Quantitative study of intestinal fluid loss in irreversible hemorrhagic shock

Porciuncula, Camilo I.; Crowell, Jack W.

doi:10.1152/ajplegacy.1963.205.2.261

Cited by 13 publications

(4 citation statements)

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“…Small intestinal fluid and electrolyte transport during hemorrhagic hypotension has been studied by several authors using different experimental animals and methods with varying results. Some investigators have found a increase in fluid and electrolyte absorption after hemorrhage, at least during the early phase (Mailman & Ingraham 1971, Fromm 1973, Mariscotti et al 1977, whereas others, mainly using dogs, have observed a decrease in absorption or a pronounced secretion (Goldberg & Fine 1945, Porciuncula & Crowell 1963, Cook et al 1971.…”

Section: Discussionmentioning

confidence: 99%

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

Redfors

Hallbäck

Haglund

et al. 1984

Acta Physiologica Scandinavica

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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.

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Section: Discussionmentioning

confidence: 99%

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

Redfors

Hallbäck

Haglund

et al. 1984

Acta Physiologica Scandinavica

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“…Previous studies on fluid and electrolyte transport in the small intestine after hemorrhage have revealed either an increase in absorption (Mailman & Ingraham 1971, Fromm 1973, Mariscotti et al 1977 or a decrease which in some studies even turned into a net fluid secretion (Goldberg & Fine 1945, Porciuncula & Crowell 1963, Cook et al 1971. The inconsistent results are probably due to the fact that hemorrhage induces varying changes in blood flow as well as varying nervous and hurnoral changes that directly or indirectly influence intestinal transport capacity.…”

mentioning

confidence: 97%

Effects of hemorrhage on intramural blood flow distribution, villous tissue osmolality and fluid and electrolyte transport in the cat small intestine

Redfors

Hallbäck

Sjövall

et al. 1984

Acta Physiologica Scandinavica

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The hemodynamic response in the parallel-coupled vascular sections of the cat small intestine were studied before, during and after a two hour period of hemorrhage (about 30 per cent of estimated blood volume). Fluid and electrolyte transport and villous tissue osmolality were also measured. Biopsies for histology were taken at the end of all experiments. The animals were divided in two groups, undamaged and damaged, according to the degree of mucosal damage observed. 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 flows. Total intestinal blood flow was lower in the damaged as compared to the undamaged group during hypovolemia. No difference in absorptive site blood flow was observed between the two groups during hypovolemia. Furthermore, no decrease of red blood cell flow in the "villi" was recorded in either group after hemorrhage. Consequently, mucosal lesions developed despite an unchanged oxygen transport capacity to the villi. The pathophysiology of the mucosal lesions is briefly discussed. Net fluid and sodium absorption was after hemorrhage increased in the undamaged group reflecting a decrease in the tissue to lumen transport of sodium. After retransfusion net fluid and sodium absorption returned to control. In the damaged group, however, net fluid and sodium absorption was decreased after hemorrhage. The increased rate of fluid and electrolyte transport observed in the undamaged small intestine after hemorrhage, is proposed to be an important mechanism for fluid replacement after hemorrhage.

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“…These derangements lead to fluid loss into the interstitium and lumen of the intestine, aggravating the relative hypovolemia due to sequestration [18]. Similar lesions have been reported in human intestinal specimens obtained during or after a period of shock and/or hypotension [10].…”

Section: Discussionmentioning

confidence: 59%

Hemorrhagic shock in the dog

et al. 1985

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Oxygen consumption, hemodynamics, and regional blood flow (with the radioactive microspheres technique) were determined in 12 anesthetized dogs subjected to hemorrhagic shock. The animals were kept in hypotension at 40 mmHg, until 15% of the maximum shed blood had been infused to keep arterial pressure stable, whereafter all the shed blood was retransfused. Cardiac output (CO) decreased to 33% and 25% of preshock values in survivors (S) and nonsurvivors (NS), respectively, and after retransfusion it was significantly higher in S. After retransfusion, NS showed a higher arterial pCO2 than S adding a respiratory component to the metabolic acidosis that occurred during and after hemorrhage. Blood flow to the brain was not impeded during shock, but as CO decreased the fraction delivered to the brain was increased 2.6-3.3-fold. Myocardial blood flow decreased to about 28% of preshock values immediately after hemorrhage, and increased to about 54% at the end of hemorrhage. After retransfusion S had a higher myocardial flow than NS. The flow to the gut paralleled the decrease in CO during hemorrhage and immediately after retransfusion NS exhibited an overperfusion in ileum and colon compared to the preshock values. Kidney blood flow fell progressively during the course of hypotension, similarly in S and NS. After retransfusion it was normalized in S but not in NS. The preshock flow to pancreas was significantly higher in S than in NS, but during and after shock the blood flow did not differ between S and NS.

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Quantitative study of intestinal fluid loss in irreversible hemorrhagic shock

Cited by 13 publications

References 0 publications

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

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

Effects of hemorrhage on intramural blood flow distribution, villous tissue osmolality and fluid and electrolyte transport in the cat small intestine

Hemorrhagic shock in the dog

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