Effects of systemic hypotension on postnatal intestinal circulation: role of angiotensin

Citation
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
ISSN journal
01931857 → ACNP
Volume
39
Issue
2
Year of publication
1999
Pages
G341 - G352
Database
ISI
SICI code
0193-1857(199902)39:2<G341:EOSHOP>2.0.ZU;2-B
Abstract
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.