[Postresuscitation care]. / Postreanimationsbehandlung.

Witnessed collapse, bystander resuscitation and the use of automated external defibillators for defibrillatable arrhythmias, are recognized as strong predictors for a good prognosis after cardiac arrest. In addition, patient care after return of spontaneous circulation (ROSC), i.e. postresuscitation care, has been identified as an important factor for survival. It is necessary to differentiate between measures for treating the underlying cause of the cardiac arrest and measures for limiting reperfusion injury after global hypoxia and ischemia. The importance of urgent coronary angiography in cases of ST-elevation myocardial infarction (STEMI) and for patients with suspected cardiac origin without STEMI, especially with hemodynamic instability is emphasized in the current European Resuscitation Council (ERC) guidelines. In order to minimize reperfusion injury targeted temperature management (32-36 °C) is advised, rewarming must be controlled and fever and hyperthermia avoided. The mean arterial pressure should be adjusted to allow sufficient urine production (1 ml/kg/h) and blood glucose should be ≤10 mmol/l (≤180 mg/dl). Analgosedation is necessary in most patients, especially with the use of targeted temperature management. Convulsive seizures must be consistently treated. Cardiac arrest centers provide a treatment strategy for postresuscitation care involving emergency percutaneous coronary angiography, targeted temperature management and comprehensive neurological evaluation for estimating the prognosis. Whether establishing these centers will actually lead to improved survival still needs to be proven.

[Prognostic assessment as the basis for limiting therapy in unconscious patients after cardiopulmonary resuscitation]. / Prognostische Einschätzung als Grundlage für die Therapiebegrenzung bewusstloser Patienten nach kardiopulmonaler Reanimation.

BACKGROUND: The prognosis of patients who have been resuscitated after cardiac arrest is still unfavourable and long-term results have only slightly improved. As a consequence, intensivists are frequently confronted with the question of limiting active therapeutic efforts for patients in prolonged coma. The history of the patient and circumstances of the resuscitation are of limited value with regard to reliable decisions. THERAPEUTIC DECISION-MAKING: Clinical and electrophysiological neurologic techniques as well as biomarkers and diagnostic imaging are, therefore, the basis for prognostication and potential consecutive therapeutic decisions. Sedation, relaxation and particularly therapeutic hypothermia have great influence on the test results. These influences have to be excluded before results can be validated. With regard to therapeutic hypothermia a reliable neurologic evaluation as a basis for limiting treatment is only possible after rewarming. Moreover results of multiple tests should be in agreement before a decision to limit treatment can be made. Finally it must be kept in mind that the absence of unfavourable test results is not proof of a good prognosis. CONCLUSION: The decision to limit treatment can not be made on the basis of a single adverse prognostic sign, but requires a comprehensive clinical diagnostic assessment.

[Fibrinolysis as a therapeutic option in acute ST-elevation myocardial infarction]. / Die Thrombolyse als therapeutische Option bei akutem ST-Streckenhebungsinfarkt.

The introduction of intravenous thrombolytic therapy started the new era of reperfusion therapy in ST elevation myocardial infarction. The addition of aspirin almost halved mortality in patients with ST elevation infarction. Primary coronary intervention (PCI) often in combination with stent implantation instead of thrombolytic therapy increases infracted-artery patency and reduces mortality, number of re-infarction and stroke even further. However, studies comparing the benefits of both therapeutic regimens often included patients with long symptom duration (up to 12 hours and more). In addition, there are differences in long term treatment after myocardial infarction in both groups since the addition of thienopyridines to standard treatment after stent implantation. The routine combination of thrombolytic therapy and immediate PCI (facilitated PCI) did not prove beneficial whereas a pharamacoinvasive strategy including thrombolytic therapy and PCI at a later time point could be beneficial. Subgroup analysis in the studies comparing PCI and thrombolytic therapy suggested a beneficial effect for patients receiving thrombolytic therapy early after symptom onset (≥ 2 h). Therefore, a strategic concept of thrombolytic therapy early after symptom onset in patients presenting with ST elevation myocardial infarction combined with either rescue intervention when indicated or planned PCI is currently tested in the so STREAM-study (STrategic Reperfusion Early After Myocardial Infarction). Hopefully this study will clarify the role of thrombolytic therapy in ST Elevation myocardial infarction compared to PCI alone.

Differential regulation of mitogen-activated protein kinases in the failing human heart in response to mechanical unloading.

Background- Mechanical unloading of the heart with a left ventricular assist device (LVAD) leads to favorable changes in the biology of the failing cardiac myocyte. To determine a potential mechanism for these improvements, we examined the regulation of mitogen-activated protein kinases (MAPKs) in the failing heart in the presence and absence of LVAD support. Methods and Results- We examined the degree of activation (ie, phosphorylation) of p44/42 extracellularly regulated kinase, p38 kinase, and c-Jun N-terminal kinase (JNK1/2), and the corresponding activity levels of these MAPKs in myocardial samples obtained from 11 patients with LVAD support and in 11 patients without LVAD support. MAPK activity was also examined in an additional 6 patients from whom paired samples were obtained before and after LVAD support. The activity of p44/42 and JNK1/2 were reduced significantly, whereas p38 activity levels were significantly increased after LVAD support. We examined functional parameters that are linked to MAPK activation, namely cardiac myocyte hypertrophy and apoptosis. Both cardiac myocyte cell size and the incidence of cardiac myocyte apoptosis were significantly reduced after LVAD support. Conclusions- Mechanical unloading of the failing heart leads to differential regulation of MAPKs. These changes in MAPK activity are associated with changes in myocyte hypertrophy and viability, suggesting a potential mechanistic basis for some of the observed salutary changes after LVAD support.

Upregulation of the cardiac bradykinin B2 receptors after myocardial infarction.

An increase in myocardial bradykinin (BK) might be a mechanism to protect the heart during acute myocardial infarction (MI). To characterize the regulation of the myocardial B2 receptor during MI, we studied the expression of this BK receptor in the right ventricle (RV), left ventricle (LV) and myocardial septum (S) 24 h after left coronary ligation. Experiments were performed in male Wistar Kyoto rats (n = 10) and compared with sham operated animals (n = 6). After total RNA extraction, the myocardial B2-receptor expression was analyzed by a RNase protection assay (n = 6), using a specific probe from the coding region of the receptor gene. After 24 h, rats with MI were normotensive and showed an impaired left ventricular function. The B2-receptor expression of the LV of these rats was significantly elevated (2.3-fold) compared to sham operated rats. Furthermore, we found a dramatic upregulation of the B2 receptor in the RV (7.8-fold) and a dramatic expression of B2 receptor mRNA in S of infarcted hearts, whereas in the S of sham operated rats no B2 receptor expression could be detected. Our data show clearly that the described increase in BK during myocardial ischemia is accompanied by an elevated B2-receptor expression in the infarcted and non-infarcted parts of cardiac ventricles.

Ischemic preconditioning prevents the impairment of hypoxic coronary vasodilatation caused by ischemia/reperfusion: role of adenosine A1/A3 and bradykinin B2 receptor activation.

We previously reported that hypoxic coronary vasodilatation (HCVD) is initiated by endothelial NO and sustained by adenosine. Prolonged ischemia/reperfusion impairs endothelium-dependent coronary vasodilatation, whereas transient ischemia (ie, preconditioning) protects the myocardium from subsequent ischemic events. Accordingly, we assessed whether prolonged ischemia/reperfusion impairs HCVD and whether preconditioning prevents this dysfunction. HCVD, elicited in isolated guinea pig hearts by a 1-minute exposure to 100% N2, consisted of an approximately 70% increase in coronary flow associated with enhanced nitrite/nitrate and adenosine overflow (+40% and 5-fold, respectively). After 30-minute global ischemia and 20-minute reperfusion, HCVD was decreased by approximately 60%, and the increases in nitrite/nitrate and adenosine overflow were abolished. Preconditioning (ie, three cycles of 5-minute global ischemia+5-minute reperfusion) prevented the impairment of HCVD and fully restored the increase in nitrite/nitrate overflow, but not that of adenosine. The protective effect of preconditioning was mimicked by perfusion with the adenosine A1 receptor agonist N6-cyclopentyladenosine and prevented by the A1 receptor antagonist N-0861. In addition, the A3 receptor agonist N6-(3-iodobenzyl)adenosine-5'-N-methyl-carboxamide had a similar protective effect. The bradykinin B2 receptor antagonist HOE 140 abolished the protective effect of preconditioning, whereas the NO synthase inhibitor N(omega)-methyl-L-arginine and the cycloxygenase inhibitor indomethacin did not. Our data indicate that preconditioning restores HCVD by a process that is triggered by activation of adenosine A1/A3 and bradykinin B2 receptors. The action of bradykinin is independent of NO and prostacyclin production. Once restored by preconditioning, HCVD is mediated by NO but no longer sustained by adenosine.

[The occurrence and survival of Campylobacter in sewage sludge]. / Untersuchungen zum Vorkommen und Uberleben von Campylobacter im Klärschlamm.

Campylobacter was found only in raw sewage sludge samples of the high-rate municipal sewage treatment plant studied. Campylobacters were isolated from 28.6% of the sewage sludge samples of grit tank and primary settling tank. 40% of the settled activated sludge samples contained Campylobacter. Campylobacter was never found in digested sludge of a mean sludge age of more than 90 days. The survival times of Campylobacter in sewage sludge samples ranged between some hours and 10 days. Therefore a low risk of the spread of Campylobacter in the environment due to agricultural application of digested sewage sludge is assumed.

A study of Campylobacter jejuni and Campylobacter coli in a river system.

Campylobacter isolates were detected in 82.1% of river water samples moderately polluted with organic wastes. In the majority of the samples less than 10 Campylobacter cfu/100 ml were detectable. The presence of waterfowl and the faecal contamination from a poultry-farm resulted in considerable higher Campylobacter contents (greater than 240/100 ml). Correlation studies showed a high correlation coefficient (P less than 0.05) between the number of campylobacters and that of total coliforms. Campylobacter isolates were never found in river water samples of 100 ml of volume with total coliform contents less than 10/ml. Campylobacter contents and the spectrum of serotypes isolated indicate hygienic precautions for drinking water supply from oligotrophic surface waters if the water is distributed without chlorination.

[Antibiotic sensitivity of Campylobacter jejuni and Campylobacter coli strains with special reference to sensitivity to erythromycin and neomycin]. / Untersuchungen über die Antibiotikaempfindlichkeit von Campylobacter jejuni- und Campylobacter coli-Stämmen unter besonderer Berücksichtigung der Empfindlichkeit gegenüber Erythromycin und Neomycin.

166 strains of C. jejuni and 46 strains of C. coli were typed against 14 antibiotics using the agar diffusion test. All strains were resistant against Penicillin G, Oxacillin and Rifampicin. Susceptibility were found against Chloramphenicol, Erythromycin, Neomycin, Oxytetracyclin, Streptomycin and Gentamycin. The minimal inhibition concentration was performed for Erythromycin and Neomycin. All strains tested were inhibited by less than or equal to 2 micrograms/ml Neomycin, one strain was resistant against 4 micrograms/ml Erythromycin.

Characterization of Campylobacter jejuni and Campylobacter coli isolated from waste water.

The raw sewage samples of the investigated municipal sewage plant (sewage flow of about 30,000 m3/d) contained about 10(3) campylobacters/100 ml. The sewage plant reduced 80.8% of organic wastes (COD), 85.0% of colony counts (20 degrees C), 92.5% of total coliforms and 88.0% of campylobacters. The sewage plant effluent contained an average of 1.3 X 10(2) campylobacters/100 ml. About 10(10) campylobacters are discharged with the effluent of the high-output sewage plant into the receiving water every day. No reduction of the indicator bacteria was found in the activated sludge tank, there was, however, a significant reduction (94.5%) of campylobacters. In total, 94 strains were differentiated by biotyping and serotyping. 59.6% were found to be Campylobacter jejuni and 40.4% were Campylobacter coli. 8 Serotypes were found among the C. jejuni strains and 12 among C. coli. The raw sewage of the investigated oxidation pond treatment plant contained an average of 51 campylobacters/100 ml. The sewage plant effluent did not show campylobacters in any case.