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Biomedical subjects

B Zwissler

Publications and source records attributed to B Zwissler.

At least 19 recordsLinked to original sources
PubMed2000

[Acute right heart failure. Etiology--pathophysiology--diagnosis--therapy].

Impaired right ventricular (RV) function may be caused by pulmonary hypertension or myocardial ischemia. It is characterized by a dilation of the RV, which is followed by an increase of wall tension and O2-consumption and a decrease of RV ejection fraction (RV 'dysfunction'). If a drop of arterial pressure occurs this my precipitate RV failure and shock (RV 'insufficiency'). Diagnosis of RV failure and monitoring of RV function is difficult. Sometimes, even a severe impairment of RV function goes undetected or is misinterpreted. Patients in the operating room or on intensive care units seem to be especially prone to RV dysfunction and failure. Since a causative therapy often is not readily available, adequate symptomatic therapy is of utmost importance. Four basic principles have to be considered: 1) Optimizing preload: The failing RV requires adequate filling for preservation of stroke volume. On the other hand, overdistension of the RV may result in RV ischemia, thereby further deteriorating RV function Hence, volume loading is important, but requires continuous monitoring. 2) Maintenance of aortic pressure: Vasopressors are indicated if there is a critical drop of coronary perfusion pressure. Norepinephrine presently is the drug of choice for this purpose. 3) Reduction of RV afterload: Whereas intravenous vasodilators are limited in their efficacy in dilating pulmonary vessels due to systemic side effects, inhaled vasodilators result in selective pulmonary vasodilation and may improve RV function. 4) Increase of RV contractility: In RV failure and shock, norepinephrine and epinephrine are the drugs of choice. Inodilators are well suited for reducing pulmonary vascular resistance due to their positive inotropic and vasodilating effects. Since systemic vasodilation may occur, these drugs must only be used in hemodynamically stable patients.

Acute Disease↗
PubMed1999

Response to inhaled nitric oxide (NO) is not associated with changes of plasma cGMP levels in patients with acute lung injury.

BACKGROUND: A clinically relevant increase of PaO subset2 or decrease of pulmonary vascular resistance (PVR) upon inhalation of NO (iNO) does occur in only 60 to 80% of patients with acute lung injury. The mechanisms for divergent responses of different patients have not yet been fully elucidated. Since NO mediates its pulmonary effects by stimulating soluble guanylate cyclase, thereby increasing levels of cyclic guanosinemonophosphate (cGMP), we hypothesized that pulmonary cGMP production upon iNO might be suppressed in patients not responding to iNO treatment. METHODS: After approval by the local ethical committee and after informed consent had been obtained, both arterial and mixed-venous cGMP levels were analyzed in 13 patients in whom iNO was administered to treat pulmonary hypertension and/or hypoxemia due to acute respiratory distress syndrome (n = 11) or reperfusion injury following lung transplantation (n = 2). Both cardiorespiratory variables and cGMP concentrations were documented simultaneously at baseline, 15 min after inhalation of 8 ppm of NO, and 15 min after withdrawal of NO, respectively. RESULTS: Inhaled NO resulted in a significant increase in PaO(2)/FiO(2) and a decrease in PVR. Arterial and mixed venous concentration of cGMP (median) also increased significantly upon iNO from 2.5 to 6.5 nM (p <0.05) and from 3.0 to 5.7 nM (p <0.05), respectively. Theses effects were fully reversible after withdrawal of iNO. No gradients between arterial and mixed venous cGMP concentrations were detected (p = 0.12). Regression analysis showed no relationship between baseline arterial cGMP concentrations and changes of either PaO(2)/FiO(2) (p = 0. 62) or PVR (p = 0.91). Similarly, no relationship was found between the rise of arterial cGMP concentration subsequent to iNO and corresponding changes of PaO(2) (p = 0.40) or PVR (p = 0.74), respectively. CONCLUSION: Inhalation of NO significantly stimulates soluble guanylate cyclase within the lungs in patients with acute lung injury. However, neither baseline cGMP nor its rise during treatment with inhaled NO can predict the clinical efficacy of iNO in humans. Furthermore, the fact that increased cGMP concentrations were detected during administration of iNO in mixed venous blood (i.e. pulmonary inflow) strongly suggest that the pharmacological effects of iNO are not fully selective for the lungs, but may also affect extrapulmonary organs.

Acute Disease↗
PubMed1998

Recombinant human interleukin-10 attenuates TNFalpha production by porcine monocytes.

BACKGROUND: Human recombinant interleukin-10 (rhIL-10) has been found to inhibit endotoxin-induced production of several proinflammatory cytokines including tumor necrosis factor alpha (TNFalpha) from human monocytes. The exogenous therapeutic administration of rhIL-10 in acute and chronic hyperinflammatory conditions has been discussed. For none of the large animal species that have been used to study the role and effects of various mediators during septicemia, crossreactivity of rhIL-10 has been shown so far. Therefore, the aim of the present investigation was to evaluate the crossreactivity of rhIL-10 in a porcine model. METHODS: To determine the effects of rhIL-10 on endotoxin-challenged porcine monocytes, we incubated porcine peripheral blood monocytes from five donors with three different concentrations of rhIL-10 (500 ng/ml, 1000 ng/ml and 2000 ng/ml, respectively) either simultaneously with, or two hours prior to lipopolysaccharide (LPS) administration. RESULTS: As compared to incubation with LPS (1 microg/ml) alone, coincubation with LPS and rhIL-10 (500 ng/ml, 1000 ng/ml and 2000 ng/ml) (n = 5) for four hours resulted in a marked and uniform reduction of immunoreactive TNFalpha. For preincubation (n = 5), only the addition of 500 ng/ml rhIL-10 led to a homogeneous decrease of TNFalpha levels in each sample. There was no consistent reduction in TNFalpha after preincubation with 1000 and 2000 ng/ml rhIL-10. Our results indicate crossreactivity of recombinant human interleukin-10 in porcine peripheral blood monocytes. Further investigations on the potential therapeutical role of exogenously administered rhIL-10 are thus possible in porcine models.

Adjuvants, Immunologic↗
PubMed1998

Influence of positive end-expiratory pressure ventilation (PEEP) on left ventricular pattern of contraction in experimental ARDS.

The aim of the present study was to investigate the pattern of ventricular dynamic contraction and its relation to changes of transseptal pressure gradient during ventilation with positive end-expiratory pressure (PEEP). For that purpose, left (LV) and right ventricular (RV) pressures as well as ventricular shortening in septal-lateral (s.l.) direction were assessed in 8 dogs (RV n = 5) exposed to experimental acute respiratory distress syndrome (eARDS) and PEEP 10 and 20 cmH2O (P10, P20). Despite maintenance of transmural central venous pressure by volume substitution, PEEP resulted in a fall of stroke index (P10 vs. eARDS: -7%, p<0.05; P20 vs. P10: -28%, p<0.05); this was accompanied by a fall of LV end-diastolic diameter (P10 vs. eARDS: -3.1%, p<0.01; P20 vs. P10: -7.4%, p<0.01). Although the transseptal LV to RV end- diastolic pressure gradient changed only minimally, there was a significant increase of paradoxic left ventricular systolic lengthening from 3.1% at eARDS to 4.5% at P10 (p<0.05 vs. eARDS) and 8.4% at P20 (p<0.05 vs. P10). Neither RV end-diastolic diameter nor s.l. shortening were significantly influenced by P10 or P20. It is concluded, that a rearrangement of LV dynamic contraction does occur during ventilation with PEEP, which is compatible with the concept of paradoxic systolic bulging of the interventricular septum towards the lumen of the right ventricle. Since this phenomenon occurred independent from changes of the end-diastolic pressure gradient between both ventricles, we suggest that systolic septal movement to the right is an active contractile process to support the function of a stressed RV.

Animals↗
PubMed1998

Inhaled nitric oxide (NO) for the treatment of early allograft failure after lung transplantation. Munich Lung Transplant Group.

OBJECTIVE: Inhalation of high concentrations of nitric oxide (NO) has been shown to improve gas exchange and to reduce pulmonary vascular resistance in individuals with ischemia-reperfusion injury following orthotopic lung transplantation. We assessed the cardiopulmonary effects of low doses of NO in early allograft dysfunction following lung transplantation. DESIGN: Prospective clinical dose-response study. SETTING: Anesthesiological intensive care unit of a university hospital. PATIENTS AND PARTICIPANTS: 8 patients following a single or double lung transplantation who had a mean pulmonary arterial pressure (PAP) in excess of 4.7 kPa (35 mmHg) or an arterial oxygen tension/fractional inspired oxygen ratio (PaO2/FIO2) of less than 13.3 kPa (100 mmHg). INTERVENTIONS: Gaseous NO was inhaled in increasing concentrations (1, 4 and 8 parts per million, each for 15 min) via a Siemens Servo 300 ventilator. MEASUREMENTS AND RESULTS: Cardiorespiratory parameters were assessed at baseline, after each concentration of NO, and 15 min after withdrawal of the agent [statistics: median (25th/75th percentiles: Q1/Q3), rANOVA, Dunnett's test, p < 0.05]. Inhaled NO resulted in a significant, reversible, dose-dependent, selective reduction in PAP from 5.5(5.2/6.0) kPa at control to 5.1(4.7/5.6) kPa at 1 ppm, 4.9(4.3/5.3) kPa at 4 ppm, and to 4.7(4.1/5.1) kPa at 8 ppm. PaO2 increased from 12.7(10.4/17.1) to 19.2(12.4/26.0) kPa at 1 ppm NO, to 23.9(4.67/26.7) kPa at 4 ppm NO and to 24.5(11.9/28.7) kPa at 8 ppm NO. All patients responded to NO inhalation (either with PAP or PaO2), all were subject to long-term inhalation (1-19 days). All were successfully weaned from NO and were discharged from the intensive care unit. CONCLUSION: The present study demonstrates that low-dose inhaled NO may be an effective drug for symptomatic treatment of hypoxemia and/or pulmonary hypertension due to allograft dysfunction subsequent to lung transplantation.

Administration, Inhalation↗
PubMed1998

Programs for assessment of spatial heterogeneity of regional organ blood flow.

Regional organ blood flow (RBF) is spatially heterogeneous. Relative dispersion (standard deviation S.D./mean) is often used to assess heterogeneity of RBF. Relative dispersion is a global measure of heterogeneity and is strongly influenced by the tissue sample size making comparisons between research groups inappropriate. Spatial correlation (s.c.) of blood flow is, on the other hand, averaged local self similarity. Both parameters change oppositely secondary to interventions. Fractal dimension (D) is a scale-independent measure of spatial heterogeneity and thus facilitates comparison of data. Programs for calculation of s.c. and D have not been published. We present two portable computer programs written in C+2 for calculating s.c. and D. The programs were validated with six computer generated data sets of known heterogeneity. The results were in agreement with data from the literature: we conclude that the programs accurately calculate spatial correlation and fractal dimension of 1-, 2-, or 3-dimensional perfusion matrices.

Humans↗
PubMed1998

Efficacy of inhaled prostanoids in experimental pulmonary hypertension.

OBJECTIVES: To evaluate the effects of inhaled prostacyclin (PGI2) and inhaled as well as intravenous prostaglandin E1 (PGE1) on thromboxane A2 mimetic-induced pulmonary vasoconstriction. Active pulmonary vasoconstriction was to be distinguished from passive resistance to blood flow. DESIGN: Prospective, randomized, crossover study. SETTING: Experimental animal laboratory. SUBJECTS: Eight anesthetized and paralyzed sheep. INTERVENTIONS: The stable thromboxane A2 mimetic, U46619, was infused in increasing dosage to obtain a stable pulmonary hypertension of approximately 30 mm Hg. Subsequently, PGE1 aerosol (0.6, 6, 58, 259 ng/kg/min), intravenous PGE, (0.5 microg/kg/min), or PGI2 aerosol (27 ng/kg/min) were administered in randomized order. MEASUREMENTS AND MAIN RESULTS: Active pulmonary vasoconstriction was assessed by determining the pulmonary pressure-flow relationship (PPFR). For measurement of pulmonary artery flow, an ultrasound flow probe was placed around the pulmonary artery after a sternotomy. Pulmonary arterial pressure was measured with a pulmonary artery flotation catheter. Flow was varied by partial occlusion of the inferior vena cava or incremental opening of an arterio-venous fistula between the large neck vessels. The primary end points were the slope of the resulting linear pressure-flow relationship, and pulmonary vascular resistance (PVR). Infusion of U46619 increased the slope of the PPFR (2.9+/-0.7 vs. 4.2+/-1.2 mm Hg/L/min [median+/-semi-interquartile range]; p < or = .05), and PVR (221+/-20 vs. 424+/-57 dyne x sec/cm5) (p < .05). Neither dose of PGE1 aerosol induced changes of the slope of PPFR or PVR. In contrast, intravenous administration of the same drug reduced the slope of the PPFR (4.0+/-1.0 vs. 3.1+/-0.4) (p < .05) but left PVR unchanged. Inhalation of PGI2 reduced both the slope of the PPFR, slightly but significantly, and PVR (424+/-98 vs. 323+/-26 dyne x sec/cm5) (p < .05). CONCLUSIONS: This study is the first to show reduction of active pulmonary vasoconstriction by PGI2 aerosol. Neither inhalation nor intravenous administration of PGE1 reduced PVR but the latter reduced the slope of PPFR. We conclude that PGE1 has potential for pulmonary vasodilation, but that it is ineffective as an aerosol, even in high doses, in sheep. PVR may fail to reflect drug-induced pulmonary vasodilation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1998

PEEP only partly restores disturbed distribution of regional pulmonary blood flow in lung injury.

The effects of lung injury, positive end-expiratory pressure (PEEP), and norepinephrine on heterogeneity of regional pulmonary blood flow (rPBF, radioactive microspheres) were investigated. We hypothesized that lung injury increases heterogeneity of rPBF and that PEEP ventilation reduces these effects. Heterogeneity of rPBF is scale dependent and was therefore assessed in detail. Local correlation (p), relative dispersion (RD), fractal dimension (D), perfusion gradients, and histograms of rPBF each measures a different aspect of heterogeneity. In eight anesthetized dogs, lung injury was induced with oleic acid and glass bead injection. Afterward, PEEP of 10-20 cmH2O was instituted. Norepinephrine was infused at 20 cmH2O PEEP. Heterogeneity increased upon lung injury (p, 0.44 +/- 0.09 vs. 0.24 +/- 0.09; RD, 0.36 +/- 0.06 vs. 0.64 +/- 0.12; both P < or = 0.05), but fractal dimension remained constant. PEEP did not change p, RD, or D. Perfusion gradients were reversed after lung injury (right, -27 +/- 18 vs. 196 +/- 115%; -24 +/- 18 vs. 282 +/- 184%; P < or = 0.05). PEEP (10 cmH2O) reduced gradients (116 +/- 73 and 143 +/- 62%, respectively; P < or = 0.05). Norepinephrine, in part, further reduced gradients (right, 50 +/- 58%; P < or = 0.05; left, 102 +/- 94%; P = NS). We conclude that oleic acid- and glass bead-induced lung injury produces abnormal distribution of rPBF. Of these changes, application of PEEP only reverses perfusion gradients.

Animals↗
PubMed1998

Hemodilution and hyperoxia locally change distribution of regional pulmonary perfusion in dogs.

In seven anesthetized dogs, the effects of acute normovolemic hemodilution (ANH) to a hematocrit of 20 and 8% and the effects of hyperoxic ventilation (100% oxygen) on distribution of regional pulmonary blood flow (rPBF; radioactive microspheres) were investigated. Normovolemia was monitored with blood volume measurements (indocyanine green dilution kinetics). Before ANH, fractal dimension (D) of rPBF in the whole lung was 1.19 +/- 0.09 (mean +/- SD). Spatial correlation (rho) of rPBF in the whole lung was 0.6 +/- 0.08. D is a resolution-independent measure for global rPBF distribution, and rho is the averaged flow relationship of directly neighboring lung samples. With regard to the entire lung, neither ANH nor hyperoxia changed D or rho. With regard to horizontal, isogravitational planes, ANH induced opposite changes of rPBF heterogeneity depending on the vertical location of the plane and the parameter used. In ventral planes, a change in relative dispersion (SD/mean) indicated decreased homogeneity. However, rho suggested more homogeneous perfusion. Hyperoxia restored baseline rPBF distribution. Our data suggest that ANH causes different alterations of heterogeneity of rPBF depending on location within the lung.

Animals↗
PubMed1998

3D-video- and robot-assisted minimally invasive ASD closure using the Port-Access techniques.

BACKGROUND: Video-assisted minimally invasive surgical methods with endovascular-based femoral cardiopulmonary bypass (CPB) and balloon occlusion of the aorta (Port-Access technique) were used to close an ostium-secundum atrial septal defect (ASD) in 7 patients. METHODS: Minor modifications were made to the system to provide drainage of the superior vena cava. The surgery was performed through a small (3.5-5cm) right anterolateral thoracotomy with 3D video and robotic arm assistance. RESULTS: The operative procedures were completely uneventful and the patients were discharged four days postoperatively in good condition and with excellent cosmesis. CONCLUSION: Using the modifications described, the Port-Access surgical method can be recommended for minimally invasive closure of an ASD.

Adolescent↗
PubMed1997

Biochemical and cellular composition of alveolar epithelial lining fluid in anesthetized healthy lambs.

Pulmonary toxicity of inhaled materials is often evaluated by (repetitive) assessment of the composition of bronchoalveolar lavage (BAL) fluid or of epithelial lining fluid (ELF) in sheep and lambs. Knowledge of the typical constituents of these fluids obtained from healthy animals is essential for identification of pathologic changes. Few studies have dealt with normal constituents of BAL fluid or ELF in sheep and lamb. The comparability of these studies, however, is limited for reasons concerning the choice of model and BAL technique. The biochemical and cellular composition of alveolar ELF obtained by a standardized BAL procedure was examined in 15 pento-barbital anesthetized 4 months old Merino lambs unexposed to inhaled substances. ELF volume was calculated by using the urea dilution method. We found 20.3 x 10(5) leucocytes per ml ELF, 87.5% of which were alveolar macrophages. Basophils and neutrophils were practically absent while 5% of the counted cells were lymphocytes. 76% of recovered cells were viable. The ELF contained 7 mg/ml total protein; enzyme activities of LDH and AP were 1692 U/l and 145 U/l, respectively.

Anesthesia, Inhalation↗
PubMed1997

[Anesthesia procedures--postoperative effects].

The perioperative morbidity and mortality is mainly influenced by the type and duration of surgery as well as the patient's preoperative state of health. Anesthesia per se, however, may also result in severe perioperative (patho) physiological changes, which may be both desired (e.g. analgesia, vasodilation in vascular surgery) or detrimental (e.g. hypothermia, ventilatory depression) and which may differ depending on the anesthetic technique used (e.g. general anesthesia vs. regional anesthesia). Yet, all anaesthetic techniques have in common, that their effects are not limited to the duration of the surgical intervention, but may expand far into the postoperative period. Therefore, many trials have been performed in the past aiming to compare the impact of different anesthetic techniques on the incidence of postoperative techniques, no significant advantage of one or the other technique has been identified up to now with respect to postoperative mortality or severe morbidity. This finding may be due to at least three factors. 1) Many side-effects related to anesthesia--due to close postoperative monitoring--are detected and treated early in the postoperative phase (e.g. in the recovery room), thereby preventing serious complications.2) Postoperative mortality related exclusively to anesthesia probably is so low, that huge patient numbers would be required to demonstrate any significant differences between different techniques. 3) Besides the factor 'anesthesia', many other factors contribute to the anesthesia related morbidity and mortality (e.g. the factor 'anesthetist') which are hardly quantified. The fact that clear advantages for a single technique have not yet been demonstrated must not, however, result in anesthetic 'nihilism'. Rather there may be good reasons in the individual patient (e.g. lack of a recovery room), to prefer a certain anesthetic technique or drug over another, in order to lower the individual risk of anesthesia. Whether the use of a certain technique-e.g. spinal or epidural anesthesia-may contribute to a reduction of specific postoperative surgical complications (e.g. rate of reocclusion subsequent to peripheral vascular surgery) is presently under investigation.

Anesthesia↗