Intestinal Tonometry Research Articles

Performance of automated air tonometry under hypothermia

Intestinal tonometry is used during hypothermic cardio-pulmonary bypass surgery to assess splanchnic perfusion. In an in vitro set-up the performance of automated air tonometry (TONOCAP) was tested for normo- and hypothermia. A 14-FG tonometry catheter was built into a testing chamber (100 cm(3)) perfused with blood from a cardio-pulmonary bypass circuit with P(a)co(2) held at 5.6-5.8 kPa (alpha-stat). P(r)co(2) from the balloon of the tonometry catheter was measured at intervals of 10 min at 37 degrees C and at 25 degrees C by the TONOCAP. Bias (precision) of P(r)co(2) - P(a)co(2 alpha-stat) and P(r)co(2) -P(a)co(2 pH-stat) at 37 degrees C blood temperature were low at 0.23 kPa (0.21) each. Tonometrically measured P(r)co(2) at 25 degrees C significantly differed from P(a)co(2 alpha-stat) bias (precision) of 2.00 kPa (0.11) but was similar to P(a)co(2 pH-stat) (0.30 kPa (0.11)). P(r)co(2) values as measured by the TONOCAP represent pH-stat approach. Identical blood gas management (pH- or alpha-stat) should be used for calculation of mucosal-arterial CO(2) difference (P(r-a)co(2) gap) or calculation of intramucosal pH.

Is intestinal tonometry a reliable method to detect histological changes after small bowel transplantation?

Postoperative complications after intestinal transplantation can be attributed to hypothermic storage and reperfusion injury. In this study, we sought to obtain evidence that intestinal pCO2 measurement can be a useful method for monitoring graft perfusion and early histological changes after small-bowel transplantation. Additionally, we evaluated the initial effects of isolated intestinal hypothermic perfusion (IHP) (at 4°C) on mucosal and serosal blood flow distribution, and we correlated these findings with other systemic and regional markers of mesenteric ischemia.

Intestinal nitric oxide output during reduced mucosal blood flow in healthy volunteers.

Nitric oxide regulates epithelial permeability and other properties of the intestinal mucosal barrier. It previously has been shown in animals that intestinal mucosal nitric oxide production is impaired during gut hypoperfusion. The study was performed to confirm the presence of intestinal mucosal nitric oxide production in humans and to investigate the effect of gut hypoperfusion due to moderate arterial hypotension on intestinal nitric oxide concentrations. Open study where each subject served as his own control. Clinical research laboratory. Nine healthy volunteers were intubated with a nasogastrointestinal tube for recordings in the distal duodenum. Intestinal nitric oxide output and motility were assessed by tonometry and manometry, respectively. Laser Doppler flowmetry and plasma angiotensin II concentration were used to investigate mucosal perfusion and a vasoregulatory response. Moderate hypotension was induced with lower body negative pressure over 1 hr. Intestinal nitric oxide production varied in parallel with the migrating motor complex. Low values were obtained during phase I and peak values during phase III. Lower body negative pressure was initiated at a well-defined point in the migrating motor complex cycle. It was followed by a 40 +/- 6% reduction of laser Doppler flow signal, a 778 +/- 138% increase in angiotensin II, and a reduction in intestinal mucosal nitric oxide production by 48 +/- 8%. After lower body negative pressure, laser Doppler signal and angiotensin II concentrations returned to baseline levels within 1 hr, whereas intestinal nitric oxide output remained decreased. Intestinal tonometry in humans exhibits a considerable mucosal nitric oxide formation that varies in relation to intestinal motility. Intestinal nitric oxide production is depressed during conditions with lowered mucosal blood perfusion.

Supraceliac aortic cross-clamping and declamping. Effects of dopexamine and dopamine on systemic and mesenteric hemodynamics, metabolism and intestinal tonometry in a rat model.

The effects of dopexamine and dopamine on mesenteric ischemia during reperfusion following aortic cross-clamping are not known. We determined intramucosal tonometric PCO2 and PCO2 gap using a rat model of supraceliac aortic cross-clamping and declamping. Under pentobarbital and fentanyl anesthesia, 24 rats were surgically instrumented with arterial, right atrial, and portal venous catheters, ultrasonic flowprobes for measurements of abdominal aortic, superior mesenteric and carotid artery blood flow, and a pediatric tonometer for intestinal mucosal PCO2 measurements. Rats were randomized to receive a continuous infusion of dopexamine (10 x microg(-1) x kg(-1) x min(-1), n=8), dopamine (10 microg x kg(-1) x min(-1), n=8 ), or physiologic saline (control, n= 8), infused at a rate of 4 ml x kg(-1) x h(-1), administered throughout the experimental protocol. After 30 min of drug infusion, the aorta was cross-clamped at the supraceliac level for 30 min. Reperfusion following declamping was observed for 180 min. Intestinal tonometric PCO2 remained unchanged during drug treatment before aortic cross-clamping, increased similarly in all groups following declamping during early reperfusion, and recovered to baseline within 30 min of reperfusion. Dopexamine treatment was associated with higher lactate levels and increased heart rate (P<0.05) during aortic cross-clamping. 1) Mesenteric ischemia, determined by intestinal tonometric PCO2 and PCO2 gap, recovers within 30 min of reperfusion following 30 min of aortic cross-clamping irrespective of drug treatment and, 2) dopexamine induced higher lactate levels and increased heart rate during aortic cross-clamping and should be carefully analyzed for potentially adverse effects on cardiac function.

Systemic and mesenteric hemodynamics, metabolism, and intestinal tonometry in a rat model of supraceliac aortic cross-clamping and declamping

Objective: To describe systemic and mesenteric hemodynamics, metabolism, and intestinal tonometry in a rat model of supraceliac aortic cross-clamping and declamping. Design: Prospective, randomized, experimental study. Setting: University cardiovascular research laboratory. Participants: Twelve male anesthetized and ventilated Sprague-Dawley rats. Intervention: Supraceliac aortic cross-clamping was performed for 30 minutes, followed by declamping and reperfusion for 180 minutes or sham clamping and sham declamping. Measurements and Main Results: Z Mean arterial blood pressure; abdominal aortic, superior mesenteric, and carotid artery blood flow; intestinal mucosal tonometry; hemoglobin; lactate; and blood gases were measured before and after 30 minutes of aortic cross-clamping and 15, 30, 60, 120, and 180 minutes after declamping during reperfusion, Aortic cross-clamping induced an increase in mean arterial pressure (117 ± 20 mmHg to 147 ± 12 mmHg), an increase in right atrial hemoglobin saturation (66% ± 11% to 81% ± 6%), an increase in lactate levels (1.7 ± 0.7 mmol/L to 4.3 ± 1.3 mmol/L), and an increase in tonometric PCO 2 (49.6 ± 5.0 mmHg to 75.6 ± 8.6 mmHg). Three hours of reperfusion after declamping resulted in significantly decreased mean arterial pressure (38 ± 10 mmHg); decreased aortic (101 ± 12 mL/min/kg to 57 ± 32 mL/min/kg), mesenteric (19 ± 4 to 13 ± 6 mL/min/kg), and carotid (12 ± 4 mL/min/kg to 5 ± 3 mL/min/kg) blood flows; and elevated lactate levels (4.2 ± 2.0 mmol/L). Tonometric PCO 2 had normalized to baseline levels (51.9 ± 3.8 mmHg), but PCO 2 gap was significantly higher than in sham clamped rats (17.9 ± 7.8 mmHg v 7.0 ± 2.6 mmHg). Conclusions: Hemodynamic and metabolic effects of aortic cross-clamping and declamping known from large animal models are reproducible using a rat model. Intestinal tonometry indicated mesenteric ischemia during aortic cross-clamping, which was reversible to preclamp values within 30 minutes of reperfusion after declamping.

Gastric mucosal tonometry: towards new methods and applications.

Gastrointestinal tonometry is a minimally-invasive method of assessing splanchnic perfusion. The measurement of regional-CO2 (PrCO2) and calculation of intra-mucosal pH (pHi) using the gastro-intestinal tonometer has been shown to be predictive of outcome in critically ill patients. Furthermore, the use of tonometrically derived data as therapeutic indices have been associated with improved outcome. The original balloon-saline method of tonometry was laborious, cumbersome and prone to systematic errors. The Tonocap (Tonometrics Division Instrumentarium Corp., Datex, Finland) is an automated on-line air based system. We present here a detailed description of the Tonocap along with a summary of the results of some of the original in-vitro, animal in-vivo and human experiments. The Tonocap is a major advance in regional monitoring and its introduction into clinical practice should allow widespread assessment of the value of gastro--intestinal tonometry in the management of the critically ill.

SPLANCHNIC HOMEOSTATIS DURING ENDOTOXIN CHALLENGE IN THE PIG AS ASSESSED BY MICRODIALYSIS AND TONOMETRY

The splanchnic region is particularly susceptible to shock. The purpose of this study was to evaluate microdialysis of the liver and small intestine as a monitor of splanchnic metabolic deterioration (elevation of lactate and hypoxanthine) in porcine endotoxic shock. Tonometry of the small intestine was used as a reference. Microdialysis probes (liver, ileum, and artery), tonometer, and pulmonary artery catheter were inserted. Eight animals were given Escherichia coli lipopolysaccharide endotoxin (20 micrograms kg-1 h-1 for 2 h). Five animals served as controls. Measurements were made every half-hour. Three hours after onset of endotoxin challenge, there were significant differences between endotoxin and control groups in intestinal lactate and hypoxanthine, as well as liver lactate, in addition to mucosal pH obtained by tonometry. Lactate elevation in blood was first seen at 4 h, while there was no significant hypoxanthine elevation in arterial blood over 5 h. Hence, data obtained from the splanchnic region became significantly different early, when compared with data obtained from arterial blood. Microdialysis of liver and small intestine as well as intestinal tonometry are sensitive tools for detection of splanchnic metabolic deterioration during endotoxin shock.

Gastric tonometry: a new monitoring modality in the intensive care unit.

In many critically ill patients, systemic measures of hemodynamic and O2 transport variables may not be sufficiently sensitive to portray the complex interaction between energy requirements and energy supply in all tissues. Gastric or intestinal tonometry has been proposed as a relative noninvasive index of the adequacy of aerobic metabolism in the gut mucosa, a tissue that is particularly vulnerable to alterations in perfusion and oxygenation. The gut mucosa lacks some of the microvascular control mechanisms that allow other tissues, such as the heart, skeletal muscle, and the brain, to increase tissue perfusion during times of stress, and, just like the canary, it will display metabolic changes indicative of dysoxia earlier than those more "vital" tissues. The tonometric measurement of mucosal PCO2 rests on the premise that equilibrium exists between mucosal and luminal PCO2. Increases in mucosal PCO2, or conversely, decreases in mucosal pH (pHi), are associated with the development of intestinal mucosa ischemia. The clinical utility of pHi to detect intestinal mucosal ischemia has been demonstrated in patients undergoing abdominal aortic surgery. Further, a low gastric mucosal pHi on admission to the ICU appears to be predictive of mortality and pHi-guided resuscitation may improve outcome in a subpopulation of patients admitted to the ICU with normal pHi, perhaps by preventing splanchnic ischemia and the development of a systemic oxygen deficit.

Intraluminal "balloonless" air tonometry: a new method for determination of gastrointestinal mucosal carbon dioxide tension.

To determine if air introduced directly into the lumen of a hollow viscus can be used instead of fluid in a Silastic balloon to estimate gastrointestinal mucosal PCO2. Prospective, unblinded comparison of two methods of mucosal PCO2 measurement. Animal surgery suite at a large, university-affiliated medical center. Standard, commercially available, tonometric catheters were positioned in the ileum (n = 4) or the stomach and ileum (n = 12) of anesthetized, immature Yorkshire swine. Using gas-tight purse-string sutures, plastic cannulas were inserted into the lumen of the stomach (n = 12) and the lumen of a 10-cm isolated segment of ileum (n = 16). Data were collected after equilibration periods of 30 or 60 mins. Before each equilibration period, the "air tonometers" (i.e., the lumens of the stomach and/or the isolated ileal segment) were lavaged with 200 mL (stomach) or 20 mL (ileum) of air. In group 1 (n = 4) and group 2 (n = 3), graded degrees of mesenteric hypoperfusion were achieved by mechanical mesenteric occlusion or pericardial tamponade, respectively. In group 3 (n = 8), graded degrees of respiratory acidosis were induced. At various intervals, PCO2 was determined simultaneously in arterial blood, gastric air, saline from the gastric tonometric balloon, ileal air, and saline from the ileal tonometric balloon. In pigs with ischemia created by mesenteric vascular occlusion (group 1), there was a moderate correlation between PCO2 values in air samples from the ileal lumen and samples of saline from the standard tonometer (r2 = .61, p < .001). In pigs with mesenteric ischemia secondary to pericardial tamponade (group 2), air and saline tonometry were well-correlated in the stomach (r2 = .71, p < .001) and ileum (r2 = .83, p < .001). In pigs with normal mesenteric perfusion (group 3) and PaCO2 > 40 torr (5.3 kPa), PaCO2 correlated with ileal mucosal PCO2, determined using air (r2 = .93, p < .001) or saline (r2 = .91, p < .001) tonometry, or gastric mucosal PCO2, determined using air (r2 = 1.00, p < .001) or saline (r2 = .97, p < .001) tonometry. Values obtained by air tonometry were highly correlated with values obtained using standard saline tonometry in the stomach (r2 = .98, p < .001; bias = -5 +/- 5 torr [-0.65 +/- 0.65 kPa]) or ileum (r2 = .96, p < .001; bias = 1 +/- 9 torr [0.13 +/- 1.17 kPa]). a) Under stable hemodynamic and respiratory conditions, air tonometry (which, in theory, can be performed using a conventional nasogastric or nasoenteric feeding tube) estimates gastrointestinal mucosal PCO2 as accurately as standard saline tonometry in the stomach or ileum; b) respiratory acidosis leads to tissue hypercarbia, a phenomenon that must be considered when tonometry is used to guide therapy in the clinical setting; c) under stable, nonischemic conditions, gastric or intestinal tonometry can be used to estimate PaCO2.