Pt. Nowicki et La. Minnich, Effects of systemic hypotension on postnatal intestinal circulation: role of angiotensin, AM J P-GAST, 39(2), 1999, pp. G341-G352
Citations number
31
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
Systemic hypotension causes a greater degree of vasoconstriction in intesti
ne from 3- than from 35-day-oId postnatal swine. To determine the basis for
this age-dependent difference, systemic hypotension (pressure reduction to
similar to 50% of baseline) was induced by creating pericardial tamponade
in postnatal swine instrumented to allow measurement of intestinal hemodyna
mics and oxygenation in vivo. Hypotension caused gut vascular resistance to
increase 77 +/- 6% in 3-day-old subjects but only 18 +/- 3% in 35-day-old
subjects. Prior blockade of alpha(1)-receptors with phentolamine, vasopress
in receptors with [d(CH2)(5),D-Phe(2),Ile(4),Ala(9)-NH2]AVP, or surgical de
nervation of the gut loop had no effect on hypotension-induced gut vasocons
triction. Losartan, which blocks angiotensin AT(1) receptors, significantly
attenuated hypotension-induced gut vasoconstriction in both age groups. BQ
-610, which blocks endothelin ETA receptors, also limited the magnitude of
vasoconstriction but only in younger subjects. This effect may have been co
nsequent to an interaction between endothelin and angiotensin, inasmuch as
a subpressor concentration of endothelin increased the contractile response
to angiotensin in mesenteric artery rings. The substantial rise in 3-day-o
ld gut vascular resistance was partly consequent to a locally mediated vaso
constriction that occurred in response to pressure and/or flow reduction du
ring hypotension, as evidenced by the significant attenuation of this const
riction when blood flow was held constant by controlled-flow perfusion to t
he gut loop during hypotension. Intestinal O-2 uptake was compromised to a
significantly greater degree in 3- than in 35-day-old subjects during hypot
ension. This difference was primarily due to the inability of younger intes
tine to increase O-2 extraction in the face of reduced blood flow and may b
e mediated, in part, by an effect of angiotensin II on intestinal capillary
perfusion.