Abstract
Objective: Mesenteric ischemia/reperfusion (I/R) is associated with cardiac dysfunction. Mesenteric lymph primes polymorphonuclear leukocytes (PMNs) for increased superoxide release following I/R. We hypothesized that mesenteric I/R causes myocardial edema resulting in myocardial dysfunction, and that diverting mesenteric lymph would preserve myocardial function.
Methods: Two canine groups were studied: lymphatic diversion (LD) and no lymphatic diversion (No LD). Preload recruitable stroke work, ±dp/dtmax, isovolumic relaxation (tau), cardiac output, and myocardial water content (MWC) were determined. I/R consisted of 60 min of ischemia followed by 180 min of reperfusion. Myocardial myeloperoxidase (MPO) was measured as an index of PMN leukosequestration. In addition, mesenteric lymph harvested after I/R was infused into normal canines and all variables measured.
Results: MWC increased from baseline in No LD. Tau and −dp/dtmax were significantly affected in No LD, but not in LD. After mesenteric I/R, mesenteric lymph primed PMNs for increased superoxide production. Lymph diversion resulted in significantly lower myocardial MPO. With reinfusion of I/R lymph, MWC and tau increased. MPO was also increased post I/R mesenteric lymph reinfusion.
Conclusions: Our data indicate that myocardial dysfunction after mesenteric I/R is due to lymph-induced, PMN-mediated microvascular alterations and myocardial edema.