Differentiation of the peptidergic vasoregulatory response to standardizedsplanchnic hypoperfusion by acute hypovolaemia or sepsis in anaesthetized pigs

This study was performed to integratively investigate the vasoregulatory re sponse during standardized splanchnic hypoperfusion in pigs. Splanchnic per fusion was reduced to 50% of baseline by: haemorrhage by 20 and 40% of the estimated total blood volume; femoral Venous infusion of live E. coli to es tablish sepsis of systemic origin; portal venous infusion of live E. coli t o establish sepsis of splanchnic origin. Invasive haemodynamic monitoring a nd radioimmunoassay analyses of arterial plasma concentrations of angiotens in II, endothelin-1 and atrial natriuretic peptide were carried out. Acute hypovolaemia reduced systemic and splanchnic Vascular resistances following transient increases and increased angiotensin II levels (+587%), whereas e ndothelin-1 and atrial natriuretic peptide levels did not change significan tly. Systemic sepsis following femoral venous infusion of E. coli resulted in increased splanchnic vascular resistance and increased levels of angiote nsin II (+274%), endothelin-1 (+134%) and atrial natriuretic peptide (+185% ). Infusion of E. coli via the portal venous route induced an increase in s planchnic vascular resistance associated with particularly elevated levels of angiotensin II (+1770%) as well as increased endothelin-1 (+201%) and at rial natriuretic peptide (+229%) concentrations. Hypovolaemia and sepsis, a lthough standardized with a predefined level of splanchnic hypoperfusion, e licited differentiated cardiovascular and vasopeptidergic responses. Sepsis , particularly of portal origin, notably increased splanchnic Vascular resi stance related to increased production of the vasoconstrictors angiotensin II and endothelin-1. The role of atrial natriuretic peptide as a vasodilato r seems to be of subordinate importance in hypovolaemia and sepsis.