[Are there still indications for albumin?].
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Biomedical subjects
Publications and source records attributed to W Hasibeder.
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We report a 29-year-old primigravid who developed cardiac failure following postpartum haemorrhage unresponsive to volume resuscitation and therapy with catecholamines and phosphodiesterase-inhibitors. Transoesophageal echocardiography (TEE) demonstrated left atrial and ventricular dilatation and global left ventricular hypokinesis. No elevation of serum MB-isoenzyme fraction was detected and other organ functions remained stable. Although emergency cardiac transplantation was considered in the presented patient, the institution of intra-aortic counterpulsation was decided on as a first treatment option. Intra-aortic balloon counter-pulsation rapidly improved cardiac function and led to weaning from pharmacological cardiac support within a few days. Mechanical circulatory assist devices can be life-saving in postpartum-haemorrhage-associated cardiac failure.
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A 53-year-old woman with a history of cervical carcinoma 14 years ago, treated with hysterectomy and radiation therapy, was admitted to the intensive care unit with severe SIRS (systemic inflammatory response syndrome) progressing to shock, multiple organ failure and death within 5 d. Bilateral hydronephrosis diagnosed by sonography and an enlarged left kidney with suspected abscesses verified in a CT-scan suggested the diagnosis of urosepsis. However, multiple microbiological examinations remained sterile. Despite surgical treatment and aggressive intensive care, she died in unresponsive shock. Pathohistologically, an angiotropic large B-cell lymphoma, a rare diffuse intravascular neoplasm of lymphoid origin, was diagnosed. The patient's history of abdominal radiation therapy 14 years earlier as well as multiple negative microbiological specimens in a patient with suspected urosepsis should have initiated the search for a non-infectious cause of the disease.
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.
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.
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.
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.
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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.
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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.
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.
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)
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.
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We present a patient with evidence of severe intravascular hemolysis after mitral valve repair, an established method for the surgical treatment of mitral valve disease to avoid prosthesis related complications. The coincidence of this uncommon complication with hemodynamic instability due to pre-existing myocardial dysfunction and Gram-negative pneumonia promoted the development of simultaneous dysfunction of liver, kidney and the cardio-respiratory system. Elimination of the source of hemolysis by re-operation with mitral valve replacement on the ninth postoperative day allowed prompt recovery from severe organ dysfunction. Free hemoglobin may have perpetuated progressive organ failure in our patient.