The important distinction between those with or without gut mucosal ischaemia
One of the features of gut mucosal ischaemia, which appears to a
common occurrence in marathon runners, is diarrhoea. This may be due to an
inhibition of the absorptive flux of water, which is dependent upon the
carrier-mediated absorption of solute (principally sodium), or due to the
active stimulation of a secretory flux as in cholera. Of these two
possibilities the former is the more likely for the ischaemia is greatest
and often confined to the superficial layers of the mucosa, where
absorption occurs, rather than the crypts where secretion evidently
occurs. In runners who develop ischaemic mucosa net absorption and weight
gain is, therefore, unlikely to occur unless the fluids the drink are
accompanied by glucose as in those fluids used to induce a net absorptiive
flux in patients with cholera.
Those who develop gut mucosa ischaemia are more likely to have
hepatic ischaemia and even ischaemia in other organs. In which case their
intracellular pH may be abnormally low, their K(atp) channel activated,
and their sodium pump impaired. If a net flux of sodium and other solute
occurs into the cells as a result of these changes the sodium
concentration in ECF may fall and the ICF volume may rise as the ECF
volume falls independently of the volume of fluid drunk.
Shires's "third spacing", to which I referred in my earlier
communication, is evidently an intracellular rather than an extracellular
event, as I had erroneously suggested. In which case any weight gain and
oedema that might occur will not induce or compound the severity of
ischaemia by increasing the intercapillary distance, as I had suggested,
but by increasing the distance between blood and mitochondria.
Knowing whether marathon runners have developed gut mucosal ischaemia
or not would seem essential in determining the causes of hyponatraemia and
more importantly in deciding the most appropriate therapy for collapsed
runners. Any organ dysfunction or failure that occurs is likely to be
confined to those who have developed gut mucosal ischaemia.
Excessive oral fluid intake would seem, therefore, more likey to
cause pathological problems in those who do not develop gut mucosal
ischaemia (?the occasional marathon runner) than in those that do (?the
serious marathon runners). As in surgery fluid intake during a marathon
would seem to be desirable for it can prevent the development of gut
mucosa ischaemia and its adverse consequences. It is much more difficult
to reverse gut mucosal ischaemia and prevent its adverse consequences.
There is, therefore, the danger that overzealous intravenous therapy in a
collapsed runner may do more harm than good.
Rapid Response:
The important distinction between those with or without gut mucosal ischaemia
One of the features of gut mucosal ischaemia, which appears to a
common occurrence in marathon runners, is diarrhoea. This may be due to an
inhibition of the absorptive flux of water, which is dependent upon the
carrier-mediated absorption of solute (principally sodium), or due to the
active stimulation of a secretory flux as in cholera. Of these two
possibilities the former is the more likely for the ischaemia is greatest
and often confined to the superficial layers of the mucosa, where
absorption occurs, rather than the crypts where secretion evidently
occurs. In runners who develop ischaemic mucosa net absorption and weight
gain is, therefore, unlikely to occur unless the fluids the drink are
accompanied by glucose as in those fluids used to induce a net absorptiive
flux in patients with cholera.
Those who develop gut mucosa ischaemia are more likely to have
hepatic ischaemia and even ischaemia in other organs. In which case their
intracellular pH may be abnormally low, their K(atp) channel activated,
and their sodium pump impaired. If a net flux of sodium and other solute
occurs into the cells as a result of these changes the sodium
concentration in ECF may fall and the ICF volume may rise as the ECF
volume falls independently of the volume of fluid drunk.
Shires's "third spacing", to which I referred in my earlier
communication, is evidently an intracellular rather than an extracellular
event, as I had erroneously suggested. In which case any weight gain and
oedema that might occur will not induce or compound the severity of
ischaemia by increasing the intercapillary distance, as I had suggested,
but by increasing the distance between blood and mitochondria.
Knowing whether marathon runners have developed gut mucosal ischaemia
or not would seem essential in determining the causes of hyponatraemia and
more importantly in deciding the most appropriate therapy for collapsed
runners. Any organ dysfunction or failure that occurs is likely to be
confined to those who have developed gut mucosal ischaemia.
Excessive oral fluid intake would seem, therefore, more likey to
cause pathological problems in those who do not develop gut mucosal
ischaemia (?the occasional marathon runner) than in those that do (?the
serious marathon runners). As in surgery fluid intake during a marathon
would seem to be desirable for it can prevent the development of gut
mucosa ischaemia and its adverse consequences. It is much more difficult
to reverse gut mucosal ischaemia and prevent its adverse consequences.
There is, therefore, the danger that overzealous intravenous therapy in a
collapsed runner may do more harm than good.
Competing interests:
None declared
Competing interests: No competing interests