Blood flow distribution, villous tissue osmolality and fluid and electrolyte transport in the cat small intestine during regional hypotension

Abstract

The hemodynamic reactions of the parallel coupled vascular circuits in the cat small intestine were studied before, during and after a two-hour period of intestinal hypotension induced by lowering the intestinal arterial inflow pressure by partially occluding the superior mesenteric artery during a continuous stimulation of the postganglionic nerves to the small intestine. Furthermore, fluid and electrolyte transport and villous tissue osmolality were measured. A histological examination of biopsies taken during and after the hypotensive period was also carried out. The animals were divided into two groups (undamaged and damaged) according to the histological appearance of the intestinal mucosa. The hemodynamic reactions were investigated with a method that made it possible to study total intestinal, absorptive site ("villous"), nonabsorptive site ("crypt") and muscle layer blood flow. Total intestinal blood flow was lower in the damaged group than in the undamaged group during the arterial hypotension. However, absorptive site blood flow was similar in the two groups. Consequently, a significantly larger fraction of blood flow was distributed to the "villi" in the damaged group. Moreover, absorptive site red blood cell flow was only slightly reduced despite the development of mucosal ulcerations. These findings are discussed in relation to the pathophysiology of the mucosal lesions. Net fluid, net sodium and net chloride absorption was unchanged in the undamaged group whereas in the damaged group a marked decrease was observed after lowering the perfusion pressure. The decrease in net sodium absorption was due to a decrease in the lumen to tissue transport of sodium. Thus, the capacity of the small intestine to absorb fluid and electrolytes is unchanged even during a marked arterial hypotension with a pronounced decrease of intestinal blood flow as long as no mucosal damage has developed.

Feline Intestinal Ischemia and Reperfusion: Relation between Radical Formation and Tissue Damage

“…One characteristic feature is a drop in arterial blood pressure often seen after the ischemic period [2,15,16], a phenomenon that has been attributed to cardiodepressive material released from the intestine at the onset of reperfusion [ 17], However, this effect is lacking in the present experiments. We do not know the reason for the absent pressure fall, but it is not due to any effect of O X A N O ' or O X A N O H as seen in table 1.…”

“…We do not know the reason for the absent pressure fall, but it is not due to any effect of O X A N O ' or O X A N O H as seen in table 1. One possible explanation could be the relatively small amount of intestine, generally below 10 g, retaind in our experiments since there is a corre lation between the amount of intestine left in the animal and the magnitude of the pressure fall [15]. Alternatively, the explanation may be sought in the flow conditions during isch emia, as revealed by pressure development in previously published experiments [8] origi nally divided into two groups with ischemic blood flow either above (hiflow) or below (loflow) 5 ml X min-1 X 100 g*1.…”

“…Using this technique we have pre viously demonstrated xanthine-oxidase de pendent radical production after 120 min of intestinal ischemia [8]. In the present study we have investigated to what extent duration of ischemia ( 15,30 or 60 min) affects the rate of radical formation during subsequent reper fusion. We have also attempted to shed some light on the nature of the relationship between the amount of radicals formed and the histo logical appearance of the intestinal mucosa.…”

Claude H. Organ, Jr. Memorial Lecture: Splanchnic hypoperfusion provokes acute lung injury via a 5-lipoxygenase–dependent mechanism

“…(17) Following hemorrhagic shock, there is selective vasoconstriction of the intestinal inflow arterioles mediated predominantly via the renin-angiotension system. (18) Despite restoration of central hemodynamics, there is persistent vasoconstriction at all levels of the intestinal microvasculature due to the net effect of multiple agents, including endothelial derived factors and circulating vasoactive substances. {19, 20) The proinflammatory response stimulated by mesenteric I/R is complex, and the process whereby local gut events translate into distant organ injury remains unclear.…”

Microcirculatory Dysfunction in Sepsis

“…Most of it is directed to the superficial villi which is the primary site of absorption. In addition, this region has the highest metabolic rate [46,47].…”