Mechanical trauma as the major cause of troponin T release after transvenous implantation of cardioverter/defibrillators.

To study the cause of myocardial injury after elective transvenous insertion of a cardioverter/defibrillator, we measured troponin T (TnT) release in 27 patients. Five patients needing only replacement of the generator with threshold testing served as controls. Compared to the control group, a significant increase in TnT occurred in the patients undergoing insertion, which was greatest in the group receiving screw-in electrodes. There was no correlation between TnT and the number and energy of the shocks and the time in fibrillation. Duration of surgery and TnT release were positively associated. Cardiac injury therefore mainly results from mechanical trauma during insertion of the electrodes and only to a lesser degree from electrical and ischemic lesions.

Pulsatility does not change cerebral oxygenation during cardiopulmonary bypass.

BACKGROUND: To determine the effect of pulsatility during cardiopulmonary bypass (CPB) on cerebral oxygenation, we measured oxyhaemoglobin (HbO2), deoxyhaemoglobin (Hb) and oxidised cytochrome aa3 (CtO2) with near-infrared spectroscopy (NIRS) in 14 patients electively scheduled for cardiac surgery. METHODS: Cerebral oxygenation was measured during steady state CPB at a core temperature of 32 degrees C. Non-pulsatile flow and pulsatile flow were performed for 10 min each. RESULTS: After 14 min of CPB, HbO2, Hb and CtO2 were significantly below prebypass values. HbO2 and CtO2 did not alter with changing flow patterns. Hb significantly increased both during the period of nonpulsatile (median: -0.7 vs. 0.25 micromol/l; P<0.05) and pulsatile flow (median: 0.25 vs. 0.5 micromol/l; P<0.001). This increase was independent of flow pattern. CONCLUSIONS: Neither oxygenated haemoglobin, nor intracellular oxygenation, represented by CtO2, indicated a beneficial effect of pulsatile perfusion during hypothermic CPB. These results, however, are only valid for short time effects within 10 min before rewarming from CPB and patients without flow-limiting stenoses of the carotid artery.

Efficacy of two methods for reducing postbypass afterdrop.

BACKGROUND: Afterdrop, defined as the precipitous reduction in core temperature after cardiopulmonary bypass, results from redistribution of body heat to inadequately warmed peripheral tissues. The authors tested two methods of ameliorating afterdrop: (1) forced-air warming of peripheral tissues and (2) nitroprusside-induced vasodilation. METHODS: Patients were cooled during cardiopulmonary bypass to approximately 32 degrees C and subsequently rewarmed to a nasopharyngeal temperature near 37 degrees C and a rectal temperature near 36 degrees C. Patients in the forced-air protocol (n = 20) were assigned randomly to forced-air warming or passive insulation on the legs. Active heating started with rewarming while undergoing bypass and was continued for the remainder of surgery. Patients in the nitroprusside protocol (n = 30) were assigned randomly to either a control group or sodium nitroprusside administration. Pump flow during rewarming was maintained at 2.5 l x m(-2) x min(-1) in the control patients and at 3.0 l x m(-2) x min(-1) in those assigned to sodium nitroprusside. Sodium nitroprusside was titrated to maintain a mean arterial pressure near 60 mm Hg. In all cases, a nasopharyngeal probe evaluated core (trunk and head) temperature and heat content. Peripheral compartment (arm and leg) temperature and heat content were estimated using fourth-order regressions and integration over volume from 18 intramuscular needle thermocouples, nine skin temperatures, and "deep" hand and foot temperature. RESULTS: In patients warmed with forced air, peripheral tissue temperature was higher at the end of warming and remained higher until the end of surgery. The core temperature afterdrop was reduced from 1.2+/-0.2 degrees C to 0.5+/-0.2 degrees C by forced-air warming. The duration of afterdrop also was reduced, from 50+/-11 to 27+/-14 min. In the nitroprusside group, a rectal temperature of 36 degrees C was reached after 30+/-7 min of rewarming. This was only slightly faster than the 40+/-13 min necessary in the control group. The afterdrop was 0.8+/-0.3 degrees C with nitroprusside and lasted 34+/-10 min which was similar to the 1.1+/-0.3 degrees C afterdrop that lasted 44+/-13 min in the control group. CONCLUSIONS: Cutaneous warming reduced the core temperature afterdrop by 60%. However, heat-balance data indicate that this reduction resulted primarily because forced-air heating prevented the typical decrease in body heat content after discontinuation of bypass, rather than by reducing redistribution. Nitroprusside administration slightly increased peripheral tissue temperature and heat content at the end of rewarming. However, the core-to-peripheral temperature gradient was low in both groups. Consequently, there was little redistribution in either case.

Mucosal tissue oxygenation of the porcine jejunum during normothermic cardiopulmonary bypass.

Cardiopulmonary bypass (CPB) has been associated with intestinal tissue hypoxia, but direct measurements of mucosal oxygenation have not been performed. In anaesthetized pigs, jejunal mucosal oxygen tension and microvascular haemoglobin oxygen saturation were measured by a Clark-type electrode and tissue reflectance spectrophotometry. In pigs, normothermic CPB with systemic oxygen transport equivalent to baseline values was performed. In control animals, mucosal oxygen tension and mucosal haemoglobin oxygen saturation were mean 5.01 (SD 1.08) kPa and 38.0 (2.3)%, respectively. CPB was associated with a decrease in mucosal oxygen tension to 2.26 (1.21) kPa, decrease in mucosal microvascular haemoglobin oxygen saturation to 26.0 (3.9)% and appearance of oscillations in mucosal microvascular haemoglobin oxygen saturation. With CPB, arterial lactate concentrations increased from 1.77 (1.37) to 3.52 (1.58) mmol litre-1, but transvisceral lactate and splanchnic venous-arterial carbon dioxide tension gradients remained unchanged. Our results support the concept that CPB is associated with diminished oxygenation of intestinal mucosa that is probably caused by regional redistribution.

Centrifugal pumps as left ventricular assist for coronary revascularization on a beating heart.

During recent years, coronary bypass surgery has progressed toward minimizing invasiveness. One important feature of this approach is performing surgery on a beating heart. During the crucial phase of such surgery, the mechanical support of the heart with a left ventricular assist device (LVAD) is a possible option. During the period from October 1, 1994 until June 30, 1997, we employed a centrifugal pump system in 118 cases of coronary artery bypass graft (CABG) procedures with LVAD support (mechanically supported CABG [SUPPCAB]). A total of 179 distal anastomoses with an average of 1.5 +/- 0.5 coronary anastomoses per patient was performed. Three types of pumps were used: 23 BioPump, 87 Isoflow, and 8 Capiox systems. The median time on mechanical support was 44 min (range, 16-116 min). The mean flow rate during support time was 3.5 +/- 0.8 L/min, which results in a calculated flow of 1.7 +/- 0.6 L/min/m2 body surface area (BSA). The average flow was 3.2 +/- 0.8 L/min with the BioPump and 3.7 +/- 0.8 L/min with the Isoflow pump, respectively (p < 0.01). The mean arterial pressure during mechanical support was 75 +/- 12 mm Hg. In 2 patients, the pump system was kept running postoperatively in the ICU. Eight of the patients received operations under resuscitation or in cardiogenic shock. Nine (7.9%) of the patients did not survive the early postoperative phase. For coronary revascularization of the anterolateral and diaphragmatic parts of the heart, the SUPPCAB procedure is feasible with excellent mechanical support of the heart by centrifugal pumps. Especially in high risk cases, this procedure can be recommended.

Splanchnic oxygen transport and lactate metabolism during normothermic cardiopulmonary bypass in humans.

UNLABELLED: The effect of normothermic (36.2 degrees C +/- 0.6 degree C) nonpulsatile cardiopulmonary bypass (CPB) on splanchnic (hepatic) blood flow (SBF), splanchnic oxygen transport (DO2spl) and oxygen consumption (VO2spl), splanchnic lactate uptake and gastric mucosal pH (pHi, gastric tonometry) was studied in 12 adults (New York Heart Association class II, ejection fraction > or = 0.4) undergoing coronary artery surgery. SBF was estimated with the constant-infusion indocyanine green (ICG) technique using a hepatic venous catheter. DO2spl, VO2spl, and splanchnic lactate uptake were calculated using the Fick principle after the induction of anesthesia, during aortic cross-clamping, after CPB, and 2 and 7 h after admission to the intensive care unit (ICU). SBF, DO2spl, and VO2spl did not decrease during CPB but increased after ICU admission, whereas pHi decreased 7 h after ICU admission. Initial ICG extraction was 0.78, which decreased to 0.54 during aortic clamping and remained low thereafter. The increased arterial blood lactate concentrations were not associated with a decreased splanchnic lactate uptake. We conclude that normothermic CPB is not associated with deterioration in the global intestinal oxygen supply. The increase of blood lactate levels and the decrease in ICG extraction, as well as in pHi, are consistent with a systemic inflammatory response to CPB. IMPLICATIONS: This study demonstrated that normothermic cardiopulmonary bypass (at flows > 2.4 L.min-1.m-2) was not associated with deterioration in global intestinal oxygen delivery, which suggests that increased blood lactate concentrations and decreased gastric mucosal pH and indocyanine green extraction are manifestations of a systemic inflammatory response to cardiopulmonary bypass.

Dopamine and intestinal mucosal tissue oxygenation in a porcine model of haemorrhage.

Haemorrhage is associated with intestinal mucosal hypoxia and impaired gut barrier function. Dopamine increases oxygen delivery to the intestinal mucosa and may thus counteract haemorrhage-induced mucosal hypoxia. Jejunal mucosal tissue oxygen tension (mucosal PO2) and jejunal oxygen saturation of mucosal microvascular haemoglobin (mucosal HbO2) were measured in 14 anaesthetized pigs. Seven animals served as controls (group C) and seven received continuous infusion of dopamine 16 micrograms kg-1 min-1 (group D) while 45% of blood volume was removed in three equal increments. Resuscitation was performed using shed blood and fluid. Mean arterial pressure and systemic oxygen delivery decreasing significantly during haemorrhage and returned to baseline after resuscitation in both groups. Mucosal PO2 decreased from 4.4 to 1.7 kPa after haemorrhage (P < 0.01) and further to 1.5 kPa after resuscitation (P < 0.01) in group C whereas group D showed an increase from 3.9 to 5.9 kPa after the start of the dopamine infusion (P < 0.05), but no significant difference from baseline after haemorrhage (2.3 kPa) (ns) or resuscitation (3.1 kPa) (ns). Mucosal HbO2 decreased from 52 to 32% after haemorrhage (P < 0.05) and increased to near baseline (37%) (ns) after resuscitation in group C whereas group D showed no significant changes from baseline (54%) throughout the experiment. Comparison between groups showed higher mucosal PO2 and HbO2 values for group D animals after the start of the dopamine infusion (P < 0.05 each), after the first two steps of haemorrhage (P < 0.01 each) and after resuscitation (P < 0.05 each). We conclude that i.v. dopamine 16 micrograms kg-1 min-1 improved tissue oxygenation of the small intestinal mucosa during moderate haemorrhage and subsequent resuscitation.

Inotropic treatment and intestinal mucosal tissue oxygenation in a model of porcine endotoxemia.

OBJECTIVE: To evaluate the dose-related effects of dopamine, dopexamine, and dobutamine on intestinal mucosal tissue oxygenation following short-time infusion of Escherichia coli lipopolysaccharide, which has previously been shown to decrease mucosal tissue oxygenation by 60% of control values. DESIGN: Prospective, randomized, unblinded study. SETTING: Animal research laboratory. SUBJECTS: Anesthetized, mechanically ventilated domestic pigs. INTERVENTIONS: Pigs were infused with 2 microg/kg of E. coli lipopolysaccharide over 20 mins via the superior mesenteric artery. Pulmonary artery occlusion pressure was maintained near 15 mm Hg, using a mixed infusion regimen of Ringer's lactate solution and hydroxyethyl starch. Following endotoxemia, a small segment of the jejunal mucosa was exposed by midline laparotomy and antimesenteric incision. The control group (n = 7) received no further interventions. Pigs in the dopamine (n = 7), dopexamine (n = 7), and dobutamine (n = 7) groups were infused with 2.5, 5, 10, and 20 microg/kg/min of the respective drug via a central venous catheter. MEASUREMENTS AND MAIN RESULTS: Systemic hemodynamics as well as systemic, mesenteric, and femoral blood gas variables were measured using an arterial, a thermodilution pulmonary artery, a superior mesenteric venous, and a femoral venous catheter. Jejunal mucosal tissue PO2 was measured by means of two Clark-type surface oxygen electrodes. Oxygen saturation of jejunal mucosal microvascular hemoglobin was determined by tissue reflectance spectrophotometry. Infusion of endotoxin resulted in pulmonary hypertension. Systemic hemodynamics remained unchanged except for brief decreases in cardiac output and arterial blood pressure. Dopamine, dopexamine, and dobutamine increased systemic oxygen delivery in a dose-related manner by 80% (p < .01), 96% (p = .00), and 129% (p = .00) of values before inotropic treatment. Dopamine increased mucosal tissue PO2 by 109% (10-microg dose, p < .01) and 164% (20-microg dose, p = .00), and mucosal hemoglobin oxygen saturation by 61% (5-microg dose, p < .05), 102% (10-microg dose, p < 01) and 121% (20-microg dose, p = .00). Dopexamine increased mucosal tissue PO2 by 89% (20-microg dose, p < .01) and mucosal hemoglobin oxygen saturation by 26% (2.5-microg dose, p < .05) and 35% (5-, 10-, and 20-microg dose, p < .05). In the dobutamine and control groups, no significant effect on either mucosal tissue PO2 or hemoglobin oxygen saturation was observed. CONCLUSIONS: In this model of porcine endotoxemia, dopamine and, to a lesser extent, dopexamine increase intestinal mucosal tissue oxygenation. Of all three inotropes used, dobutamine has the most pronounced effect on systemic oxygen delivery, but it does not improve mucosal tissue oxygenation. Selective vasodilation within the intestinal mucosa, mediated mainly by dopamine-1 receptors, seems to explain the observed intestinal mucosal effect of dopamine and dopexamine.

The effects of progressive anemia on jejunal mucosal and serosal tissue oxygenation in pigs.

Anemia may promote intestinal hypoxia. We studied the effects of progressive isovolemic hemodilution on jejunal mucosal (Po2muc), and serosal tissue oxygen tension (Po2ser, Clark-type surface electrodes), mucosal microvascular hemoglobin oxygen saturation (Hbo2muc), and hematocrit (Hctmuc; tissue reflectance spectophotometry) in a jejunal segment. Twelve domestic pigs were anesthetized, paralyzed, and mechanically ventilated. Laparatomy was performed, arterial supply of a jejunal segment isolated, and constant pressure pump perfused. Seven animals were progressively hemodiluted to systemic hematocrits (Hctsys) of 20%, 15%, 10%, and 6%. Baseline for Po2muc, Po2ser and Hbo2muc was 23.5 +/- 2.1 mm Hg, 57.5 +/- 4 mm Hg, and 47.0% +/- 6.4% which were not different from the five controls. Despite a significant increase in jejunal blood flow, jejunal oxygen delivery decreased and oxygen extraction ratio increased significantly at Hctsys 10% and 6%. Po2ser decreased significantly below or at Hctsys of 15%, whereas Po2muc and Hbo2muc were maintained to Hctsys of 10%, but less than 10% Hbo2muc and mesenteric venous pH decreased significantly, implying that physiological limits of jejunal microvascular adaptation to severe anemia were reached. Decrease of Hctmuc was less pronounced than Hctsys. In conclusion, redistribution of jejunal blood flow and an increase in the ratio of mucosal to systemic hematocrit are the main mechanisms maintaining mucosal oxygen supply during progressive anemia.

Effects of short-term endotoxemia and dopamine on mucosal oxygenation in porcine jejunum.

Effects of Escherichia coli lipopolysaccharide (2 micrograms.kg-1.20 min-1; LPS), given systemically (S) or via superior mesenteric artery (M), and consecutive dopamine infusion (16 micrograms.kg-1.20 min-1) on jejunal mucosal tissue O2 tension (PO2muc) and serosal tissue O2 tension (PO2ser; Clark-type surface electrodes) and jejunal mucosal microvascular hemoglobin O2 saturation (HbO2muc; tissue reflectance spectrophotometry) were investigated in a hemodynamically stable pig model. Twenty-one pigs were anesthetized, paralyzed, and mechanically ventilated. After laparotomy, a mesenteric venous catheter was inserted and a jejunal antimesenteric enterotomy performed. LPS-infused animals developed similar degrees of pulmonary hypertension. No differences in cardiac output and mean arterial blood pressure between groups were found. PO2muc and HbO2muc were significantly lower in M animals compared with control (C) [210 min; PO2muc: 7.12 +/- 1.81 (M), 19.01 +/- 3.12 mmHg (C); HbO2muc: 28.78 +/- 3.36 (M), 49.09 +/- 3.84% (C)], whereas S animals ranged in between (PO2muc: 13.36 +/- 2.2 mmHg; HbO2muc: 40.68 +/- 4.43%). Of measured PO2muc values, 12.6 (C), 20.6 (S), and 46.3% (M) ranged from 0 to 5 mmHg. PO2ser was lower in LPS animals compared with control [59.43 +/- 5.4 (C), 45.00 +/- 6.12 (S), 47.33 +/- 4.34 (M) mmHg]. Dopamine increased PO2muc and HbO2muc to similar absolute values and significantly decreased frequency of PO2muc (0-5 mmHg) in M animals. We conclude that LPS impairs mucosal tissue oxygenation independently of systemic hemodynamics. Mucosal microvascular dysfunction depends on regional LPS concentrations. Under conditions of compromised tissue oxygenation, dopamine significantly improves PO2muc and HbO2muc.

[Percutaneous "high risk" angioplasty with prophylactic cardiopulmonary support. High risk PTCA with mechanical circulatory support]. / Die perkutane "Hochrisiko" -Angioplastie unter prophylaktischem Kardiopulmonalen Support. Hochrisiko PTCA mit mechanischer Kreislaufassistenz.

With improved technology and development of several mechanical assist devices, the indications of percutaneous transluminal coronary revascularization have been extended. In 39 patients (30 men, mean age = 60.1 +/- 8.1 years) with angina pectoris or heart failure, with poor operative risk-benefit ratio and ejection fraction < 35% and/or target vessel supplying > 50% of the viable myocardium, we performed assisted percutaneous transluminal coronary revascularization. Intraortic balloon counterpulsation (n = 16), extracorporal circulation (n = 21), or hemopump (n = 2) were used for mechanical support. Complete 6-week follow up was possible in 27 patients. An improvement of left-ventricular function (patients with EF < or = 35% demonstrated an improvement: 27 +/- 7 vs 36 +/- 10%, p < 0.05), heart failure (patients with EF < or = 35% demonstrated an improvement of maximal oxygen uptake: 14 +/- 4 vs 17 +/- 4 ml/kg/min; p < 0.05) and a marked improvement of angina (23/38 demonstrated CCS-improvement of at least one class) was found. Hospital mortality was as low as 2.6%. Major postinterventional complications included nonfatal myocardial infarction (n = 2), fatal retroperitoneal bleeding (n = 1), pulmonary edema (n = 1), nonfatal ventricular fibrillation (n = 1), cerebrovascular event without residual (n = 1), and deep vein thrombosis (n = 4). In conclusion, assisted percutaneous revascularization was successful in a high risk subset of patients with increased surgical risk and/or poor ventricular function.

[Surgical coronary revascularization of the beating heart]. / Chirurgische Koronarrevaskularisation am schlagenden Herzen.

Despite the fact that all the progress in technology, surgical technique and pathophysiological knowledge has made aortocoronary bypass surgery a safe routine procedure, there are certain clinical settings where an alternative approach seems to be advantageous. In 50 patients with age ranging from 51 to 74 years with advanced coronary heart disease and poor left ventricular (LV) function, as well as in patients with good LV function and single or double vessel disease not amenable for PTCA and in patients with acute ischemia or recent myocardial infarction, we performed coronary artery bypass grafting (CABG) without cardioplegic arrest during a short period of left ventricular unloading by means of a left ventricular assist device (LVAD). During LVAD support we administered Esmolol to decrease the heart rate and to keep the heart flaccid to facilitate easier peripheral anastomosis on a breathing heart. Preoperative ejection fraction ranged from 15 to 56%. In two patients of the acute MI-group, we continued the left ventricular mechanical support postoperatively, one of them survived. We performed on average 1,4 distal anastomoses and used in 34 cases the left internal mammary artery. All but three patients survived the procedure in stable conditions and could leave intensive care after a mean stay of 1.5 days. There were no perioperative myocardial infarctions. In our view, CABG during LVAD support without heart lung machine and cardioplegia is a safe and life saving procedure. No ischemic damage is applied to the heart and it can be recommended for cautions use in select patients.

Dopamine-1-receptor stimulation and mucosal tissue oxygenation in the porcine jejunum.

OBJECTIVE: To evaluate the effects of dopamine-1-receptor stimulation on intestinal mucosal tissue oxygenation. DESIGN: Prospective, experimental, controlled trial. SETTING: Animal research laboratory. SUBJECTS: Anesthetized domestic pigs (30 to 45 kg). INTERVENTIONS: A small segment of the jejunal mucosa and serosa was exposed by midline laparotomy and antimesenteric incision. Fenoldopam, a selective dopamine-1-receptor agonist, was infused in steps, exponentially increasing from 0.6 to 9.6 micrograms/kg/min via a central venous catheter (n = 8, fenoldopam group), whereas a second group (n = 6, saline group) was only given the solvent. MEASUREMENTS AND MAIN RESULTS: Systemic hemodynamics as well as systemic and jejunal acid base and blood gas variables were measured using an arterial catheter, a thermodilution pulmonary artery catheter, and a jejunal venous catheter. Jejunal mucosal and serosal tissue PO2 were measured by means of Clark-type surface oxygen electrodes. Oxygen saturation and relative concentration of mucosal microvascular hemoglobin were measured by means of tissue reflectance spectrophotometry. In the fenoldopam group, systemic oxygen delivery (12.5 +/- 0.8 mL/kg/min at baseline) increased by 56% (p < .001) above baseline values. Mean arterial pressure remained unchanged. Fenoldopam produced a 51% increase in mucosal PO2 (23.8 +/- 2.8 torr [3.2 +/- 0.4 kPa] at baseline; p < .001) and a 31% increase in mucosal hemoglobin oxygen saturation (55.4 +/- 8.3% at baseline; p < .001), but not change in serosal PO2 (58 +/- 4.8 torr [7.7 +/- 0.6 kPa] at baseline). CONCLUSIONS: Fenoldopam improves tissue oxygenation of the porcine jejunum in a dose-related manner. This effect is limited to the inner mucosal layer. Dopamine-1-receptor agonists should be evaluated in patients presenting with signs of intestinal mucosal ischemia.

Dopamine and mucosal oxygenation in the porcine jejunum.

The effect of intravenously delivered dopamine on jejunal tissue oxygenation was studied in 12 pigs anesthetized with midazolam and sufentanil and mechanically ventilated. A small segment of the jejunal mucosa and serosa was exposed by midline laparotomy and antimesenteric incision. Mucosal and serosal tissue PO2, mucosal microvascular hemoglobin oxygen saturation, and mucosal hemoglobin concentration were measured by means of Clark-type oxygen electrodes and tissue reflectance spectrophotometry, respectively. In five animals electromyogenic potentials of the jejunal wall were recorded. Measurements were performed under baseline conditions and after intravenous infusion of 2, 4, 8, 16, 32, and again 2 micrograms.kg-1.min-1 of dopamine. The drug produced a dose-related increase in mucosal PO2 (from 26.5 Torr at baseline to 49 Torr at 32 micrograms of dopamine; P < 0.001) and mucosal hemoglobin oxygen saturation (from 55.1 to 70.1%; P < 0.03) but no change in serosal PO2 (from 70.6 to 65.5 Torr). In nine animals baseline mucosal PO2 and mucosal hemoglobin oxygen saturation showed rhythmic oscillations with a frequency of 2.5-5 cycles/min that could not be related to electromyogenic potentials. Dopamine decreased the oscillation amplitude of these two parameters (P < 0.001), and at doses > 16 micrograms.kg-1.min-1 they were no longer present. Dopamine therefore improves mucosal oxygenation of the porcine jejunum in a selective and dose-related manner. At higher doses the preexisting oscillatory pattern of mucosal oxygenation, which is most likely due to vasomotion, is impeded.

Vasomotion induces regular major oscillations in jejunal mucosal tissue oxygenation.

The mucosa of the small intestine has some unique microcirculatory features that may result in significant tissue oxygenation changes even under physiological conditions. To prove this hypothesis we investigated mucosal and serosal oxygenation in an autoperfused, innervated jejunal segment in pigs. Eight animals (30-40 kg) were anesthetized, paralyzed, and normoventilated. A small segment of the jejunal mucosa and serosa was exposed by a midline laparotomy and an antimesenteric incision. Mucosal and serosal oxygen tensions were measured using Clark-type surface oxygen electrodes. Mucosal hemoglobin saturation and concentration were determined by tissue reflectance spectrophotometry. Systemic hemodynamics, mesenteric-venous acid base, and blood gas variables, as well as systemic acid-base and blood gas variables and jejunal electromyogenic potentials, were recorded. Measurements were performed after a rest period at 0, 30, 60, and 90 min. All animals remained hemodynamically stable. At time 0 the jejunal oxygen extraction ratio was 0.33 +/- 0.05, the mean serosal PO2 was 60.25 +/- 7.69, the mean mucosal PO2 was 25.47 +/- 4.41 mmHg, and the mean mucosal hemoglobin saturation was 46.36 +/- 6.22%. Mean values did not change with time. In contrast to serosal PO2, mucosal PO2, mucosal hemoglobin oxygen saturation, and hemoglobin concentration showed rhythmic oscillations with a frequency of 3.4-5 cycles/min that were unrelated to systemic hemodynamic parameters, respiratory frequency, and intestinal peristalsis. From this we concluded that the jejunal mucosa demonstrates significant, regular changes in oxygenation parameters that are locally mediated. We speculate that the physiological basis for this phenomenon is the countercurrent arrangement of microvessels in conjunction with vasomotion.(ABSTRACT TRUNCATED AT 250 WORDS)

Sodium-taurocholate-induced acute necrotizing pancreatitis does not affect jejunal oxygenation in pigs.

OBJECTIVE: To study the influence of experimentally induced acute necrotizing pancreatitis on jejunal oxygen transport, jejunal oxygen consumption, and mucosal PO2. DESIGN: Prospective, randomized trial. SETTING: Animal laboratory. SUBJECTS: Domestic pigs aged 7 to 8 wks. INTERVENTIONS: Two groups of pigs were anesthetized with midazolam and sufentanyl, mechanically ventilated, and hemodynamically monitored. In controls (n = 9) and in animals with acute necrotizing pancreatitis (n = 9), a segment of the jejunum was isolated and autoperfused in situ. Through an antimesenteric enterotomy, an area of jejunal mucosa was exposed for mucosal PO2 measurements. Acute necrotizing pancreatitis was induced by the injection of 10 mL of 10% sodium-taurocholate into the main pancreatic duct. Both groups received normal saline solution to keep pulmonary artery occlusion pressure constant. MEASUREMENTS: Mucosal PO2 was assessed with a modified Clark-type multiwire surface electrode. After two baseline measurements, systemic and regional oxygen transport variables and mucosal PO2 were determined at designated intervals (20, 40, 60, 100, 120, 160, 200, 240, 280 mins). MAIN RESULTS: Systemic hemodynamics and oxygen transport were maintained in both groups. In contrast to controls, all animals with pancreatitis showed gross macroscopic and histologic evidence of severe acute necrotizing pancreatitis at autopsy. There were no significant differences between groups in jejunal blood flow, oxygen transport, oxygen consumption, oxygen extraction ratio, or mucosal PO2. CONCLUSIONS: Our results demonstrate that, under conditions of sustained systemic hemodynamics, jejunal oxygen transport and mucosal oxygenation are well maintained during the early course of sodium-taurocholate-induced acute necrotizing pancreatitis.