. Symbiosis is critical and imbalances are associated with disease, occurring within hours of serious illness and injury. There are many characteristics of space flight that negatively influence the microbiome, especially deep space itself, with its increased radiation and absence of gravity. Prolonged weightlessness causes many physiologic changes that are detrimental; some resemble aging and will adversely affect the ability to tolerate critical illness or injury and subsequent treatment. Critical illness-induced intra-abdominal hypertension (IAH) may induce malperfusion of both the viscera and microbiome, with potentially catastrophic effects. Evidence from animal models confirms profound IAH effects on the gut, namely ischemia and disruption of barrier function, mechanistically linking IAH to resultant organ dysfunction. Therefore, a pathologic dysbiome, space-induced immune dysfunction and a diminished cardiorespiratory reserve with exacerbated susceptibility to IAH, imply that a space-deconditioned astronaut will be vulnerable to IAH-induced gut malperfusion. This sets the stage for severe gut ischemia and massive biomediator generation in an astronaut with reduced cardiorespiratory/immunological capacity. Fortunately, experiments in weightless analogue environments suggest that IAH may be ameliorated by conformational abdominal wall changes and a resetting of thoracoabdominal mechanics. Thus, review of the interactions of physiologic changes with prolonged weightlessness and IAH is required to identify appropriate questions for planning exploration class space surgical care.
Highlights
Humans are destined to explore space, yet critical illness and injury may be catastrophically limiting for extraterrestrial travel
Humans are superorganisms living in symbiosis with their microbiomes, whose genetic diversity dwarfs that of humans
intra-abdominal hypertension (IAH) and abdominal compartment syndrome have been conceptualized as having a largely mechanical pathogen esis, occurring when the physical capacity of the abdominal container is exceeded by the addition of surgical packing, abdominal viscera edema, hematomata and/or ascites all of which increases the intra-abdominal volume (IAV)
Summary
Cardiac β-receptor sensitivity Dysrhythmias Perfusion and MAP= Cardiac reserve Cardiac atrophy Vasoconstriction Venous capacitance Stomach Nausea – vomiting Gastroparesis – GRV Gastroesophageal reflux. Microbial Biome Pathogenicity Antibiotic resistance Cell wall thickness Biofilm density
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