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Dallas, TX
Galveston, TX
Dr. Tao is an Assistant Professor at The University of Texas Southwestern Medical Center. Dr. Mathru is the Clara Tibbetts Phillips Professor of Anesthesiology and the Director of the Surgical Intensive Care Unit, The University of Texas Medical Branch.
Correspondence to: Mali Mathru, MD, Department of Anesthesiology, The University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555-0591; e-mail: mamathru{at}utmb.edu
The intestines have been a major focus of investigations in critically ill patients, either as the "motor" or as the target organ of multiorgan dysfunction. Mucosal ischemia, and bacterial and endotoxin translocation have been implicated in a variety of situations such as shock, trauma, burn, sepsis, and cardiopulmonary bypass. It is generally believed that vasoactive substances and cytokines cause intense regional vasospasm and blood flow redistribution, leading to gut mucosal ischemia.1
In the current issue of CHEST (see page 688), Lehtipalo et al used a porcine model of graded regional hypotension of the intestines to evaluate the effects of therapy with positive end-expiratory pressure (PEEP) and dopexamine on gut blood flow and mucosal perfusion. This is an interesting approach since gut mucosal dysfunction and ARDS are important components of multiorgan dysfunction syndrome.2
Their data showed that applying a PEEP of 10 cm H2O caused a predicted increase in central venous pressure, and therefore a decrease in intestinal perfusion pressure (IPP). The use of dopexamine predictably induced an increase in cardiac output, a decrease in systemic vascular resistance (SVR), and a decrease in mean arterial pressure (MAP), which further reduced IPP. At an IPP of 
45 mm Hg, there was a decrease in mucosal perfusion. Intestinal oxygen uptake became supply-dependent at an IPP of 33 mm Hg, along with increased lactate production.
The article adds to the information about the mechanical threshold of intestinal hypoperfusion. While a MAP of 45 mm Hg appears to be low for most clinical settings, an IPP of 45 mm Hg can be easily encountered in patients with right heart failure or in those receiving high levels of PEEP. In their experimental model, an occluder was placed on the superior mesenteric artery, and an ultrasonic flow probe was placed on the mesenteric vein. One has to ask whether the observed findings can be seen in an intact subject with complete innervation of the mesenteric vessels, given a host of neurohormonal responses during acute and chronic stress that might influence the intestinal vascular tone and the presence of an effective autoregulation and redistribution system.1
Experimental evidence suggests that different vascular beds have different slopes for their pressure-flow relationships and different zero-flow pressure intercepts. Accordingly, similar increases in MAP induce different degrees of increasing blood flow in various vascular beds.3
It would also be interesting to find out what added effects the vasoactive drugs that are used in the critical care setting, especially 
-agonists, would have on gut mucosal perfusion. Would they improve gut blood flow by increasing the perfusion pressure or compromise it by constricting intestinal vessels? Obviously, more studies are necessary to address this interesting topic.
Another interesting question that this article raises is the effect of dopexamine on gut mucosal blood flow. While many investigators have shown that dopexamine has attenuated mucosal ischemia4 5 and has improved mucosal tissue histology,6 others have found that it failed to show a direct effect on mucosal permeability or a direct influence on multiorgan dysfunction in critically ill patients,7 and clinical trials have failed to show improvement in survival among patients after major abdominal surgery.8 In the current article, dopexamine, either alone or added to PEEP, further reduced IPP but did not significantly influence mucosal perfusion. With the reduction in SVR that is associated with dopexamine, it appears reasonable to believe that the reduction in IPP was due to a decrease in perfusion pressure. These findings, along with the observed threshold of gut perfusion, suggest that the gut may be an organ in which perfusion is pressure-dependent. On the other hand, since the decrease in SVR did not cause an increase in mucosal perfusion, one may suspect that blood was preferentially shunted away from the mucosa into other areas of the intestines or the body.
Given the larger amount of data on mucosal blood flow, and the numerous proposed mechanisms contributing to its regulation, more comprehensive studies are necessary to further characterize intestinal and mucosal blood flow. In addition, correlative studies using clinically available means of quantitating tissue ischemia, such as mucosal tonometry,9 may provide therapeutic end points in the treatment of the critically ill. The findings of Lehtipalo et al certainly address the issue from a mechanical point of view and provide a guideline for hemodynamic management to maintain a target MAP, not only for such well-known pressure-dependent organs as the heart, but also for the motor of multiorgan dysfunction, the intestines.
Footnotes
This article was supported by the Department of Anesthesiology, The University of Texas Medical Branch.
References
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