Gastric Mucosal Perfusion Research Articles

Comparison of gastric reactance with commonly used perfusion markers in a swine hypovolemic shock model

BackgroundThe gut has been hypothesized to be a protagonist tissue in multiple organ dysfunction syndrome (MODS) for the past three decades. Gastric reactance (XL) is a potential perfusion marker derived from gastric impedance spectroscopy (GIS), which is an emerging tool through which living tissue can be continuously measured to determine its pathophysiological evolution. This study aimed to compare the performance of XL [positive predictive values (PPV), negative predictive values (NPV), and area under the curve (AUC)] against commonly used perfusion markers before and during hypovolemic shock in swine subjects.MethodsProspective, controlled animal trial with two groups, control group (CG) N = 5 and shock (MAP ≤ 48 mmHg) group (SG) N = 16. Comparison time points were defined as T-2 (2 h before shock), T-1 (1 h before shock), T0 (shock), T1 (1 h after shock), and T2 (2 h after shock). Shock severity was assessed through blood gases, systemic and hemodynamic variables, and via histological examination for assessing inflammation-edema and detachment in the gastric mucosa. Macroscopic assessment of the gastric mucosa was defined in five levels (0—normal mucosa, 1—stippling or epithelial hemorrhage, 2—pale mucosa, 3—violet mucosa, and 4—marmoreal mucosa). Receiver Operating Characteristic (ROC) curves of perfusion markers and XL were calculated to identify optimal cutoff values and their individual ability to predict hypovolemic shock.ResultsComparison among the CG and the SG showed statistically significant differences in XL measurements at T-1, T0, T1, and T2, while lactate showed statistically significant differences until T1 and T2. Statistically significant differences were detected in mucosa class (p < 0.001) and in inflammation-edema in the gastric body and the fundus (p = 0.021 and p = 0.043). The performance of the minimum XL value per subject per event (XL_Min) was better (0.81 ≤ AUC ≤ 0.96, 0.93 ≤ PPV ≤ 1.00, 0.45 ≤ NPV ≤ 0.83) than maximum lactate value (Lac_Max) per subject per event (0.29 ≤ AUC ≤ 0.82, 0.82 ≤ PPV ≤ 0.91, 0.24 ≤ NPV ≤ 0.82). Cutoff values for XL_Min show progressive increases at each time point, while cutoff values for Lac_Max increase only at T2.ConclusionsXL proved to be an indirect and consistent marker of inadequate gastric mucosal perfusion, which shows significant and detectable changes before commonly used markers of global perfusion under the hypovolemic shock conditions outlined in this work.

Relationship between Gastric Blood Perfusion and Gastric Mucosal Injury Induced by Acute Cerebrovascular Disease in Rats

This study aims to discuss the relationship between gastric perfusion and gastric mucosal injury induced by acute cerebrovascular disease in rats. Healthy adult male Wistar rats weighing 280-320 g are randomly divided into the following 4 groups: middle cerebral artery occlusion-reperfusion group, middle cerebral artery occlusion -sham group, gastric ischemia-reperfusion group and gastric ischemia-sham group, with 12 in each group. In gastric ischemia-reperfusion group, the similar changes occur to the mucous membrane of the rats, such as hyperaemia, edema, spotty or patchy hemorrhage and partial mucous exfoliation. There is no significant difference between middle cerebral artery occlusion-reperfusion group and gastric ischemia-reperfusion group in the number of gastrin cells and the expression of gas, but the number of gastrin cells and the expression of gas are significantly higher than those of their corresponding sham operation group, resulting in statistically significant difference. The gastric mucosal blood flow is significantly increased in the middle and high dose groups, which has significant difference compared with normal saline group (p<0.05). One of the important mechanisms of Calcitonin gene-related peptide protecting ischemic gastric mucosal injury is to increase gastric mucosal blood perfusion and improve microcirculation.

A randomized-controlled trial of arginine infusion in severe sepsis on microcirculation and metabolism.

Sepsis is hypothesized as an arginine deficient state, with lack of nitric oxide (NO) for adequate microcirculation and local perfusion. This study aimed to investigate if prolonged (72-h) intravenous l-arginine administration in sepsis patients improves microcirculation. Secondly, effects on arginine and protein metabolism, and organ function were studied. Critically ill patients with a diagnosis of septic shock participated in a long-term (72h) randomized double-blind placebo-controlled parallel-group study. l-arginine-HCl (1.2μmolkg-1min-1; n=9) or l-alanine (isocaloric control: 2.4μmolkg-1min-1; n=9) was continuously infused. Primary study outcome was microcirculation, assessed as gastric mucosal perfusion by gastric tonometry (Pr-aCO2 gap) and skin perfusion by Laser Doppler flowmetry. Secondary endpoints were whole body (WB) arginine and protein metabolism, organ function and clinical outcomes. We measured global hemodynamics continuously for safety monitoring. Statistical analyses were performed by mixed model for repeated measures with treatment by time interaction as estimate for between-group difference. Pr-aCO2 increased only in the l-arginine group (p=0.006), without a significant between-group difference (p=0.17). We found no significant differences in skin perfusion parameters. l-arginine infusion resulted in a larger increase of plasma arginine and ornithine concentrations (p<0.01), WB (endogenous) arginine appearance (p<0.001), WB NO synthesis (p=0.027) and WB arginine to urea conversion (p<0.001) than infusion of l-alanine. We found no effect on global hemodynamics, and protein metabolism by l-arginine infusion. Organ function parameters were unaffected, except for a significant difference between groups in intra-abdominal pressure over time (p=0.029). Prolonged intravenous l-arginine administration does not improve local perfusion and organ function despite an increase in WB NO synthesis. Administration is safe with regard to global hemodynamics, but the observed increase in Pr-aCO2 and intra-abdominal pressure warrants careful application of l-arginine infusion and further research, especially in the early stage of septic shock.

Local gastric RAAS inhibition improves gastric microvascular perfusion in dogs.

During circulatory shock, gastrointestinal microcirculation is impaired, especially via activation of the renin-angiotensin-aldosterone system. Therefore, inhibition of the renin-angiotensin-aldosterone system might be beneficial in maintaining splanchnic microcirculation. The aim of this study was to analyze whether locally applied losartan influences gastric mucosal perfusion (µflow, µvelo) and oxygenation (µHbO2) without systemic hemodynamic changes. In repetitive experiments six anesthetized dogs received 30 mg losartan topically on the oral and gastric mucosa during normovolemia and hemorrhage (-20% blood volume). Microcirculatory variables were measured with reflectance spectrometry, laser Doppler flowmetry and incident dark field imaging. Transpulmonary thermodilution and pulse contour analysis were used to measure systemic hemodynamic variables. Gastric barrier function was assessed via differential absorption of inert sugars. During normovolemia, losartan increased gastric µflow from 99 ± 6 aU to 147 ± 17 aU and µvelo from 17 ± 1 aU to 19 ± 1 aU. During hemorrhage, losartan did not improve µflow. µvelo decreased from 17 ± 1 aU to 14 ± 1 aU in the control group. Application of losartan did not significantly alter µvelo (16 ± 1 aU) compared to the control group and to baseline levels (17 ± 1 aU). No effects of topical losartan on macrohemodynamic variables or microcirculatory oxygenation were detected. Gastric microcirculatory perfusion is at least partly regulated by local angiotensin receptors. Topical application of losartan improves local perfusion via vasodilation without significant effects on systemic hemodynamics. During mild hemorrhage losartan had minor effects on regional perfusion, probably because of a pronounced upstream vasoconstriction.

The effects of hypervolemic infusion on microcirculation perfusion of patients during laparoscopic colorectal surgery.

The aim of this study is to assess the effects of hypervolemic infusion with different solutions on microcirculation perfusion during laparoscopic colorectal surgery.Thirty-six patients were randomly divided into Ringer lactate solution [RL] group, succinylated gelatin injection [Gel] group, and hypertonic saline hydroxyethyl starch 40 injection [HS] group. Hypervolemic infusion was performed during the induction period of general anesthesia. Arterial blood-gas parameters, noninvasive hemodynamics, gastric tonometry values, and central venous pressure (CVP) were compared at baseline (T1); the end of hypervolemic infusion (T2); 5 min (T3), 15 min (T4), 30 min (T5), and 60 min (T6) during pneumoperitoneum; 5 min (T7), 15 min (T8), and 25 min (T9) after pneumoperitoneum. Patients were also grouped by age for further comparisons.The hematocrit levels of all groups after T2 decreased. The gastric mucosal-arterial carbon dioxide partial pressure (Pg-aCO2) started to decrease after T2 and rebounded after T5. There was no difference in the gastric mucosal perfusion when compared between 3 groups. The blood Na of HS group increased significantly after T2, then gradually restored and returned to baseline by T8. The plasma bicarbonate (HCO3) levels of RL and Gel groups elevated from T2 to T7, after which they started to decrease, but this phenomenon was not significant in HS group. In both RL and Gel groups, blood pressure has a significant fluctuation in elder patients.Hypervolemic infusion of these solutions during the induction of anesthesia can improve gastric mucosal perfusion. HS can maintain a more stable hemodynamic effect when used with caution in patients with preoperative hypernatremia.

Melatonin pretreatment improves gastric mucosal blood flow and maintains intestinal barrier function during hemorrhagic shock in dogs.

Melatonin improves hepatic perfusion after hemorrhagic shock and may reduce stress-induced gastric lesions. This study was designed to investigate whether pretreatment with melatonin may influence gastric mucosal microcirculatory perfusion (μflow), oxygenation (μHbO2 ), or intestinal barrier function during physiological and hemorrhagic conditions in dogs. In a randomized crossover study, five anesthetized foxhounds received melatonin 100μgkg-1 or vehicle (ethanol 5%) intravenously in the absence or presence of hemorrhagic shock (60minutes, -20% blood volume). Systemic hemodynamic variables, gastric mucosal perfusion, and oxygenation were recorded continuously; intestinal barrier function was assessed intermittently via xylose absorption. During hemorrhagic shock, melatonin significantly attenuated the decrease in μflow, compared with vehicle (-19±9 vs -43±10aU, P<.05), without influence on μHbO2 . A significant increase in xylose absorption was detected during hemorrhage in vehicle-treated dogs, compared with sham-operated animals (13±2 vs 8±1 relative amounts, P<.05); this was absent in melatonin-treated animals (6±1 relative amounts). Melatonin did not influence macrocirculation. Melatonin improves regional blood flow suggesting improved oxygen delivery in gastric mucosa during hemorrhagic shock. This could provide a mechanism for the observed protection of intestinal barrier function in dogs.

Effect of Topical Iloprost and Nitroglycerin on Gastric Microcirculation and Barrier Function during Hemorrhagic Shock in Dogs

Background: Topical drug application is used to avoid systemic side effects. The aim of this study was to analyze whether locally applied iloprost or nitroglycerin influence gastric mucosal perfusion, oxygenation, and barrier function during physiological and hemorrhagic conditions. Methods: In repeated experiments, 5 anesthetized dogs received iloprost, nitroglycerin, or normal saline during physiological and hemorrhagic (-20% blood volume) conditions. Macro- and microcirculatory variables were recorded continuously. Gastric barrier function was assessed via translocation of sucrose into the blood. Results: During hemorrhage, gastric mucosal oxygenation decreased from 77 ± 4 to 37 ± 7%. This effect was attenuated by nitroglycerin (78 ± 6 to 47 ± 13%) and iloprost (82 ± 4 to 54 ± 9%). Sucrose plasma levels increased during hemorrhage from 7 ± 4 to 55 ± 15 relative amounts. This was alleviated by nitroglycerin (5 ± 8 to 29 ± 38 relative amounts). These effects were independent of systemic hemodynamic variables. Conclusions: During hemorrhage, topical nitroglycerin and iloprost improve regional gastric oxygenation without affecting perfusion. Nitroglycerin attenuated the shock-induced impairment of the mucosal barrier integrity. Thus, local drug application improves gastric microcirculation without compromising systemic hemodynamic variables, and it may also protect mucosal barrier function.

Melatonin improves gastric mucosal microcirculatory perfusion and maintains intestinal barrier function during haemorrhagic shock in dogs

Vollmer, C.1; Wallenfang, M.1; Weber, A.2; Bauer, I.1; Mathes, A.1; Picker, O.1 Author Information

Hypothermia Improves Oral and Gastric Mucosal Microvascular Oxygenation during Hemorrhagic Shock in Dogs

Hypothermia is known to improve tissue function in different organs during physiological and pathological conditions. The aim of this study was to evaluate the effects of hypothermia on oral and gastric mucosal microvascular oxygenation (μHbO2) and perfusion (μflow) under physiological and hemorrhagic conditions. Five dogs were repeatedly anesthetized. All animals underwent each experimental protocol (randomized cross-over design): hypothermia (34°C), hypothermia during hemorrhage, normothermia, and normothermia during hemorrhage. Microcirculatory and hemodynamic variables were recorded. Systemic (DO2) and oral mucosal (μDO2) oxygen delivery were calculated. Hypothermia increased oral μHbO2 with no effect on gastric μHbO2. Hemorrhage reduced oral and gastric μHbO2 during normothermia (−36 ± 4% and −27 ± 7%); however, this effect was attenuated during additional hypothermia (−15 ± 5% and −11 ± 5%). The improved μHbO2 might be based on an attenuated reduction in μflow during hemorrhage and additional hypothermia (−51 ± 21 aU) compared to hemorrhage and normothermia (−106 ± 19 aU). μDO2 was accordingly attenuated under hypothermia during hemorrhage whereas DO2 did not change. Thus, in this study hypothermia alone improves oral μHbO2 and attenuates the effects of hemorrhage on oral and gastric μHbO2. This effect seems to be mediated by an increased μDO2 on the basis of increased μflow.

Metabolic fate of S-nitrosoglutathione after oral administration: Where does NO go?

Increasing the gastric mucosal perfusion by nitric oxide (NO) action can reduce the gastric injuries caused by non-steroidal anti-inflammatory drugs (NSAIDs). We have shown previously that topical administration of the NO donor S-nitrosoglutathione (GSNO) on the gastric mucosa of rats increases gastric blood flow, pointing to a possible oral therapeutic approach for treating NSAIDs side effects. In the present study, we found that oral administration of GSNO solutions (7–365 μmol/kg) to Swiss mice leads to a significant dose–response increase in the plasmatic levels of nitrite and nitrate (NOx) measured by chemiluminescence, with peak levels (160 mM) achieved after 1 h. At the same time, intact GSNO could not be detected in the plasma of the GSNO-treated animals by high-sensitivity Ultra Performance Liquid Chromatography (UPLC), 1 h after oral administration. These results indicate that gastric vasodilatation is not associated with a direct action of GSNO molecules, what is in accordance with the fact that GSNO vanishes completely 1 h after incubation in human plasma, as shown by UPLC analysis. In addition, no signal of free NO could be detected after incubation of human plasma with GSNO 50 μM by using a nanomolar-sensitive NO selective electrode (ISO-NOP and APOLLO 4000), over a 1 h period. These findings strongly suggest that the fate of GSNO after contact with the biological milieu involves its primary reaction with proteins by S-nitrosation or/and S-nitrosylation with the transfer of its NO moiety to other effector molecules, which are ultimately responsible for the observed increase in gastric blood flow.

Moderate-dose Vasopressin Therapy May Impair Gastric Mucosal Perfusion in Severe Sepsis

The effects of moderate-dose vasopressin on gastric mucosal perfusion and its relation to global and hepatosplanchnic hemodynamic and oxygen transport variables were investigated in patients with severe sepsis. Vasopressin was administered at a dose of 0.04 IU · kg⁻¹ · h⁻¹ over 4 h in 12 patients with severe sepsis who were receiving norepinephrine. During the study period, the norepinephrine infusion rate was reduced to keep mean arterial blood pressure constant. Hepatosplanchnic blood flow, oxygen delivery, and oxygen consumption (via hepatic venous catheterization using the Fick principle and continuous indocyanine green infusion technique), global hemodynamics (transpulmonary thermodilution method), and the difference between the gastric mucosal and arterial carbon dioxide tension (Pco₂-gap) were measured at baseline and 4 h after the start of the vasopressin infusion. The administration of 0.04 IU · kg⁻¹ · h⁻¹ vasopressin over 4 h was associated with minimal changes in global hemodynamics. Heart rate decreased slightly from 99 [81-115] (median [interquartile range]) to 96 [74-109] beats/min (P = 0.016) and cardiac index from 3.7 [2.8-4.7] to 3.5 [2.7-3.6] L · min⁻¹ · m⁻² (P = 0.003). Global oxygen delivery index decreased significantly from 461 [375-637] to 419 [352-551] ml · min⁻¹ · m⁻² (P = 0.002), whereas hepatosplanchnic blood flow and oxygen uptake remained unchanged. Gastric mucosal Pco₂-gap increased significantly from 13.3 [8.0-16.7] to 17.1 [10.3-28.7] mmHg (P = 0.002), suggesting that blood flow may have been redistributed away from the gut mucosa. Vasopressin at a dosage of 0.04 IU · kg⁻¹ · h⁻¹ may impair gastric mucosal perfusion with minimal global hemodynamic effects.

The effects of methylene blue infusion on gastric tonometry and intestinal fatty acid binding protein levels in septic shock patients

Objective We prospectively studied the effect of methylene blue (MB) infusion on gastric mucosal metabolism perfusion ratio, assessed by gastric tonometry, and on mucosal cell damage, assessed by urinary levels of intestinal fatty acid binding protein, in septic shock patients. Methods Methylene blue (MB) infusion (1 mg/kg per hour) during 4 hours in 10 consecutive patients with a proven or suspected bacterial infection and with severe vasodilatory shock, defined as a mean arterial pressure 70 mm Hg or lower for at least 1 hour despite adequate volume resuscitation and norepinephrine infusion at a rate ≥0.2 μg/kg per minute. Results Methylene blue infusion did not significantly change the P(g-a)CO 2 gradient ( P = .16). Post hoc analysis of the subgroup of patients with an elevated baseline P(g-a)CO 2 gradient, defined as ≥20 mm Hg, showed that the median P(g-a)CO 2 gradient (interquartile range [IQR]) decreased from 45 (41-56) mm Hg before infusion to 41 (28-52) at the end of the 4-hour infusion and decreased further to 32 (26-36) mm Hg 2 hours after cessation of MB infusion ( P = .012). The median urinary intestinal fatty acid binding protein concentration at baseline was elevated (210 [79-437] pg/ μmol creatinine) and did not change significantly after 24 hours (116 [53-601] pg/ μmol creatinine, P = .15). The median mean arterial blood pressure (IQR) increased from 70 (69-71) mm Hg at baseline to 77 (67-83) mm Hg after 1 hour ( P = .04), the norepinephrine dose did not change significantly. The median (IQR) cardiac index decreased from 4.4 (3.2-5.5) L min -1 m -2 at baseline to 3.6 (3.3-4.7) L min -1 m -2 after 2 h, returning back to baseline values after cessation of MB infusion P = .02). Conclusion Although MB infusion in patients with septic shock and advanced multi-organ failure increases mean arterial blood pressure and decreases cardiac index, it does not compromise the gastric mucosal perfusion metabolism ratio as indicated by tonometry, and by the release of a mucosal cellular injury marker.

British consensus guidelines on intravenous fluid therapy for adult surgical patients (GIFTASUP) – Cassandra’s view

British consensus guidelines on intravenous fluid therapy for adult surgical patients (GIFTASUP) – Cassandra’s view

Changes of splanchnic perfusion after applying positive end expiratory pressure in patients with acute respiratory distress syndrome

Background:Positive end-expiratory pressure (PEEP) improves oxygenation and can prevent ventilator- induced lung injury in patients with acute respiratory distress syndrome (ARDS). Nevertheless, PEEP can also induce detrimental effects by its influence on the cardiovascular system. The purpose of this study was to assess the effects of PEEP on gastric mucosal perfusion while applying a protective ventilatory strategy in patients with ARDS.Materials and Methods:Thirty-two patients were included in the study. A pressure–volume curve was traced and ideal PEEP, defined as lower inflection point + 2cmH2O, was determined. Gastric tonometry was measured continuously (Tonocap). After baseline measurements, 10, 15 and 20cmH2O PEEP and ideal PEEP were applied for 30 min each. By the end of each period, hemodynamics, CO2 gap (gastric minus arterial partial pressures), and ventilatory measurements were taken.Results:PEEP had no effect on CO2 gap (median [range], baseline: 18 [2–30] mmHg; PEEP 10: 18 [0–40] mmHg; PEEP 15: 17 [0–39] mmHg; PEEP 20: 16 [4–39] mmHg; ideal PEEP: 19 [9–39] mmHg; P = 0.19). Cardiac index also remained unchanged (baseline: 4.7 [2.6–6.2] l min−1 m−2; PEEP 10: 4.4 [2.5–7] l min−1 m−2; PEEP 15: 4.4 [2.2–6.8] l min−1 m−2; PEEP 20: 4.8 [2.4–6.3] l min−1 m−2; ideal PEEP: 4.9 [2.4–6.3] l min−1 m−2; P = 0.09).Conclusion:PEEP of 10–20 cmH2O does not affect splanchnic perfusion and is hemodynamically well tolerated in most patients with ARDS, including those receiving inotropic supports.

Gastric Mucosal Perfusion in Dogs: Effects of Halogenated Anesthetics and of Hemorrhage

The gastrointestinal tract is one of the first organs affected by hypoperfusion during hemorrhagic shock. The hemodynamics and oxygen transport variables during hemorrhagic shock and resuscitation can be affected by the anesthetics used. In a model of pressure-guided hemorrhagic shock in dogs, we studied the effects of three halogenated anesthetics—halothane, sevoflurane, and isoflurane—at equipotent concentrations on gastric oxygenation. Thirty dogs were anesthetized with 1.0 minimum alveolar anesthetic concentration (MAC) of either halothane, sevoflurane, or isoflurane. A gastric tonometer was placed in the stomach to determine mucosal gastric CO2 (PgCO2) and for the calculation of gastric-arterial PCO2 gradient (PCO2 gap). The dogs were splenectomized and hemorrhaged to hold mean arterial pressure at 40–50 mm Hg over 45 min and then resuscitated with the shed blood volume. Hemodynamics, systemic oxygenation, and PCO2 gap were measured at baseline, after 45 min of hemorrhage, and at 15 and 60 min after blood resuscitation. Hemorrhage induced reductions of mean arterial pressure and cardiac index, while systemic oxygen extraction increased (p <. 05), without significant differences among groups (p >. 05). Halothane group showed significant lower PCO2 gap values than the other groups (p <. 05). After 60 min of shed blood replacement, all groups restored hemodynamics, systemic oxygenation, and PCO2 gap to the prehemorrhage levels (p >. 05), without significant differences among groups (p >. 05). We conclude that halothane is superior to preserve the gastric mucosal perfusion in comparison to isoflurane and sevoflurane, in dogs submitted to pressure-guided hemorrhagic shock at equipotent doses of halogenated anesthetics.

Increased Gastric–End Tidal PCO2 Gap during Exercise at High Altitude Measured by Gastric Tonometry

Using automated air gastric tonometry, the hypothesis that gastric perfusion is reduced while exercising at high altitude was explored. This prospective observational study of 5 well acclimatized healthy volunteers was performed during a medical research expedition to Chamlang base camp (5000 m), Hongu valley, Nepal. We used gastric tonometry at rest and during graded submaximal exercise. The end tidal partial pressure of carbon dioxide was subtracted from the gastric mucosal partial pressure of carbon dioxide to calculate the P(CO2) gradient, which is a marker of gastric mucosal perfusion. When compared with rest, there was no increase in the mean P(CO2) gradient at the lower work rate (0.22 vs. 0.18, p 0.10), but an increase was seen between rest and the higher work rate (0.22 vs. 0.77, p = 0.04). We conclude that exercising while at high altitude can lead to a raised P(CO2) gradient when gastric tonometry is performed, indicating reduced perfusion. This may represent reduced gastric mucosal perfusion under these conditions.

Effects of dobutamine, norepinephrine, and vasopressin on cardiovascular function in anesthetized neonatal foals with induced hypotension

To determine the effects of dobutamine, norepinephrine, and vasopressin on cardiovascular function and gastric mucosal perfusion in anesthetized foals during isoflurane-induced hypotension. 6 foals that were 1 to 5 days of age. 6 foals received 3 vasoactive drugs with at least 24 hours between treatments. Treatments consisted of dobutamine (4 and 8 Sang/kg/min), norepinephrine (0.3 and 1.0 Sang/kg/min), and vasopressin (0.3 and 1.0 mU/kg/min) administered IV. Foals were maintained at a steady hypotensive state induced by a deep level of isoflurane anesthesia for 30 minutes, and baseline cardiorespiratory variables were recorded. Vasoactive drugs were administered at the low infusion rate for 15 minutes, and cardiorespiratory variables were recorded. Drugs were then administered at the high infusion rate for 15 minutes, and cardiorespiratory variables were recorded a third time. Gastric mucosal perfusion was measured by tonometry at the same time points. Dobutamine and norepinephrine administration improved cardiac index. Vascular resistance was increased by norepinephrine and vasopressin administration but decreased by dobutamine at the high infusion rate. Blood pressure was increased by all treatments but was significantly higher during the high infusion rate of norepinephrine. Oxygen delivery was significantly increased by norepinephrine and dobutamine administration; O2 consumption decreased with dobutamine. The O2 extraction ratio was decreased following norepinephrine and dobutamine treatments. The gastric to arterial CO2 gap was significantly increased during administration of vasopressin at the high infusion rate. Norepinephrine and dobutamine are better alternatives than vasopressin for restoring cardiovascular function and maintaining splanchnic circulation during isoflurane-induced hypotension in neonatal foals.

Positive end-expiratory pressure does not affect indocyanine green plasma disappearance rate or gastric mucosal perfusion after cardiac surgery*

Positive end-expiratory pressure (PEEP) may affect hepato-splanchnic blood flow. We studied whether a PEEP of 10 mbar may negatively influence flow-dependent liver function (indocyanine green plasma disappearance rate, ICG-PDR) and splanchnic microcirculation as estimated by gastric mucosal PCO2 (PRCO2). In a randomized, controlled clinical study, we enrolled 28 patients after elective cardiac surgery using cardiopulmonary bypass. In 14 patients (13 male, 1 female; age 48-74, mean 63 +/- 7 yr) we assessed ICG-PDR and PRCO2 on intensive care unit admission with PEEP 5 mbar, after 2 h with PEEP of 10 mbar and again after 2 h at PEEP 5 mbar. Inspiratory peak pressure was adjusted to maintain normocapnia. Fourteen other patients (8 male, 6 female; age 46-86, mean 68 +/- 11 yr) in whom PEEP was 5 mbar throughout served as controls. All patients underwent haemodynamic monitoring by measurement of central venous pressure, left atrial pressure and cardiac index using pulmonary artery thermodilution. While doses of vasoactive drugs and cardiac filling pressures did not change significantly, cardiac index slightly increased in both groups. ICG-PDR remained unchanged either within or between both groups (PEEP10 group: 24.0 +/- 6.9, 22.0 +/- 7.9 and 25.5 +/- 7.7% min-1 vs. controls: 22.0 +/- 7.5, 23.8 +/- 8.4 and 21.4 +/- 6.5% min-1) (P = 0.05). The difference between PRCO2 and end-tidal PCO2 (PCO2-gap) did not change significantly (PEEP10 group: 1.1 +/- 0.9, 1.3 +/- 0.7 and 1.3 +/- 0.9 kPa vs. controls: 0.8 +/- 0.5, 0.9 +/- 0.5 and 0.9 +/- 0.5 kPa). A PEEP of 10 mbar for 2 h does not compromise liver function and gastric mucosal perfusion in patients after cardiac surgery with maintained cardiac output.

Increasing Cardiac Output by Epinephrine After Cardiac Surgery: Effects on Indocyanine Green Plasma Disappearance Rate and Splanchnic Microcirculation

The effects of increasing cardiac output by epinephrine on indocyanine green plasma disappearance rate (ICG-PDR) and gastric mucosal PCO(2) (P(R)CO(2)) were studied as indicators of splanchnic microcirculation. A prospective clinical study. Intensive care unit of a university hospital. With ethics approval and written consent, 12 elective cardiac surgical patients (5 female, 7 male, 71 +/- 8 years) were studied. Patients underwent pulmonary artery and left atrial catheterization for clinical indications. Measurements were made at intensive care unit admission and 1 hour after (increased) epinephrine treatment. Mean epinephrine dose was changed from 0.02 to 0.08 microg/kg/min. Heart rate significantly increased from 97 +/- 11 to 106 +/- 12 beat/min. Central venous (10 +/- 3 v 10 +/- 4 mmHg) and left atrial (10 +/- 5 v 11 +/- 5 mmHg) pressures were unchanged. Cardiac index and stroke volume index significantly increased from 2.7 +/- 0.5 to 3.2 +/- 0.5 L/min/m(2) and from 28 +/- 6 to 31 +/- 5 mL/m(2), respectively. Although systemic O(2) delivery and O(2) consumption significantly increased, ICG-PDR did not change significantly (ie, from 18.0% +/- 5.6% to 19.5% +/- 6.4% per minute). P(R)CO(2) and PCO(2) gap (difference between regional and end-tidal PCO(2)) significantly increased from 5.4 +/- 1.0 to 5.9 +/- 1.1 kPa and 1.2 +/- 0.8 to 1.5 +/- 0.7 kPa, respectively. Increasing cardiac output by epinephrine in patients after cardiac surgery was not associated with a change in flow-dependent liver function but a deterioration in gastric mucosal perfusion.

Gastric Intramucosal Perfusion during Descending Aortic Repair under Femoro-Femoral Bypass

The changes in gastric mucosal perfusion during distal aortic perfusion with femoro-femoral bypass (F-F bypass) were assessed by air-automated gastric tonometry. A prospective study was performed in six patients who underwent descending aortic surgery for aortic aneurysm under F-F bypass with mild hypothermia (34 degrees C). Gastric intramucosal pH (pHi) and PaCO2-PgCO2 gap (PCO2 gap) were measured. Data are presented as means and standard deviations and analyzed by using one-way analysis of variance followed by Scheffe test. Perioperative variables of hepatorenal functions are also evaluated. The PCO2 gap significantly increased during F-F bypass (3.0 +/- 2.1 mm Hg at control, 14.2 +/- 5.5 mm Hg during F-F bypass; p = 0.004), indicating abnormal gastric mucosal perfusion during F-F bypass. Significantly low pHi was found at weaning from F-F bypass (7.35 +/- 0.05 at control, 7.21 +/- 0.10 at weaning; p = 0.009), which might be related to progressing systemic metabolic acidosis. No impairment of hepatorenal functions was observed after the surgery. Distal perfusion with F-F bypass during descending aortic surgery could impair the gastric mucosal perfusion, but may have little effect on postoperative visceral dysfunction.