[Mucosa-pH as a parameter of mucosa oxygenation in liver transplantation].
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Biomedical subjects
Publications and source records attributed to J Groh.
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Isoflurane has been reported to inhibit hypoxic pulmonary vasoconstriction. However, the effects of one-lung ventilation and isoflurane on regional pulmonary blood flow (Qr) have not been investigated in detail. Therefore, using radionuclide labelled microspheres we measured Qr in rabbits (n = 8) in the left lateral decubitus position during two- and one-lung ventilation under i.v. baseline anaesthesia and during additional administration of 1.5% isoflurane. Macrohaemodynamic variables were recorded continuously. Isoflurane increased non-dependent lung blood flow during two-lung ventilation. One-lung ventilation caused a homogeneous decrease in Qr throughout the hypoxic lung, irrespective of isoflurane administration (P < 0.001). However, isoflurane significantly augmented Qr of the hypoxic lung during one-lung ventilation (P < 0.05). During all phases, Qr of the upper lobe was higher compared with that in the lower lobe in isogravitational slices of both lungs; a ventrodorsal perfusion gradient was found in the left upper lobe. We conclude that 1.5% isoflurane increased perfusion of the non-dependent lung, inhibited hypoxic pulmonary vasoconstriction-induced redistribution of pulmonary blood flow and did not influence isogravitational perfusion gradients.
We evaluated the hemodynamic profile of eltanolone and fentanyl versus thiopental and fentanyl anesthetic induction in patients with documented coronary artery disease. Fifty patients scheduled for coronary artery bypass grafting were randomly assigned to two treatment groups (25 patients each). Anesthesia was induced by eltanolone (0.5 mg/kg) or by thiopental (3 mg/kg). Each patient also received 3 micrograms/kg fentanyl and 0.1 mg/kg vecuronium. Heart rate, arterial, pulmonary arterial, central venous, and pulmonary capillary wedge pressures, and cardiac output were determined in the awake state, 2 min after induction of anesthesia, and at 1 and 5 min after intubation, which was performed 3 min after induction. Between-group statistics showed significantly (P < 0.05) lower mean arterial pressure and systemic vascular resistance for eltanolone-treated patients at all measuring points. Pulmonary capillary wedge pressure was lower at 1 min after intubation; left ventricular stroke work index was lower at 1 and 5 min after intubation in the eltanolone group. We conclude that the lower mean arterial pressure with eltanolone as compared to thiopental is a result of greater peripheral vasodilation.
OBJECTIVE: The purpose of this study was to evaluate the reliability and accuracy of a new continuous intra-arterial blood gas monitoring system (IABG; PB3300, Puritan Bennett) over a prolonged period of time (> 7 days). DESIGN: Prospective criterion standard study. SETTING: Anesthesiological intensive care unit in a university hospital. PATIENTS: 11 sensors were tested in 10 mechanically ventilated patients with severe respiratory failure. INTERVENTIONS: PO2, PCO2, and pH measured using IABG were compared to values obtained from 2 conventional blood gas analyzers. The quality of blood pressure tracings was assessed using a scoring system consisting of 5 grades. RESULTS: The median study period was 205h/sensor (range: 169-506h). 320 blood samples were obtained. The ranges of measured parameters were: PO2 = 46-433 mmHg, PCO2 = 25-79 mmHg, pH = 7.25-7.55. The mean (SD) differences for the whole study period were: -4.3 (11.9) mmHg for PO2, for the clinically important range (PO2 < 150 mmHg) -1.9 (5.4) mmHg, -2.8 (4.5) mmHg for PCO2, and -0.03 (0.04) for the pH value. The MD (SD) in relation to the sensor lifetime were for days 1-3: -1.1 (5.1) mmHg for PO2, -0.4 (3.9) mmHg for PCO2, and -0.01 (0.03) for the pH value; for days 4-6: -1.5 (6.0) mmHg for PO2, -3.3 (4.0) mmHg for PCO2, and -0.03 (0.03) for the pH value; for days 7-9: -2.5 (4.7) mmHg for PO2, -5.1 (4.6) mmHg for PCO2, and -0.04 (0.04) for the pH value; for days > 9: -4.9 (4.4) mmHg for PO2, -5.3 (4.1) mmHg for PCO2, and -0.05 (0.03) for the pH value. CONCLUSIONS: The IABG reliably measured blood gases and pH values with acceptable clinical performance based on the overall results. There was, however, a decline in the agreement of the sensors and conventional values with increasing sensor lifetime. The mean differences (bias) and the standard deviation of differences (precision) of PO2, PCO2 and the pH values were acceptable for clinical purposes up to day 6. The arterial blood pressure tracings and blood withdrawal were not adversely affected. No side effects due to the sensors occurred. In summary, a prolonged sensor use for a period of up to 6 days appears to be reasonable. This system offers on-line information on oxygenation, ventilation, and acid-base status and allows immediate detection of acute and potentially life-threatening events.
Circulating leukocytes are retained in the microcirculation of the lung. The site of leukocyte retention, however, is still a subject of controversy, and the effects of microvascular blood flow on the leukocyte-endothelium interaction in pulmonary microvessels are unknown. We used in vivo fluorescence microscopy to analyze microhemodynamics and the flow behavior of in vivo-labeled leukocytes in pulmonary arterioles, venules, and alveolar capillaries. Microvascular blood flow was altered by variation of cardiac output. Leukocytes were found to roll and to stick on arteriolar and more pronouncedly on venular endothelium. During their passage through alveolar capillaries, a fraction of passing leukocytes became static for 0.1 to > 5 s. Under control conditions, leukocytes were concentrated approximately 8-fold more in arterioles and 24-fold more in venules than in the blood passing through these vessels. The concentration in capillaries was 1.5 times greater than in venules. The velocity of rolling leukocytes in arterioles and venules correlated significantly with the shear rate in these vessels, whereas the density of sticking cells was negatively correlated with the shear rate. The differences between leukocyte rolling and sticking in arterioles and in venules cannot be explained by respective hemodynamic conditions. In alveolar capillaries, the percentage of temporarily static leukocytes and the time of their stasis were inversely correlated with red-blood-cell (RBC) velocity. We conclude that leukocytes are retained in pulmonary arterioles, venules, and alveolar capillaries according to microvascular blood flow and endothelial factors.
BACKGROUND: Non-invasive mechanical ventilation (NIPPV) is an accepted choice of treatment in patients with chronic pulmonary disease and/or acute respiratory failure. Recently NIPPV was also proposed in the postoperative weaning period. PATIENTS AND METHODS: Six of 30 patients after lung transplantation were were extubated despite a weaning failure was predicted using well accepted weaning criteria. Therefore, the 6 patients were treated with intermittent-noninvasive ventilation using assisted modes of mechanical ventilation (PSV/CPAP). RESULTS: Both, oxygenation (increase in paO2: 18 mm Hg during PSV, 11 mm Hg during CPAP) and pulmonary mechanics (decrease in respiratory rate: 14/min during PSV, 10/min during CPAP; increase in tidal volume: 5 ml/kg during PSV, 3 ml/kg KG during CPAP) improved and the energy expenditure decreased (19% during PSV, 12% during CPAP). CONCLUSION: Non-invasive ventilation after lung transplantation enables earlier extubation and prevents weaning failure.
Continuous monitoring of blood gases and pH could add substantially to patient safety. During the last decade, efforts have been made to develop continuous optochemical blood gas sensors. The initial evaluation of such fibreoptic-based systems showed major patient-interface problems [11]. We evaluated a new intra-arterial blood gas monitoring system (PB3300, Puritan-Bennett, Carlsbad CA) under routine clinical conditions. METHODS. After institutional review board approval and with written informed consent, 38 sensors were tested in 25 patients with acute respiratory failure (e.g., the acute respiratory distress syndrome, complications after lung transplantation). Two conventional bench-top blood gas analysers (ABL 520 and ABL 300, Radiometer, Copenhagen) served as criterion standards. The mean differences (bias) and standard deviations (SD) of the differences (precision) were calculated according to the method of Bland and Altman [2]. In addition, linear regression analysis and correlation coefficients were calculated. The quality of blood pressure tracings was assessed using a grading system. RESULTS. The median sensor lifetime was 81.3 h; 869 blood samples (median 14 per sensor) were analysed for the comparison of continuous and conventional blood gas analysis. The ranges for measured parameters were: pH: 6.92 to 7.55; PCO2: 20 to 83 torr; PO2: 31 to 518 torr. The mean differences (SD) were: pH: -0.03 (0.03) or -0.4 (0.4)%; PCO2: -2.6 (4.1) torr or -6.9 (10.9)%; PO2: -3.4 (10.5) torr or -2.9 (7.0)%. The results of linear regression analysis and the correlation coefficients are depicted in Table 2. The mean grade of blood pressure tracings was satisfactory for the clinical setting. CONCLUSIONS. The continuous blood gas monitor is sufficiently accurate and precise for clinical use. Bias and precision are better than those known from former studies evaluating fibreoptic blood gas monitors under experimental conditions [7]. Cost-effectiveness was not an issue of this study.
BACKGROUND: Contradictory results have been reported in previous studies investigating the effect of isoflurane on hypoxic pulmonary vasoconstriction by indirect approaches. The current study measured the effects of one-lung ventilation (1LV) and isoflurane 1.5% by direct visual observation of the pulmonary microcirculation. METHODS: Ten New Zealand White rabbits were anesthetized with intravenous thiopental, alpha-chloralose, and piritramid. Arterial, central venous, pulmonary arterial, left atrial, and airway pressures and cardiac output were recorded continuously. 1LV was facilitated by a bronchial blocker in the right main bronchus. A transparent window was implanted into the right thoracic wall for videofluorescence microscopy of the subpleural pulmonary microcirculation. After intravenous injection of fluorescein isothiocyanate-labeled red blood cells, vessel diameters, red blood cell flux, red blood cell velocity, and dynamic microhematocrit were measured in pulmonary arterioles and venules during two-lung ventilation and 1LV during baseline anesthesia and with supplementary isoflurane 1.5%. RESULTS: During intravenous anesthesia, 1LV caused significant reduction of vessel diameters and red cell flux and velocity and an increase in microvascular hematocrit in pulmonary arterioles and venules. The decreases in arteriolar diameters and red blood cell flux and velocity induced by 1LV were significantly attenuated by isoflurane as compared with those measured during baseline anesthesia (P = 0.010, P = 0.029 and P = 0.047). Accordingly, 1LV-induced reduction of venular red cell flux (P = 0.023) and velocity (P = 0.036) were less pronounced during isoflurane. Isoflurane caused a significant decrease in arterial pressure. Venous admixture increased and arterial oxygen tension decreased significantly during 1LV; the changes were more pronounced during 1LV with isoflurane 1.5% than during 1LV with baseline anesthesia. CONCLUSIONS: 1LV leads to a marked reduction of microvascular diameters and blood flow in the hypoxic lung. Isoflurane 1.5% inhibits hypoxic pulmonary vasoconstriction in pulmonary arterioles and increases regional blood flow in the hypoxic lung.
To determine the site of sequestration of leukocytes in the lung, we investigated the kinetics of fluorescently labeled erythrocytes and leukocytes in pulmonary arterioles, venules, and alveolar capillaries in vivo by using fluorescence videomicroscopy. The subpleural pulmonary microcirculation of the ventilated rabbit lung was visualized via a transparent window implanted into the right thoracic wall. Fluorescein isothiocyanate-labeled erythrocytes were administered intravenously, whereas leukocytes were labeled in vivo by intravenous injection of rhodamine 6G. Rolling and adherence of leukocytes on the surface of the vessel walls were observed in arterioles as well as in venules. The median velocity of nonadherent leukocytes was significantly higher in arterioles than in venules (84 +/- 12 vs. 15 +/- 3% of erythrocyte velocity, respectively). In alveolar capillaries the majority of leukocytes were retained at distinct sites for periods of 0.1 to > 5 s (median 0.61 s). The relative velocity of leukocytes moving in capillaries was comparable to that determined in arterioles (80 +/- 9% of erythrocyte velocity). These measurements indicate that leukocyte sequestration in the lung is governed by the retention of leukocytes in capillaries and by the interaction of leukocytes with microvascular endothelium of arterioles and venules. We propose that the kinetics of these phenomena determine the equilibrium between circulating and sequestered leukocytes.
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OBJECTIVE: Our previous randomized clinical trial showed a 4-month home physiotherapy program was effective for patients with ankylosing spondylitis. This followup study reports on 22 control patients who received the previously withheld treatment and 24 experimental patients who received followup treatment as needed. METHODS: The primary outcome measure was spinal mobility measured by fingertip-to-floor distance using a portable measuring device specially designed and validated for this study. RESULTS: Following treatment, fingertip-to-floor distance did not change in control patients (P2 = 0.145). Between 4 and 8 months, fingertip-to-floor distance did not change in experimental patients (P2 = 0.143); however, initial improvement achieved was maintained. The experimental group at 4 months was better than the control group at 8 months (P2 = 0.038). CONCLUSION: The home physiotherapy treatment program must be delivered as rigorously as it was in the initial trial to be effective. The benefit from this treatment program can be maintained with very little intervention.
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Platelet concentrates transfused for correction of thrombocytopenia or reduced platelet function do not consistently improve primary haemostasis in the recipient. Insufficient therapeutic effects may be caused by impaired donor platelet function and by unfavourable donation and storage conditions, as well as by immunological interactions with the recipient blood. The present study was designed to investigate whether the effect of platelet transfusion on recipient platelet function can be predicted by in vitro methods. METHODS. Blood samples were taken from 12 thrombocytopenic patients before (20 ml, P0) and after (10 ml, P(vivo)) transfusion of one unit of platelets previously stored for 24-120 h in acid citrate dextrose. An additional sample was taken from the platelet concentrate (TK) immediately before transfusion. P0 was divided into two specimens and TK platelets were added to one of them (P(vitro) in order to obtain a platelet count similar to that in P(vivo). Bleeding time (BT) and bleeding volume (BV) of the samples P0, P(vivo) and P(vitro) were measured using the method of Kratzer and Born (Fig. 2); mean values were calculated for each sample from six measurements. Aggregability of TK platelets was determined in addition by aggregometry. In contrast to previous studies, physiological Ca2+ concentrations were restored and secondary haemostasis was inhibited by low-molecular-weight heparin (Fragmin P, Pfrimmer Kabi GmbH und Co. KG, Erlangen) in the platelet-rich plasma used for aggregometry. RESULTS. Platelet counts increased in all patients after transfusion (P(vivo) vs P0, Table 1) and were nearly identical in P(vitro) and P(vivo) (r = 0.94, P < 0.001; Fig. 3). Parameters of primary haemostasis were significantly improved by addition of platelets to P0 in vitro (BT P < 0.05, BV P < 0.01) as well as by platelet transfusion (BT P < 0.05, BV P < 0.01). Direct comparison of P(vitro) and P(vivo) yielded a very close correlation of BT (r = 0.88, P < 0.001) and BV (r = 0.89, P < 0.01) in both samples. Although aggregometry revealed decreasing platelet function with increased storage time, aggregability was considerably higher compared to previous studies of platelet concentrates stored for 2-5 days. CONCLUSION. A new technique has been developed which allows reliable prediction of the effect of platelet concentrates on primary haemostasis of the recipient by in vitro measurement of bleeding time and bleeding volume prior to transfusion using the method of Kratzer and Born.
An experimental model has been developed for morphometric and microhemodynamic analysis of discrete arteriolar networks in the ventilated lung. We implanted a transparent window into the right thoracic wall of anesthetized rabbits. Autologous red blood cells were labeled with FITC in vitro. Using a fluorescence video microscopic technique the vessels of superficial arteriolar networks were mapped and classified hierarchically. Networks were investigated under zone 2 conditions (alveolar > left atrial pressure) during continuous monitoring of macrohemodynamics. We comprehensively measured segment length, diameter (D) and branching pattern in the whole network. Microhemodynamic parameters (red blood cell flux (Frbc), red blood cell velocity (Vrbc) and microhematocrit (H mu) were determined in terminal branches. As a result of network analysis the branching rules were found to be similar to those found by cast techniques in human and cat lungs. In terminal arterioles D (21 +/- 4 microns), Frbc (1472 +/- 662 cells/s), Vrbc (863 +/- 250 microns/s) and H mu (0.28 +/- 0.067) were heterogeneously distributed. Geometric, as well as microhemodynamic parameters fitted best to a lognormal distribution. This study represents an example of in vivo analysis of discrete microvascular networks. The measurements in hierarchically equivalent segments of pulmonary arteriolar vessel trees have been shown to be appropriate for estimation of topological, geometrical and microhemodynamic heterogeneity in pulmonary arteriolar networks.
Bleeding is causally related to about 50% of postoperative deaths following liver resection. Main factors contributing to increased perioperative bleeding in liver surgery include surgical trauma, reduced activity of clotting factors and inhibitors due to impaired hepatic synthesis, low platelet count and poor platelet function as well as impaired clearance of activated clotting factors by the reticuloendothelial system of the liver (Kupffer cells). Hemostasis may be further impaired by transfusion of blood components, since citrate added for conservation is not adequately metabolized by the failing liver. Surgical bleeding leads to a loss of pro- and anticoagulatory factors as well as to activation of coagulation. Finally, hyperfibrinolysis induced by release of tissue plasminogen activator (t-PA, primary hyperfibrinolysis) and disseminated coagulation (secondary hyperfibrinolysis) contribute to increased bleeding. Therefore early diagnosis and treatment of coagulation disorders is of paramount importance during liver surgery. Screening parameters of hemostasis and fibrinolysis should be available on a 24-hour basis in centers performing liver surgery. Screening for disorders of secondary hemostasis includes evaluation of prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen concentration and the activity of the most important inhibitor, antithrombin III (AT III). Thrombelastography is the leading method for diagnosis of hyperfibrinolysis, which can also be assessed by determination of D-dimer, fibrinogen and fibrin degradation products. Evaluation of primary hemostasis is frequently restricted to platelet count, which is only a rough parameter. In contrast, measurement of in vitro bleeding time and volume enables repeated quantification of platelet function in patients with impaired hemostasis.