Effects of ischemia and dimethyl sulfoxide on equine jejunal vascular resistance, oxygen consumption, intraluminal pressure, and potassium loss

Abstract

SUMMARY Physiologic effects of 1 hour of ischemia and 1 hour of reperfusion on equine jejunum and protective effects of systemic administration of dimethyl sulfoxide ( dmso , 1 g/kg of body weight) were investigated in 18 ponies, using neurally intact segments of jejunum perfused at constant flow with heparinized blood. Ponies were allotted to 4 groups: group 1, saline solution administered (control, n = 3); group 2, dmso administered ( dmso , n = 3); group 3, ischemia induced and saline solution administered (ischemia, n = 6); and group 4, ischemia induced and dmso administered (ischemia- dmso , n = 6). Intestinal vascular resistance ( r , mm of Hg/ml/min/100 g), oxygen consumption (V o 2 , ml/min/100 g), frequency and amplitude of rhythmic changes in intraluminal pressure, intestinal compliance ( c , ml/mm of Hg), and arteriovenous potassium concentration difference (Δ av [K + ], mEq/L) were determined and compared with stable preischemic values within groups. There were no significant changes in any variable in ponies of groups 1 or 2. In ponies of group 3, significant ( P ≤ 0.05) changes included: an initial increase in r during reperfusion, followed by a decrease to values below preischemic values by 15 minutes of reperfusion; decreased V o 2 during the entire reperfusion period; increased amplitude of rhythmic contractions during initial reperfusion; decreased frequency of rhythmic contractions during ischemia; and increased Δ av [ k + ] during initial reperfusion. Changes in ponies of group 4 were identical to changes in ponies of group 3, with the exception that dmso administration prevented the decrease in r during reperfusion. Although the action of dmso in modulating postischemic vascular reactivity may warrant further investigation, its failure to maintain tissue V o 2 or prevent tissue potassium loss suggested that dmso was not effective in preventing equine jejunal injury resulting from complete arterial occlusion followed by reperfusion.