Mucosal Perfusion Research Articles

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.

The role of pain-mediating sensory nerves in histamine-induced inflammation of nasal mucosa

Topical application of histamine on the nasal mucosa causes an inflammatory reaction with increased mucosal swelling and perfusion. In the nasal mucosa histamine receptors are found in the vascular epithelium and at free sensory nerve endings. The aim of this randomized double-blind placebo controlled study was to investigate if this inflammatory reaction to locally administered histamine was dependent upon the stimuli of pain-mediating sensory nerves, or if it mainly was the result of direct stimuli of the vascular epithelium. Eighteen healthy non-allergic subjects were treated with sprays of lidocaine or saline (placebo) in the nose, followed by challenge with histamine. Using a cross-over design the participants later returned and were allocated to the opposite treatment followed by histamine. Nasal congestion, and concentration, velocity and perfusion of erythrocytes were measured with rhinostereometry and laser Doppler flowmetry. Symptoms of blockage, discharge and itching were scored. When comparing the lidocaine group to the placebo group, we found no significant differences in the reaction to histamine concerning any of the measured parameters or subjective symptoms. In conclusion, our results suggest that the stimuli of pain-mediating sensory nerves do not significantly contribute to the inflammatory effect of histamine on human nasal mucosa.

Synthetic Atrial Natriuretic Peptide Improves Systemic and Splanchnic Circulation and Has a Lung-Protective Effect During Endotoxemia in Pigs

Pharmacological blockade of the renin-angiotensin system is thought to maintain gut perfusion during circulatory stress and thereby avoid later failure of distant organs. In this controlled experimental study, we investigated the effects of carperitide, a synthetic atrial natriuretic peptide that inhibits the renin-angiotensin system, on the systemic and splanchnic circulation during fluid-resuscitated endotoxemia in pigs. Sixteen domestic pigs of both sexes were randomly divided into 2 groups. The pigs were anesthetized and their lungs ventilated before receiving either saline (Group A: n = 8) or carperitide (Group B: n = 8). After a baseline measurement was taken, the pigs from both groups received a continuous infusion (1.7 microg x kg(-1) x h(-1)) of endotoxin for 240 min. Group B received a continuous infusion of carperitide (0.05 microg x kg(-1) x min(-1)) starting 30 min before the endotoxin infusion and lasting until the end of the study, whereas Group A received the same volume of saline. Fluid resuscitation was titrated to maintain pulmonary artery wedge pressure between 10 and 12 mm Hg. Systemic and regional hemodynamics, oxygenation variables, and the arterial-to-intestinal PCO(2) gap were measured at baseline and after endotoxin infusion for 240 min. The primary end points were cardiac index, superior mesenteric artery flow index, and PCO(2) gap at the end of this study (T240). Cardiac index and superior mesenteric artery flow index in Group B were significantly higher than those in Group A at T240 (83 +/- 15 vs 135 +/- 23 mL x kg(-1) x min(-1), P < 0.001; 2.6 +/- 1.4 vs 7.9 +/- 4.8, P = 0.01), respectively. Carperitide administration resulted in a significantly better maintenance of intestinal mucosal perfusion assessed by the PCO(2) gap at T240 (33.0 +/- 14.5 vs 11.6 +/- 10.0 mm Hg, P = 0.004). The PaO(2)/FIO(2) ratio in Group B was significantly greater than that in Group A from T60 to T240. In this porcine fluid-resuscitated endotoxemia model, a low dose of carperitide administered before endotoxemia maintained systemic and splanchnic circulation, and prevented the deterioration of oxygenation. Atrial natriuretic peptide infusion is a potentially beneficial therapy with respect to systemic and splanchnic circulation as well as the respiratory system during sepsis.

Impact of laryngeal mask airway cuff pressures on the incidence of sore throat in children

Hyperinflation of laryngeal mask airway cuffs can cause harm to the upper airway mainly by exerting high pressures on pharyngeal and laryngeal structures thus impairing mucosal perfusion. Although cuff manometers can be used to guide the monitoring of cuff pressures, their use is not routine in many institutions. In a prospective audit, we assessed the incidence of sore throat following day-case-surgery in relation to the intracuff pressure within the laryngeal mask airway. Four hundred children (3-21 years) were consecutively included in this study. The laryngeal mask airway was inflated as deemed necessary by the attending anesthetist. Cuff pressures were measured using a calibrated cuff manometer (Portex Limited, Hythe, Kent, UK, 0-120 cm H2O, pressures exceeding the measurement range were set at 140 cm H2O for statistical purposes) at induction of anesthesia. Forty-five children (11.25%) developed sore throat, 32 (8%) sore neck and 17 (4.25%) sore jaw. Of those that developed sore throat, 56.5% had cuff pressures exceeding >100 cm H2O. In contrast, when cuff pressures were <40 cm H2O, there were no episodes of sore throat, whilst there was only a 4.6% occurrence of sore throat if cuff pressures were between 40-60 cm H2O. We have demonstrated that intra cuff pressure in laryngeal mask airways is closely related to the development of sore throat with higher pressures increasing its likelihood. Hence, cuff pressures should be measured routinely using a manometer to minimize the incidence of sore throat.

Vasopressin decreases intestinal mucosal perfusion: a clinical study on cardiac surgery patients in vasodilatory shock

Low to moderate doses of vasopressin have been used in the treatment of cathecholamine-dependent vasodilatory shock in sepsis or after cardiac surgery. We evaluated the effects of vasopressin on jejunal mucosal perfusion, gastric-arterial pCO2 gradient and the global splanchnic oxygen demand/supply relationship in patients with vasodilatory shock after cardiac surgery. Eight mechanically ventilated patients, dependent on norepinephrine to maintain mean arterial pressure (MAP) > or = 60 mmHg because of septic/post-cardiotomy vasodilatory shock and multiple organ failure after cardiac surgery, were included. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h for 30-min periods. Norepinephrine was simultaneously decreased to maintain MAP at 75 mmHg. At each infusion rate of vasopressin, data on systemic hemodynamics, jejunal mucosal perfusion, jejunal mucosal hematocrit and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial pCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained. The cardiac index, stroke volume index and systemic oxygen delivery decreased and systemic vascular resistance and systemic oxygen extraction increased significantly, while the heart rate or global oxygen consumption did not change with increasing vasopressin dose. Jejunal mucosal perfusion decreased and the arterial-gastric-mucosal pCO2 gradient increased, while splanchnic oxygen or lactate extraction or mixed venous-hepatic venous oxygen saturation gradient were not affected by increasing infusion rates of vasopressin. Infusion of low to moderate doses of vasopressin in patients with norepinephrine-dependent vasodilatory shock after cardiac surgery induces an intestinal and gastric mucosal vasoconstriction.

Ischemic preconditioning of small bowel mitigates the late phase of reperfusion injury: heme oxygenase mediates cytoprotection

Background Ischemia and reperfusion (IR) injury of the intestine is a major cause of morbidity and mortality following small bowel transplantation. The current study evaluates the effect of ischemic preconditioning (IPC) on the intestinal microcirculation in the late phase of IR injury of the intestine. Methods Sixty rats were randomly allocated to 5 study groups (n = 12 per group): (1) sham, (2) IR (3) IPC, (4) pyrrolidine dithiocarbamate (PDTC) (HO-1 inducer), and (5) zinc protoporhyrin (ZnPP) (HO-1 inhibitor). Mucosal perfusion and leukocyte–endothelial interactions were measured with the aid of an intravital microscope. At the end of the experiments, blood samples for lactate dehydrogenase (LDH) levels and biopsies of ileum for histologic evaluation were obtained. Results IPC significantly improved the mucosal perfusion and decreased the leukocyte–endothelial interactions. Histologic examination showed that ileal mucosa was significantly less injured in the IPC and PDTC groups as compared with the IR group. Conclusions IPC protects the intestine from late reperfusion injury. HO-1 is involved in this protection. These findings may be of significant importance in clinical small bowel transplantation.

Goal-directed Perioperative Fluid Management

Goal-directed Perioperative Fluid Management

Mechanosensation and Mucosal Blood Perfusion in the Esophagus of Healthy Volunteers Studied with a Multimodal Device Incorporating Laser Doppler Flowmetry and Endosonography

Both mechanical and ischemic mechanisms can cause gastrointestinal pain. We investigated whether discomfort and pain caused by bag distension in the esophagus of healthy subjects correlated best with mechanical forces (stress), deformation (strain), or mucosal perfusion. Twenty-nine subjects underwent ramp bag distension using a novel catheter design incorporating high-frequency intraluminal ultrasound, laser Doppler flowmetry, and manometry. Perfusion, pressure, and geometric data were analyzed at visual analog scale (VAS) levels 1-7 in 19 subjects. The circumferential stress increased exponentially as a function of volume, whereas strain showed a linear increase. The perfusion showed a modest decline, on average 15% from baseline to VAS = 7. A significant association was found between the sensory response and stress and strain (P < 0.05). No significant association was found between the sensory response and perfusion. In conclusion, the discomfort and pain response to bag distension in the esophagus is likely to be caused by mechanical rather than ischemic mechanisms.

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.

New Insight in Loss of Gut Barrier during Major Non-Abdominal Surgery

BackgroundGut barrier loss has been implicated as a critical event in the occurrence of postoperative complications. We aimed to study the development of gut barrier loss in patients undergoing major non-abdominal surgery.Methodology/Principal FindingsTwenty consecutive children undergoing spinal fusion surgery were included. This kind of surgery is characterized by long operation time, significant blood loss, prolonged systemic hypotension, without directly leading to compromise of the intestines by intestinal manipulation or use of extracorporeal circulation. Blood was collected preoperatively, every two hours during surgery and 2, 4, 15 and 24 hours postoperatively. Gut mucosal barrier was assessed by plasma markers for enterocyte damage (I-FABP, I-BABP) and urinary presence of tight junction protein claudin-3. Intestinal mucosal perfusion was measured by gastric tonometry (PrCO2, Pr-aCO2-gap). Plasma concentration of I-FABP, I-BABP and urinary expression of claudin-3 increased rapidly and significantly after the onset of surgery in most children. Postoperatively, all markers decreased promptly towards baseline values together with normalisation of MAP. Plasma levels of I-FABP, I-BABP were significantly negatively correlated with MAP at ½ hour before blood sampling (−0.726 (p<0.001), −0.483 (P<0.001), respectively). Furthermore, circulating I-FABP correlated with gastric mucosal PrCO2, Pr-aCO2-gap measured at the same time points (0.553 (p = 0.040), 0.585 (p = 0.028), respectively).Conclusions/SignificanceThis study shows the development of gut barrier loss in children undergoing major non-abdominal surgery, which is related to preceding hypotension and mesenterial hypoperfusion. These data shed new light on the potential role of peroperative circulatory perturbation and intestinal barrier loss.

Ischemic Intestinal Injury during Cardiopulmonary Bypass Does Not Show an Association with Neutrophil Activation

Background: Neutrophil activation and tissue sequestration are crucial events in intestinal ischemia-reperfusion injury, but their role in the gut wall after clinical cardiopulmonary bypass (CPB) remains unclear. We tested whether local post-CPB inflammatory response in the gut wall would be associated with intestinal mucosal perfusion. Methods: Twenty pigs underwent 60 min of aortic clamping and 75 min of normothermic perfusion. Intestinal biopsies were taken after 120 min of reperfusion. Based on ileal myeloperoxidase activity (MPO), the animals were divided into 2 groups, CPB-induced increase in MPO (MPO+) versus no such increase (MPO–), for comparison of the parameters that measure gut mucosal perfusion. Ileal p_CO_₂ and intramucosal pH were determined, and arterial gases were analyzed. Additionally, several hemodynamic parameters and blood thrombin-antithrombin complexes (TAT) were measured. Results: Myocyte degeneration, endothelial activation and vasculitis were more pronounced in the MPO+ group (p < 0.05), while the MPO– group showed significantly increased pi_CO_₂ and lower mucosal pH values during reperfusion. Hemodynamics and TAT levels did not differ between the groups. Conclusion: Tissue sequestration of neutrophils was poorly associated with perturbed mucosal perfusion after CPB. Mechanisms of gut wall injury after a low-flow/reperfusion setting can differ from those in reperfusion injury after total ischemia.

Ischemic Colitis Secondary to Extrinsic Compression by Large Ovarian Cystic Neoplasm

Purpose: INTRODUCTION: Ischemic colitis is most often caused by inadequate colonic perfusion, either occlusive or non-occlusive. We describe an unusual mechanism of ischemic colitis namely, extrinsic compression on the colon by a large malignant mass. CASE: A 60 y/o Caucasian female developed recurrent ovarian carcinoma three years after the total abdominal hysterectomy with bilateral salpingo-oopherectomy and omentectomy. CT scan showed a large pelvic cystic mass, 12.5 × 13 cm extrinsically compressing the sigmoid colon and both ureters. There were hepatic cystic metastases as well. Cardiac function and hemodynamics were normal. Patient was on no vasospastic medications or NSAIDs. A colonoscopy was performed to evaluate new onset diarrhea, fecal incontinence and left lower quadrant abdominal pain. Colonoscopy revealed extrinsic compression on a sigmoid colon. There were mucosal ulcerations overlying the compressed portions of the sigmoid colon. Biopsies were consistent with ischemic colitis. A water soluble contrast lower GI x-ray revealed tight compression of sigmoid colon by the pelvic mass. Patient declined diverting colostomy and ultimately succumbed to her malignancy in hospice. DISCUSSION: Our patient had ischemic colitis in association with tight extrinsic compression on the involved colonic mucosa. This represents an unusual mechanism of ischemic colitis. We speculate that extrinsic compression interferes with blood flow to the colon by compressing serosal blood vessels, as well as by raising intramucosal pressure and thereby reducing mucosal perfusion. CONCLUSION: Tight extrinsic compression of the colon should be considered as a contributory cause in some cases of ischemic colitis.

Effect of Age, Feeding, and Omeprazole Administration on Gastric Tonometry in Healthy Neonatal Foals

Gastric tonometry is commonly used in humans as an assessment of intestinal mucosal perfusion. Values in healthy foals are currently unknown. Age, enteral feeding, and omeprazole administration would significantly alter gastric tonometry measurements in neonatal foals. Nine clinically normal foals were used to assess the effect of age and feeding, and 8 similar foals were used to assess the effect of omeprazole. At 1, 7, and 14 days of age, gastric intramucosal PCO2 (PgCO2) and arterial blood gas samples were obtained at baseline, immediately after feeding milk, and 1 and 2 hours after fasting for calculation of the intramucosal-arterial PCO2 difference (DeltaCO2). To evaluate the effect of omeprazole, foals were evaluated twice as above, 2 hours after fasting, comparing administration of omeprazole to no drug. There was a significant effect of age and feeding on PgCO2 and DeltaCO2, whereas arterial PCO2 was not significantly affected by these factors. Postfeeding DeltaCO2 values were significantly lower than fasted values. Baseline and postfeeding DeltaCO2 increased with age. There was no significant effect of age on data collected after 1 or 2 hours of fasting. The 90% reference interval for DeltaCO2 data collected after fasting was 0-54 mmHg. Foals had a significantly higher mean gastric pH and significantly higher DeltaCO2 and PgCO2 following omeprazole relative to no treatment. Because of the high and variable DeltaCO2, which is exacerbated by omeprazole administration, the reference interval in foals is extremely wide.

Dysphagia Following Anterior Cervical Arthrodesis Is Associated with Continuous, Strong Retraction of the Esophagus

The prevalence of dysphagia after anterior cervical decompression and arthrodesis is estimated to be 50% within one month and 21% at twelve months. However, its exact etiology is not well understood. The objective of the present study was to explore the relationship between intraoperative intra-esophageal pressure due to surgical retraction, esophageal mucosal blood flow at the level of surgery, and postoperative dysphagia. Our hypothesis was that sustained elevated pressure on the esophagus during anterior cervical arthrodesis is associated with postoperative dysphagia. Seventeen selected patients scheduled for anterior cervical arthrodesis were studied. Throughout the procedure, intraluminal pressure in the upper esophageal sphincter was measured (mm Hg) with a custom-made manometer probe and mucosal perfusion was measured at the level of surgery with a laser Doppler flowmeter. The type of retraction chosen by the surgeon was noted. Postoperatively, the patients were specifically evaluated for dysphagia on the first postoperative day and at six weeks, three months, and six months postoperatively with use of the M.D. Anderson Dysphagia Inventory. Four of the eleven patients who had dynamic retraction and five of the six patients who had static retraction during surgery had postoperative dysphagia. In the group of patients with dysphagia, the average M.D. Anderson Dysphagia Inventory score decreased from 93.8 +/- 12.1 preoperatively to 67.7 +/- 11.4 on the first postoperative day (p < 0.001). The patients with dysphagia had a significantly higher average intraluminal pressure (60.8 +/- 54.3 compared with 54.4 +/- 51.8 mm Hg; p < 0.0001) as well as significantly lower average mucosal perfusion (26.1 +/- 18.1 compared with 40.8 +/- 26.2 tissue perfusion units; p < 0.0001) in comparison with the asymptomatic patients. Patients with dysphagia following anterior cervical arthrodesis were exposed to higher intraoperative esophageal pressure and decreased esophageal mucosal blood flow during surgical retraction as compared with patients without dysphagia. In this small series, dynamic retraction seemed to be associated with a lower prevalence of postoperative dysphagia.

Persistent villi hypoperfusion explains intramucosal acidosis in sheep endotoxemia*

To test the hypothesis that persistent villi hypoperfusion explains intramucosal acidosis after endotoxemic shock resuscitation. Controlled experimental study. University-based research laboratory. A total of 14 anesthetized, mechanically ventilated sheep. Sheep were randomly assigned to endotoxin (n = 7) or control groups (n = 7). The endotoxin group received 5 microg/kg endotoxin, followed by 4 microg x kg(-1) x hr(-1) for 150 mins. After 60 mins of shock, hydroxyethylstarch resuscitation was given to normalize oxygen transport for an additional 90 mins. Endotoxin infusion decreased mean arterial blood pressure, cardiac output, and superior mesenteric artery blood flow (96 +/- 10 vs. 51 +/- 20 mm Hg, 145 +/- 30 vs. 90 +/- 30 mL x min(-1) x kg(-1), and 643 +/- 203 vs. 317 +/- 93 mL x min(-1) x kg(-1), respectively; p < .05 vs. basal), whereas it increased intramucosal-arterial PCO2 (deltaPCO2) and arterial lactate (3 +/- 3 vs. 14 +/- 8 mm Hg, and 1.5 +/- 0.5 vs. 3.7 +/- 1.3 mmol/L; p < .05). Sublingual, and serosal and mucosal intestinal microvascular flow indexes, and the percentage of perfused ileal villi were reduced (3.0 +/- 0.1 vs. 2.3 +/- 0.4, 3.2 +/- 0.2 vs. 2.4 +/- 0.6, 3.0 +/- 0.0 vs. 2.0 +/- 0.2, and 98% +/- 3% vs. 76% +/- 10%; p < .05). Resuscitation normalized mean arterial blood pressure (92 +/- 13 mm Hg), cardiac output (165 +/- 32 mL x min(-1) x kg(-1)), superior mesenteric artery blood flow (683 +/- 192 mL x min(-1) x kg(-1)), and sublingual and serosal intestinal microvascular flow indexes (2.8 +/- 0.5 and 3.5 +/- 0.7). Nevertheless, deltaPCO2, lactate, mucosal intestinal microvascular flow indexes, and percentage of perfused ileal villi remained altered (10 +/- 6 mm Hg, 3.7 +/- 0.9 mmol/L, 2.3 +/- 0.4, and 78% +/- 11%; p < .05). In this model of endotoxemia, fluid resuscitation corrected both serosal intestinal and sublingual microcirculation but was unable to restore intestinal mucosal perfusion. Intramucosal acidosis might be due to persistent villi hypoperfusion.

EVALUATION OF INTESTINAL PRECONDITIONING IN A PORCINE MODEL USING CLASSIC ISCHEMIC PRECONDITIONING OR LUNG RECRUITMENT MANEUVERS

To test the hypotheses that repeated brief intestinal ischemic insults would elicit an intestinal preconditioning response to a subsequent intestinal I/R injury and that a similar response would be elicited by repeated lung recruitment maneuvers (RMs). Randomized experimental controlled animal study. University hospital animal laboratory. Eighteen anesthetized pigs. Animals were randomized to one of three groups, with six animals in each group. Control group 75-min superior mesenteric artery (SMA) occlusion followed by 60-min reperfusion. Ischemic preconditioning group, three 5-min-long SMA occlusions preceding 75-min SMA occlusion and 60-min reperfusion. Recruitment maneuver (RM) group, three 2-min-long RMs preceding 75-min SMA occlusion and 60-min reperfusion. We measured systemic and mesenteric hemodynamic parameters, jejunal mucosal perfusion, net mesenteric lactate flux, jejunal tissue oxygen tension, and mesenteric oxygenation. Every 15 min, jejunal microdialysate samples were collected and analyzed for glucose, lactate, and glycerol. Jejunal tissue samples were collected postmortem. After occlusion of SMA, regional parameters in all groups indicated abolished perfusion and gradually increasing intraluminal microdialysate lactate and glycerol levels. At reperfusion, regional parameters indicated mesenteric hyperperfusion, whereas microdialysis markers of mucosal anaerobic metabolism and cell injury decreased, although not reaching baseline. Histological examination revealed severe mucosal injury in all groups. There were no significant differences between groups in the observed parameters. No protective preconditioning response could be observed when performing repeated brief intestinal ischemic insults or repeated lung RMs before an intestinal I/R injury.

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.

NOREPINEPHRINE AND INTESTINAL MUCOSAL PERFUSION IN VASODILATORY SHOCK AFTER CARDIAC SURGERY

Patients with norepinephrine-dependent vasodilatory shock after cardiac surgery (n = 10) were compared with uncomplicated postcardiac surgery patients (n = 10) with respect to jejunal mucosal perfusion, gastric-arterial PCO2 gradient, and splanchnic oxygen demand/supply relationship. Furthermore, the effects of norepinephrine-induced variations in MAP on these variables were evaluated in vasodilatory shock. Norepinephrine infusion rate was randomly and sequentially titrated to target MAPs of 60, 75, and 90 mmHg (0.25 +/- 0.24, 0.37 +/- 0.21, and 0.55 +/- 0.39 microg/kg per minute, respectively). Data on jejunal mucosal perfusion, jejunal mucosal hematocrit, and red blood cell (RBC) velocity (laser Doppler flowmetry) as well as gastric-arterial PCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained. Splanchnic oxygen extraction was 71 +/- 16% in the vasodilatory shock group and 41 +/- 9% in the control group (P < 0.001), whereas splanchnic lactate extraction did not differ between the two groups. Jejunal mucosal perfusion (61%; P < 0.001), RBC velocity (35%; P < 0.01), and gastric-arterial mucosal PCO2 gradient (150%; P < 0.001) were higher in the vasodilatory shock group compared with those of the control group. Jejunal mucosal perfusion, jejunal mucosal hematocrit, RBC velocity, gastric-arterial mucosal PCO2 gradient, splanchnic oxygen extraction, and splanchnic lactate extraction were not affected by increasing infusion rates of norepinephrine. In patients with norepinephrine-dependent vasodilatory shock after cardiac surgery, intestinal mucosal perfusion was higher, whereas splanchnic and gastric oxygen demand/supply relationships were impaired compared with postoperative controls, suggesting that intestinal mucosal perfusion is prioritized in vasodilatory shock. Increasing MAP from 60 to 90 mmHg with norepinephrine in clinical vasodilatory shock does not affect intestinal mucosal perfusion and gastric or global splanchnic oxygen demand/supply relationships.

Endoscopic Reflectance Spectrophotometry and Visible Light Spectroscopy in Clinical Gastrointestinal Studies

The use of reflectance spectrophotometry (RS) for mucosal hemodynamic measurement relies on the recognition of changes in indexes of mucosal hemoglobin concentration and oxygen saturation. Endoscopic application in clinical studies has confirmed important observations demonstrated in animal experiments. The vasoconstriction induced by propranolol, vasopressin, glypressin, or somatostatin in the portal hypertensive gastric mucosa and the reduction of gastroduodenal mucosal perfusion by nonsteroidal anti-inflammatory drugs (NSAIDs) or smoking, mesenteric venoconstriction associated with systemic hypoxia, and acid-induced duodenal hyperemia are important examples. Prognostic predictions include the development of stress-induced gastric ulcerations in patients with significant reductions in gastric perfusion after thermal or head injury, or the demonstration of delayed gastric or duodenal ulcer healing when the hyperemia at the ulcer margin fails to materialize. In mechanical-ventilator-dependent patients with sepsis, a significantly reduced gastric mucosal RS measurement portends a grave prognosis (mortality >80%). Recent advances in technology resulted in the construction and validation of instruments for visible light spectroscopy. Measurements focused on tissue oxygen saturation demonstrated epinephrine and vessel-ligation-induced vasoconstriction, the absence of ischemia in radiation-induced rectal telangiectasias, and gut ischemia responsive to revascularization treatment. Endoscopic RS and visible light spectroscopy are suitable for assessing the role of blood flow in conditions with a lesser degree of ischemia and for testing the hypothesis that functional dyspepsia and dysmotility syndromes may be due to gut ischemia.