Role of endothelium and nitric oxide in the in vitro response of equine colonic venous rings to vasoconstrictor agents.

OBJECTIVE

To determine in vitro contractile responses of equine colonic veins to various vasoconstrictor agents.

METHODS

Colonic veins collected from 8 adult horses.

METHODS

Veins were cut into 4-mm-wide rings, placed in organ baths at 37 C, and attached to a force-transducer interfaced with a polygraph; 2 g of tension was applied, and rings were allowed to equilibrate for 45 minutes. Bath solution was replaced, and tension was reapplied at 15-minute intervals. Cumulative concentration responses (10(-8) to 10(-4) M) were determined for each agent, using separate rings (n = 8). Three vein groups were evaluated: endothelium-intact, endothelium-denuded, and N omega-nitro-L-arginine methyl ester (L-NAME, 10(-5) M)-treated. Maximal responses by each vein to each agent were considered 100%; responses to lower concentrations were calculated as percentage of maximum.

RESULTS

Considering all vein groups, comparison of the doses that caused 50% of the maximal contraction revealed relative sensitivity of colonic veins to be: angiotensin II (ANG) > thromboxane B2 analogue (TXB) > 5-hydoxytryptamine (5HT) > norepinephrine (NE) > histamine (HST) > prostaglandin F2 alpha (PGF) > vasopressin (VP). Compared with ANG, PGF, TXB, and VP, treatment with HST, 5HT, and NE evoked significantly greater responses. Endothelium-denuded and L-NAME-treated colonic veins had significantly greater maximal contractile responses than did endothelium-intact veins.

CONCLUSIONS

Response of colonic veins to vasoconstrictor agents was differential; sensitivity was not altered by endothelium removal or L-NAME treatment; maximal responses of endothelium-intact veins were greater than those of endothelium-denuded and L-NAME-treated veins; and responses of endothelium-denuded and L-NAME-treated veins were not different.

CONCLUSIONS

Alterations in colonic veins that mimic conditions associated with large-colon volvulus may contribute to blood flow alterations, edema formation, and vascular responses to hypovolemic and endotoxic shock.