SummaryThe relationship between breath hydrogen excretion and intestinal ischemia was investigated in nine mechanically ventilated dogs under pentobarbital anesthesia. An ileal segment was isolated in situ, ligated a t each end, and insufflated with hydrogen. Expired air was collected at intervals. Blood volume was reduced 30% by three successive equivalent hemorrhages 10 min apart. Local bowel ischemia was produced by clamping the blood supply to the isolated segment for 10 min. Graded hemorrhage produced stepwise reductions in breath hydrogen concentration, to 77 + 13, 66 -t-15, and 35 f 8% (mean f S.E.) of baseline after the first, second, and third hemorrhages, respectively. These reductions correlated highly (r = 0.84; P < 0.01) with declines in mean aortic blood pressure. Occlusion of blood supply caused a significant ( P < 0.025) decrease in breath hydrogen concentration and excretion to 39 k 14% of baseline. Termination of occlusion was followed within 2 min by a 7-fold increase in breath Hz concentration above the original baseline, probably reflecting reactive hyperemia. Breath hydrogen measurements appear to reflect functional (hemorrhagic shock-induced) and mechanical (vascular occlusion induced) enteric ischemia in dogs.
SpeculationMonitoring of breath Hz excretion in the infant at risk for necrotizing enterocolitis may indicate the development of enteric hypoperfusion. Inhibition of transfer of Hz into the portal circulation in the presence of reduced mesenteric blood flow may contribute to distention of the bowel in necrotizing enterocolitis and further impede intestinal perfusion.Exhaled hydrogen (H2) is an accurate, noninvasive index of intestinal carbohydrate malabsorption, (6,12,13,17,18,20). Hz in breath is the product of: (1) incomplete absorption of sugar substrate; (2) intraluminal fermentation of substrate by enteric flora yielding Hz; (3) transfer of Hz into the portal circulation; (4) perfusion of the lungs resulting in diffusion of HZ into the air spaces; and (5) excretion of HZ from the alveoli. Although the availability of carbohydrate and bacteria governs production of Hz, the transfer of Hz from the intestinal lumen to the lung appears to be dependent on circulatory factors. By fitting absorption parameters for inert gases to models of interaction between perfusion and diffusion, Levitt and Levitt (14) demonstrated that the rate of absorption of HZ from the intestine is primarily a function of intestinal blood flow, being only marginally affected by diffusion. Enteric perfusion being the rate-limiting step in absorption of hydrogen, changes in intestinal blood flow sufficient to produce ischemia should be reflected in breath Hp excretion. The purpose of the present study was to determine the effects of functional (hemorrhagic shock-induced) and mechanical (vascular occlusioninduced) reduction in intestinal perfusion on Hp excretion in breath.
MATERIALS AND METHODS
PREPARATION OF INTESTINAL SEGMENTSTransfer of Hz from the intestinal lumen to alveolar air was measured using closed i...