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B Heindl

Publications and source records attributed to B Heindl.

16 recordsLinked to original sources
PubMed2003

Sevoflurane but not isoflurane can reduce prostacyclin production of endothelial cells.

BACKGROUND AND OBJECTIVE: Little is known about the interaction of newer volatile anaesthetics with endothelial eicosanoid production. Sevoflurane may possibly reduce prostacyclin formation. Thus, we compared the influences of sevoflurane and isoflurane on endothelial prostacyclin production. METHODS: Production of prostacyclin of human umbilical vein endothelial cells was measured by the ELISA technique under basal conditions and after stimulation with calcium ionophore A 23187 10 micromol or histamine 0.1 micromol in the absence and presence of 1 and 2 minimal alveolar concentrations (MAC) of sevoflurane or isoflurane. RESULTS: The basal production of prostacyclin was unaffected by the volatile anaesthetics. Stimulation of endothelial cells increased prostacyclin formation 3-5-fold. Sevoflurane at 2 MAC, but not at 1 MAC, could reduce stimulated prostacyclin production by about half (P < 0.05). Isoflurane had no inhibitory effect. Inhibition of cyclo-oxygenase function by acetylsalicylic acid abolished the induced burst of prostacyclin formation completely. CONCLUSIONS: Sevoflurane, but not isoflurane, can reduce stimulated endothelial prostacyclin production in a concentration-dependent manner. Because at least 2 MAC of sevoflurane were required, this effect should be of minor importance under clinical conditions of balanced anaesthesia.

Analysis of Variance↗
PubMed2001

Aspirin, but not the more selective cyclooxygenase (COX)-2 inhibitors meloxicam and SC 58125, aggravates postischaemic cardiac dysfunction, independent of COX function.

Inhibition of cyclooxygenase (COX) might favour non-enzymatic formation of cardiodepressive isoprostanes from arachidonic acid by radicals generated during reperfusion. This could explain deleterious effects of acetylsalicylic acid (ASA) on cardiac function. We examined the influence of COX inhibition on myocardial function after low-flow ischaemia and reperfusion, employing either ASA (100 micromol/l), the partially selective COX-2 inhibitor meloxicam (0.3 micromol/l and 3.0 micromol/l), or the highly selective COX-2 inhibitor SC 58125 (1.0 micromol/l and 3.0 microgmol/l). Isolated, buffer-perfused guinea pig hearts, performing pressure-volume work before and after consecutive low-flow ischaemia and reperfusion, were used for the study. Measurement of coronary and aortic flow, ejection time and heart rate served to calculate external heart work (EHW), before and after ischaemia. Additionally, release of prostacyclin and thromboxane A2, production of lactate, consumption of pyruvate and tissue concentration of the isoprostane 8-iso-PGF2alpha were measured. ASA significantly reduced recovery of EHW (46+/-18% vs. 82+/-15% for controls), whereas meloxicam and SC 58125 did not (64+/-15% and 74+/-13% recovery, respectively). Paradoxically, ASA increased reactive hyperaemia and consumption of pyruvate in the early reperfusion phase in comparison to all other groups, while lactate production did not differ. Prostacyclin production did not increase during reperfusion and was not significantly different between groups at any time point. In contrast, thromboxane A2 release increased about fivefold in the 2nd min of reperfusion under control conditions and in the presence of SC 58125, but was inhibited by ASA and by meloxicam in both concentrations. Isoprostane content of heart tissue was not detectably influenced under the mild reperfusion conditions used here. We conclude that ASA can aggravate postischaemic cardiac dysfunction, independent of COX inhibition. The deleterious effect in the present model might be due to uncoupling of mitochondrial oxidative phosphorylation rather than to direct effects of reduced eicosanoid release or radical induced formation of isoprostanes.

Animals↗
PubMed2000

Endothelial function and hemostasis.

The vascular endothelium influences not only the three classically interacting components of hemostasis: the vessel, the blood platelets and the clotting and fibrinolytic systems of plasma, but also the natural sequelae: inflammation and tissue repair. Two principal modes of endothelial behaviour may be differentiated, best defined as an anti- and a prothrombotic state. Under physiological conditions endothelium mediates vascular dilatation (formation of NO, PGI2, adenosine, hyperpolarizing factor), prevents platelet adhesion and activation (production of adenosine, NO and PGI2, removal of ADP), blocks thrombin formation (tissue factor pathway inhibitor, activation of protein C via thrombomodulin, activation of antithrombin III) and mitigates fibrin deposition (t- and scuplasminogen activator production). Adhesion and transmigration of inflammatory leukocytes are attenuated, e.g. by NO and IL-10, and oxygen radicals are efficiently scavenged (urate, NO, glutathione, SOD). When the endothelium is physically disrupted or functionally perturbed by postischemic reperfusion, acute and chronic inflammation, atherosclerosis, diabetes and chronic arterial hypertension, then completely opposing actions pertain. This prothrombotic, proinflammatory state is characterised by vaso-constriction, platelet and leukocyte activation and adhesion (externalization, expression and upregulation of von Willebrand factor, platelet activating factor, P-selectin, ICAM-1, IL-8, MCP-1, TNF alpha, etc.), promotion of thrombin formation, coagulation and fibrin deposition at the vascular wall (expression of tissue factor, PAI-1, phosphatidyl serine, etc.) and, in platelet-leukocyte coaggregates, additional inflammatory interactions via attachment of platelet CD40-ligand to endothelial, monocyte and B-cell CD40. Since thrombin formation and inflammatory stimulation set the stage for later tissue repair, complete abolition of such endothelial responses cannot be the goal of clinical interventions aimed at limiting procoagulatory, prothrombotic actions of a dysfunctional vascular endothelium.

Arteriosclerosis↗
PubMed2000

Development of a knowledge-base for automatic monitoring of renal function of intensive care patients over time.

Renal dysfunction is a major problem in the management of critically ill patients. Monitoring of renal parameters over time is a prerequisite for detection of any significant deterioration of kidney function. Thus, we developed a knowledge-base for the dynamic monitoring of renal function of critically ill patients. A database with renal parameters of 750 intensive care patients was analyzed for distribution of parameters within predefined intervals of the creatinine clearance. Additionally, a subgroup of 11 patients with (quite) normal renal function over 11 days was selected and the daily variability of renal parameters was analyzed. An interdisciplinary expert team selected a set of nine clinically relevant renal parameters and formulated, on the basis of the data analysis and the parameter set, eight definitions of renal function, which represent four levels of renal performance. These definitions were arranged into an hierarchical structure, considering only clinically relevant changes of renal function. A change from one functional state to another inside of 2 days indicates a relevant alteration of renal function. Monitoring of time courses can additionally be performed by statistical analysis of the daily variability of parameters and comparison with their 'normal' variability. Moreover, rules were established for the plausibility check of results and interpretations of single parameters and parameter sets formulated.

Artificial Intelligence↗
PubMed2000

Sevoflurane and isoflurane do not enhance the pre- and postischemic eicosanoid production in guinea pig hearts.

UNLABELLED: Eicosanoids and volatile anesthetics can influence cardiac reperfusion injury. Accordingly, we analyzed the effects of sevoflurane and isoflurane applied in clinically relevant concentrations on the myocardial production of prostacyclin and thromboxane A2 (TxA2) and on heart function. Isolated guinea pig hearts, perfused with crystalloid buffer, performed pressure-volume work. Between two working phases, hearts were subjected to 15 min of global ischemia followed by reperfusion. The hearts received no anesthetic, 1 minimum alveolar anesthetic concentration (MAC) isoflurane (1.2 vol%), or 0.5 and 1 MAC sevoflurane (1 vol% and 2 vol%), either only preischemically or pre- and postischemically. In additional groups, cyclooxygenase function was examined by an infusion of 1 microM arachidonic acid (AA) in the absence and presence of sevoflurane. The variables measured included the myocardial production of prostacyclin, TxA2 and lactate, consumption of pyruvate, coronary perfusion pressure, and the tissue level of isoprostane 8-iso-PGF2alpha. External heart work, determined pre- and postischemically, served to assess recovery of heart function. Volatile anesthetics had no impact on postischemic recovery of myocardial function (50%-60% recovery), perfusion pressure, lactate production, or isoprostane content. Release of prostacyclin and TxA2 was increased in the early reperfusion phase 5-8- and 2-4-fold, respectively, indicating enhanced AA liberation. Isoflurane and sevoflurane did not augment the eicosanoid release. Only 2 vol% sevoflurane applied during reperfusion prevented the increased eicosanoid formation in this phase. Infusion of AA increased prostacyclin production approximately 200-fold under all conditions, decreased pyruvate consumption irreversibly, and markedly attenuated postischemic heart work (25% recovery). None of these effects were mitigated by 2 vol% sevoflurane. In conclusion, only sevoflurane at 2 vol% attenuated the increased liberation of AA during reperfusion. Decreased eicosanoid formation had no effect on myocardial recovery in our experimental setting while excess AA was deleterious. Because eicosanoids influence intravascular platelet and leukocyte adhesion and activation, sevoflurane may have effects in reperfused tissues beyond those of isoflurane. IMPLICATIONS: In an isolated guinea pig heart model, myocardial eicosanoid release was not increased by isoflurane or sevoflurane, either before or after ischemia. Sevoflurane (2 vol%) but not isoflurane attenuated the increased release of eicosanoids during reperfusion.

Anesthetics, Inhalation↗
PubMed2000

Nonuniform behavior of intravenous anesthetics on postischemic adhesion of neutrophils in the guinea pig heart.

UNLABELLED: Adhesion of polymorphonuclear neutrophils (PMN) to the coronary endothelium is a crucial step in the development of ischemic myocardial injury. We tested the possible effects of six widely used IV anesthetics on non- and postischemic coronary adhesion of PMN in isolated perfused guinea pig hearts. Hearts (n = 5-11/group) were perfused under conditions of constant coronary flow. After 15 min global warm ischemia, PMN (10(6)) were infused in the second minute of reperfusion. The number of cells reemerging in the coronary effluent within 2 min was expressed as a percentage of the total number of administered PMN. Anesthetics were given 20 min before ischemia and during reperfusion. In addition, the ability of the drugs to influence the oxidative burst reaction of PMN was assessed by measuring luminol-enhanced chemiluminescence in response to 0.1 microM N-formyl-L-methionyl-L-leucyl-L-phenylalanine. Under nonischemic conditions, 26.3% +/- 0.5% of the injected PMN did not acutely reemerge from the coronary system. Subjecting the hearts to ischemia augmented retention to 40.0% +/- 1.6% (P < 0.05). This postischemic stimulation of adhesion was fully prevented by ketamine (10 microM: 22.8% +/- 1.6%, 20 microM: 26.6% +/- 0.7%), thiopental (25 microM: 24.0% +/- 1.7%, 50 microM: 24.0% +/- 1.4%), and midazolam (1.5 microM: 29.0% +/- 0.9%, 3 microM: 26.4% +/- 1.4%). Propofol also inhibited the augmented postischemic retention at 25 microM (28.7% +/- 2.4%). However, 50 microM propofol, etomidate (0.5 and 1 microM), and fentanyl (1 microM) all had no effect. Only thiopental reduced the nonischemic adhesion value (14.0% +/- 3.7%). This may be linked to the direct antioxidative action of thiopental (50% reduction in oxidative burst activity). Whereas ketamine, midazolam, and propofol did not significantly influence oxidant production by PMN, etomidate and the lipid solvent Intralipid enhanced the burst reaction. This activating effect of the lipid component could explain the biphasic behavior of propofol emulsion. Despite some possible differences in efficacy, several IV anesthetics may protect the heart from PMN-mediated reperfusion injury. IMPLICATIONS: Ketamine, thiopental, and midazolam, but not etomodate or fentanyl, reduce postischemic adhesion of neutrophils in the coronary system of isolated perfused guinea pig hearts, suggesting a role in mitigating myocardial reperfusion injury.

Anesthetics, Intravenous↗
PubMed1999

The volatile anesthetic sevoflurane mitigates cardiodepressive effects of platelets in reperfused hearts.

UNLABELLED: Adherent platelets in the coronary system can impair cardiac pump function. The volatile anesthetics sevoflurane, halothane, and isoflurane have been shown to reduce platelet adhesion. Additionally, an inhibitory effect on platelet cyclo-oxygenase-dependent formation of thromboxane A2 (TxA2) has been proposed for sevoflurane. Therefore, we analyzed the influence of sevoflurane on cardiac performance and TxA2 production after intracoronary application of platelets in isolated guinea pig hearts. Isolated guinea pig hearts perfused with Krebs-Henseleit buffer and performing pressure-volume work were employed. We compromised myocardial function by subjecting hearts to ischemia (20 min low-flow plus 10 min stopped-flow) and reperfusion. During low-flow perfusion the coronary endothelium was stimulated by thrombin prior to and during infusion of a bolus of 10(8) washed human platelets. Intervention groups contained either sevoflurane in a concentration being equivalent to 1 MAC in the platelet suspension or in the perfusate or 1 microM SQ29,548 (an isoprostane- and thromboxane-receptor antagonist) in the perfusate. The parameter external heart work (EHW), determined pre- and postischemically, served as criterion for loss of myocardial function. Additionally, formation of transudate and the production of TxA2 were measured during the reperfusion phase. Coronary perfusion pressure and myocardial production of lactate and consumption of pyruvate were also determined. Adherent platelets significantly enhanced loss of EHW after ischemia and reperfusion, but strongly attenuated coronary vascular leak. Sevoflurane reduced platelet adhesion when applied to the perfusate, but not when given only to the platelet suspension. However, platelets pretreated with sevoflurane lost their cardiodepressive effects, as did platelets in hearts treated with SQ29,548. Surprisingly, TxA2 formation in hearts was not different after platelet application in comparison to the ischemia control group but was significantly reduced when sevoflurane was applied to the perfusate. Neither metabolic parameters, coronary perfusion pressure, vascular leak nor glycoprotein expression of platelets were influenced by sevoflurane. CONCLUSIONS: 1) Pretreatment of hearts with sevoflurane reduces intracoronary platelet adhesion, most likely via an endothelial mechanism. 2) Pretreatment of platelets with sevoflurane does not reduce platelet adhesion, but nevertheless averts cardiodepressive effects derived from or generated by adherent platelets. 3) Transudate formation of hearts during reperfusion was reduced after platelet application, independent of the adherence of platelets.

Adult↗
PubMed1999

Ketamine does not inhibit inflammatory responses of cultured human endothelial cells but reduces chemotactic activation of neutrophils.

BACKGROUND: Ketamine is a widely used general anaesthetic, which has been reported to inhibit neutrophil function and neutrophil-endothelial interaction. To date, however, it is unknown whether ketamine has any direct effects on endothelial cells with respect to inflammation. Therefore, we investigated the influence of varying concentrations of ketamine (0.5, 1, and 3 microM) on the endothelial expression of cytokines and adhesion molecules with relevance for inflammation. METHODS: Cultured human umbilical vein endothelial cells were stimulated with tumor necrosis factor alpha (TNFalpha, 2.5 ng/ml) for 4 h in the absence or presence of ketamine. The adhesion molecules ICAM-1 and E-selectin on the endothelial cells were measured by flow cytometry. Release of the proinflammatory cytokines IL-6 and IL-8 by endothelial cells was quantified by ELISA. The acute effect of ketamine on leukocyte activation by the supernatant of endothelial cells pre-stimulated with TNFalpha (4 h) was tested by flow cytometric measurement of CD11b, a leukocyte activation marker, after 15 min of coincubation. RESULTS: TNFalpha caused dramatic upregulation of both adhesion molecules (15-fold and 5-fold vs. control for ELAM-1 and ICAM-1, respectively) and of both cytokines (500-fold and 1.8-fold for IL-6 and IL-8, respectively). No concentration of ketamine employed in our study had any effect on these inflammatory parameters. However, activation of leukocytes by supernatant of TNFalpha-conditioned endothelial cells (70% increase of CD11b) was attenuated by coincubation of the PMN with 0.5 and 5 microM ketamine (47% and 44% increase, respectively). CONCLUSION: These data suggest that ketamine exerts its antiinflammatory actions primarily via inhibition of leukocyte reactivity. Indeed, no inhibition of endothelial responses was detectable in our study.

Anesthetics, Dissociative↗
PubMed1999

S(+)-ketamine, but not R(-)-ketamine, reduces postischemic adherence of neutrophils in the coronary system of isolated guinea pig hearts.

UNLABELLED: Polymorphonuclear neutrophils (PMN) play a crucial role in the initiation of reperfusion injury. In a previous study, we found that ketamine reduced the postischemic adherence of PMN to the intact coronary system of isolated guinea pig hearts. Because ketamine is a racemic mixture (1:1) of two optical enantiomers, we looked for possible differences in action between the stereoisomers. Seventy-six guinea pig hearts were perfused in the "Langendorff" mode under conditions of constant flow (5 mL/min) using modified Krebs-Henseleit buffer. After 15 min of global warm ischemia, freshly isolated human PMN (10(6)) were infused as a bolus into the coronary system during the second minute of reperfusion. PMN adhesion was expressed as the numeric difference between PMN recovered in the effluent and those applied. Series A hearts received 5 microM S(+), 5 microM R(-), or 10 microM racemic ketamine starting 20 min before ischemia and during reperfusion. In Series B hearts, 10 microM nitro-L-arginine, an inhibitor of NO synthase, was added to the perfusate. In Series C, PMN were preincubated for 15 min with 5 microM S(+)- or R(-)-ketamine. Coronary vascular leak was assessed by measuring the rate of formation of transudate on the epicardial surface. Ischemia/reperfusion without anesthetics increased coronary PMN adherence from 25.5% +/-2.3% (basal) to 35.3%+/-1.5% of the number applied. S(+)-ketamine reduced postischemic adherence in each series (A, 25.5%+/-5.1%; B, 22.5%+/-1.7%; C, 25.3%+/-7.7%), as did racemate (A, 26.4%+/-3.7%). Although 5 microM R(-)-ketamine had no effect on adhesion (A, 30.5%+/-6.7%; B, 34.3%+/-5.1%; C, 34.3%+/-4.3%), it significantly increased vascular leak in the presence of NOLAG. These findings indicate stereoselective differences in biological action between the two ketamine isomers: S(+)-ketamine inhibited PMN adherence, R(-)-ketamine worsened coronary vascular leak in reperfused isolated hearts. IMPLICATIONS: In this study, we demonstrated stereoselective differences in the biologic action of the two ketamine isomers in an animal model of myocardial ischemia. Polymorphonuclear neutrophil adherence to the coronary vasculature after ischemia was inhibited by S(+)-ketamine, whereas R(-)-ketamine increased coronary vascular fluid leak.

Anesthetics, Dissociative↗
PubMed1999

Sevoflurane and isoflurane protect the reperfused guinea pig heart by reducing postischemic adhesion of polymorphonuclear neutrophils.

BACKGROUND: Polymorphonuclear neutrophils (PMNs) contribute to reperfusion injury. Because volatile anesthetics can reduce PMN adhesion in the reperfused, nonworking heart, the authors analyzed whether this action of volatile anesthetics affects cardiac performance after ischemia and reperfusion and further clarified the underlying mechanism. METHODS: Isolated guinea pig hearts perfused with crystalloid buffer and performing pressure-volume work were used. Hearts were subjected to 15 min global ischemia and 20 min reperfusion. In the intervention groups an intracoronary bolus of 3 x 10(6) PMNs was applied in the second min of reperfusion, either in the absence or presence of 0.5 or 1 minimum alveolar concentration sevoflurane or isoflurane. The number of sequestered PMNs was calculated from the difference between coronary input and output (coronary effluent) of PMNs. Performance of external heart work, determined pre- and postischemically, served as criterion for recovery of myocardial function. Additionally, the expression of the integrin CD11b on the cell surface of PMN was measured before and after coronary passage. RESULTS: Injection of PMN in the reperfusion phase, but not under nonischemic conditions, reduced recovery of external heart work significantly (from 55+/-7% to 19+/-11%). Addition of sevoflurane or isoflurane in concentrations of 0.5 and 1 minimum alveolar concentration to the perfusate reduced postischemic PMN adhesion from 36+/-8% to basal values (20+/-7%) and prevented decline of cardiac function. CD11b expression on PMNs increased significantly during postischemic coronary passage under control conditions. Again, both anesthetics in both concentrations inhibited that activation. CONCLUSIONS: Volatile anesthetics reduce PMN adhesion in the reperfused coronary system and thereby preserve cardiac function. Reduced expression of the adhesion molecule CD11b on PMNs in the presence of sevoflurane or isoflurane is, at least in part, responsible for the cardioprotective effect.

Anesthetics, Inhalation↗
PubMed1998

[Attitude towards physician-assisted suicide among German doctors. A representative survey of the medical district association of Würzburg].

BACKGROUND AND OBJECTIVE: The widespread legalization of "physician assisted suicide" (PAS) in The Netherlands and comparable tendencies in other European countries have given rise to discussions of this topic in Germany. This questionnaire was undertaken because of the dearth of previous informative studies in Germany. SUBJECTS AND METHODS: Among all registered practicing doctors in the medical district of Würzburg (n = 1821) a randomly selected group of 150 (males and females) was asked to participate in a personal interview-enquiry about active and passive euthanasia. 93 (62%, 32% women, 61% men) agreed: 44.1% were doctors working in a hospital, 45.2% worked in their own practice, the others worked elsewhere or (3) were retired. All specialties and medical activities were represented. About 40% were general practitioners or worked in internal medicine. RESULTS: 81.7% of the group were against active PAS. All rejected it for non-moribund patients. CONCLUSIONS: The results of this study differ from similar enquiries in other countries in demonstrating a relatively strong rejection of active assistance in patient-suicide. Those German specialists who would most likely be confronted with this problem (e.g. neurologists, intensivists, anaesthetists, oncologists) tended towards a greater readiness to agree to physician-assisted suicide. A dialogue between doctors in different specialties is an urgent requirement and should be intensively pursued.

Attitude of Health Personnel↗
PubMed1998

Disparate effects of adhesion and degranulation of platelets on myocardial and coronary function in postischaemic hearts.

OBJECTIVE: Beside the major effect of acute thrombus formation, little is known about the interaction of platelets with the coronary endothelium in an ischaemia-reperfusion situation. The present study was designed to investigate, separately, the consequences of platelet adhesion and degranulation during myocardial reperfusion. METHODS: Isolated guinea pig hearts perfused with Krebs-Henseleit buffer and performing pressure-volume work were used. We infringed myocardial function by imposing ischaemia (20 min of low-flow perfusion with 1 ml/min and 10 min of global ischaemia) and reperfusion (15 min with 5 ml/min). During low-flow perfusion, the coronary endothelium was stimulated by thrombin before and during infusion of a bolus: 10(8) washed human platelets +/- the Arg-Gly-Asp (RGD) analogon lamifiban, the supernatant of 10(8) thrombin-stimulated platelets, fibrinogen (2 microM), lamifiban (2 microM) or Tyrode's solution (control group). The parameter external heart work (EHW), determined pre- and postischaemically, served as criterion for recovery of myocardial function. Additionally, the formation of capillary transudate was measured during the reperfusion phase to assess coronary permeability. Coronary perfusion pressure was monitored continuously and myocardial production of lactate and consumption of pyruvate were measured. Electron microscopy of hearts was performed after platelet application to verify platelet adhesion in the coronary system. RESULTS: Recovery of EHW by hearts without platelet application was 64 +/- 3% and was significantly reduced to 49 +/- 5% by platelet infusion (n = 8 each). Infusion of supernatant of thrombin-stimulated platelets did not impair recovery of heart work. In the reperfusion phase (6th-10th min), hearts that either had received platelets or supernatant of platelets exhibited a significantly reduced production of capillary transudate (70 microliters/min vs. 180 microliters/min for the controls). Intracoronary bolus application of fibrinogen or lamifiban also reduced coronary leak. Coronary perfusion pressure and metabolic parameters were not statistically different between the groups at any time. CONCLUSIONS: Platelet adhesion to the coronary endothelium in a situation of myocardial ischaemia impairs cardiac recovery, whereas constituents released by platelets may have beneficial effects on the integrity of the coronary endothelium. In particular, fibrinogen seems to contribute to the permeability reducing effect, possibly by interaction with endothelial receptors recognising the RGD sequence.

Acetates↗
PubMed1998

Volatile anaesthetics reduce adhesion of blood platelets under low-flow conditions in the coronary system of isolated guinea pig hearts.

BACKGROUND: Inhibitory effects of volatile anaesthetics on platelet aggregation have been demonstrated in several studies. However, the influence of volatile anaesthetics on intracoronary platelet adhesion has not been elucidated so far. METHODS: Isolated hearts of guinea pigs were perfused with buffer in the absence or presence of volatile anaesthetics (0.5 and 1 MAC) at constant coronary flow rates of 5 ml/min for 25 min, then 1 ml/min for 30 min and again 5 ml/min for 10 min. Before, during and after low-flow perfusion, a bolus of human platelets was applied into the coronary system. To simulate thrombogenic conditions, 0.3 U/ml human thrombin was infused during low-flow perfusion and reperfusion. The number of platelets sequestered to the endothelium was calculated from the difference between coronary in- and output of platelets. The myocardial production of lactate and consumption of pyruvate and coronary perfusion pressure were also determined. RESULTS: At a flow rate of 5 ml/min only about 3% of the applied platelets did not emerge from the coronary system, in any group. In contrast, 13.1 +/- 1.2% (mean +/- SEM) of infused platelets became adherent in low-flow perfusion in the control group without anaesthetic. The adherence was reduced with each 1 MAC isoflurane (to 6.2 +/- 1.2%), sevoflurane (to 4.4 +/- 0.9%) or halothane (to 3.2 +/- 1.5%) (each P < 0.05 vs. control). Volatile anaesthetic, 0.5 MAC, did not inhibit platelet adhesion to a statistically significant extent in any case. Perfusion pressure and metabolic parameters were not statistically different between the control and the hearts exposed to anaesthetics. CONCLUSION: Volatile anaesthetics in a concentration of 1 MAC can reduce the adhesion of platelets in the coronary system under reduced flow conditions. This action does not arise from vasodilation or inhibition of ischaemic stress.

Anesthetics, Inhalation↗
PubMed1997

A case-based consiliarius for therapy recommendation (ICONS): computer-based advice for calculated antibiotic therapy in intensive care medicine.

We report here on the system ICONS which utilizes case-based reasoning for medical decision support. As an application domain we have chosen the medical field of 'calculated antibiotic therapy' in an intensive care medicine setting. The system ICONS which runs on a personal computer suggests adequate antibiotic therapy regimen satisfying medical and economic conditions. To speed up the process of finding an adequate antibiotic therapy for a current patient, case-based reasoning is used for finding previously documented similar cases and for modifying them according to the requirements of the current patient. To reduce the memory capacity for the documentation of cases, collections of similar cases are clustered to prototypes. Medical knowledge is represented within a hierarchy of such prototypes and cases and an additional context-sensitive background knowledge-base. A knowledge acquisition tool was programmed that allows revisions of the background medical knowledge-base by simple and comprehensive methods. In addition to the advantage of producing site-specific and time-dependent knowledge, case-based reasoning is a practical method for speeding-up the process of generating and evaluating hypotheses in medical classification tasks.

Anti-Bacterial Agents↗
PubMedDate not supplied

Multiparametric time course prognoses by means of case-based reasoning and abstractions of data and time.

In this paper we describe an approach to utilize Case-Based Reasoning methods for trend prognoses for medical problems. Since using conventional methods for reasoning over time does not fit for course predictions without medical knowledge of typical course pattern, we have developed abstraction methods suitable for integration into our Case-Based Reasoning system ICONS. These methods combine medical experience with prognoses of multiparametric courses. We have chosen the monitoring of the kidney function in an Intensive Care Unit (ICU) setting as an example for diagnostic problems. On the ICU, the monitoring system NIMON provides a daily report based on current measured and calculated kidney function parameters. We abstract these parameters to a daily kidney function state. Subsequently, we use these states to generate course-characteristic trend descriptions of the renal function over the course of time. Using Case-Based Reasoning retrieval methods, we search in the case base for courses similar to the current trend descriptions. Finally, we present the current course together with similar courses as comparisons and as possible prognoses to the user.

Artificial Intelligence↗