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Biomedical subjects

K Stangl

Publications and source records attributed to K Stangl.

At least 55 records · Page 3Linked to original sources
PubMed1999

Interaction of adenosine and prostacyclin in coronary flow regulation after myocardial ischemia.

The role of adenosine and prostacyclin in post-ischemic vasodilation was investigated using a model of sequential perfusion of two isolated hearts. Two guinea pig hearts were sequentially perfused (10 ml/min) without (control, n = 4) or with preceding 10-min ischemia (n = 6) of Heart I. Under control conditions no hemodynamic changes were observed in Heart II during sequential perfusion. After 10 min of ischemia of Heart I coronary perfusion pressure decreased by 23% in Heart II at the onset of sequential perfusion. Adenosine A1 and A2 receptor antagonists 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (2 microM) and 3,7-dimethyl-1-propargylxanthine (DMPX) (20 microM) infused simultaneously inhibited this decrease in coronary perfusion pressure by 74%, whereas indomethacin (5 microM) had no effect. DPCPX, DMPX and indomethacin in combination induced a significant increase in coronary perfusion pressure. Adenosine release (HPLC) into the coronary effluent after ischemia was significantly enhanced in the presence of indomethacin. These results suggest that after myocardial ischemia prostacyclin has an inhibitory effect on adenosine release.

Adenosine↗
PubMed1999

Antithrombin increases pulmonary endothelins: inhibition by heparin and Ca2+ channel antagonism.

We investigated the mechanism of antithrombin III-induced vascular release of endothelins in rat isolated lung. The antithrombin III-stimulated release of big endothelin-1 and endothelin-1 (1.7-fold and 1.3-fold over baseline) was abolished by nicardipine (L-type Ca2+ channel blocker), heparin, and N-acetyl heparin (a derivative devoid of antithrombin affinity), whereas staurosporine and genistein (inhibitors of protein kinase C and tyrosine kinase, respectively) were ineffective. Thus, (i) the antithrombin III-induced release of endothelins requires extracellular Ca2+, but not protein kinase C or tyrosine kinase activation, and (ii) heparin binding to antithrombin III is not necessary for its inhibitory effect.

Analysis of Variance↗
PubMed1999

A1/A2 polymorphism of glycoprotein IIIa and association with excess procedural risk for coronary catheter interventions: a case-controlled study.

BACKGROUND: A five-fold increase in risk of stent thrombosis in carriers of A1/A2 (Leu33Pro) polymorphism of glycoprotein Illa has been described. Whether this increased procedural risk applies to other coronary interventions is unknown. We investigated the role of A1/A2 polymorphism as a putative risk factor. METHODS: We genotyped 1000 consecutive patients with angiographically confirmed coronary-artery disease and 1000 controls matched for age and sex. 653 of the 1000 patients received interventions (271 coronary angioplasty, 102 directional coronary atherectomy, and 280 stenting) and were assessed for a 30-day composite endpoint of need for target-vessel revascularisation, myocardial infarction, and death. FINDINGS: The composite endpoint occurred in 41 (6.3%) patients. There was no evidence that the A2 allele was associated with excess procedural risk (relative risk 1.36 [95% CI 0.70-2.70], p=0.37). Nor, in subgroup analyses, did A2 predict events that complicated coronary angioplasty (1.17 [0.40-2.70]), directional coronary atherectomy (1.50 [0.30-8.70]), or stenting (1.45 [0.60-3.50]). Neither heterozygotes (A1/A2) nor homozygotes (A2/A2) were over-represented in any subgroup, including those with acute coronary syndromes, early disease manifestation (age <40 years), and histories of myocardial infarction. INTERPRETATION: A1/A2 polymorphism is not a major risk factor for 30-day adverse events that complicate coronary angioplasty, directional coronary atherectomy, or stenting. Furthermore, A1/A2 polymorphism has no apparent impact on more chronic processes such as atherogenesis of the coronary arteries.

Aged↗
PubMed1999

Influence of polymorphonuclear leukocytes and plasma on coronary vasomotion after ischemia.

BACKGROUND: The role of plasma and neutrophils in endothelial dysfunction following myocardial ischemia was investigated. METHODS: Isolated rabbit hearts were perfused at constant pressure with a modified Krebs-Henseleit solution. After a 30-minute global ischemia the hearts were perfused at the onset of reperfusion for 10 minutes with either NaCl (group I, n = 6), autologous plasma alone (group II, n = 5), autologous polymorphonuclear leukocytes alone (PMN, group III, n = 6), or PMN and plasma in combination (group IV, n = 5). Before and after ischemia the effects of intracoronary endothelial dependent and independent vasodilation by acetylcholine (1 x 10(-7)mol/L) and glycerol trinitrate (1 x 10(-6) mol/L) were investigated. RESULTS: A similar increase in coronary flow was induced in groups I, II, and III by acetylcholine and glycerol trinitrate before and after ischemia. In contrast, in group IV the endothelial dependent vasodilation was significantly depressed (p < 0.05). In groups II and IV a moderate but significant reduction in the recovery of the left ventricular pressure was observed after ischemia and reperfusion. CONCLUSIONS: These results suggest that after myocardial ischemia, plasma is required for neutrophil-mediated endothelial dysfunction.

Animals↗
PubMed1999

Cardiodepressant mediators are released after myocardial ischaemia: modulation by catecholamines and adenosine.

The interaction of recently characterized cardiodepressant mediators with catecholamines and adenosine after myocardial ischaemia was investigated using a model of sequential perfusion of two isolated guinea-pig hearts. Sequential perfusion was initiated after 10, 20, and 30 min (group I, II, and III) of global ischaemia in the first heart. At the onset of sequential perfusion LVdP/dtmax and min of Heart II decreased by 46 and 44% in group I, by 28 and 34% in group II, and increased by 60 and 24% in group III. Infusion of the beta1-receptor antagonist metoprolol (2.8 micromol L(-1)) into Heart II did not modulate contractile changes after 10 min of ischaemia in Heart I, prevented the attenuation of the cardiodepressant effect after 20 min of ischaemia, and completely reversed the positive inotropic effect after 30 min of ischaemia. The A1- and A2-receptor antagonists DPCPX (2 micromol L(-1)) and DMPX (20 micromol L(-1)) enhanced the positive inotropic and lusitropic effects in Heart II (LVdP/dtmax +154%, LVdP/dtmin +71%) during sequential perfusion after 30 min of ischaemia in Heart I. It is concluded that the effects of cardiodepressant mediators released after myocardial ischaemia are counteracted by a time-dependent release of catecholamines. Endogenous cardiac adenosine, in turn, attenuates the modulatory effects of catecholamines.

Adenosine↗
PubMed1999

Phase-related changes in right ventricular cardiac output under volume-controlled mechanical ventilation with positive end-expiratory pressure.

OBJECTIVE: To examine determinants of right ventricular function throughout the ventilatory cycle under volume-controlled mechanical ventilation with various positive end-expiratory pressure (PEEP) stages. DESIGN: Prospective observational animal pilot study. SETTING: Animal research laboratory at a university hospital. SUBJECTS: Eight healthy swine under volume- controlled mechanical ventilation. INTERVENTIONS: Flow probes were implanted in eight swine in order to continuously measure blood flow in the pulmonary artery and inferior vena cava. After a recovery phase of 14 days, the swine were subjected to various PEEP stages (0, 5, 10 cm H2O) during volume-controlled positive pressure ventilation. MEASUREMENTS AND MAIN RESULTS: Continuous flow measurement took place in the pulmonary artery and inferior vena cava. Data on standard hemodynamic parameters were additionally acquired. Respiration-phase-specific analysis of right ventricular cardiac output and of additional hemodynamic function parameters followed, after calculation of mean values throughout five respiration cycles. PEEP at 5 cm H2O led to significant decreases in inferior vena cava flow (4.1%), and in right ventricular cardiac output (5.2%); the respective decreases at PEEP 10 cm H2O were 13.9% and 18.3%. In the inspiration phase at PEEP 10 cm H2O, results revealed an overproportionally pronounced decrease in comparison with the expiration phase in inferior vena cava flow (-24.6% vs. -10%) and right ventricular cardiac output (-35% vs. -13.5%). This phenomenon is presumably caused by a PEEP-related increase in mean airway pressure by the amount of 10.7 cm H2O in inspiration. CONCLUSIONS: Increases in PEEP during volume-controlled mechanical ventilation leads to respiration-phase-specific reduction of right ventricular cardiac output, with a significantly pronounced decrease during the inspiration phase. This decrease in cardiac output should be taken into particular consideration for patients with already critically reduced cardiac output.

Airway Resistance↗
PubMed1999

Mutations in the human paraoxonase 1 gene: frequencies, allelic linkages, and association with coronary artery disease.

Oxidative damage is a major cause of atherosclerosis. Since human paraoxonase has been postulated as a factor which plays a role in protection from low density lipoprotein oxidation, recent studies have dealt with the impact of hereditary PON1 gene polymorphisms as risk factors for coronary artery disease (CAD). The results from these studies are conflicting. In a case-control study, 1000 Caucasian patients with angiographically confirmed CAD were recruited and matched by age and gender to 1000 control individuals. PON1 mutations in codons 55 and 192 were evaluated by polymerase chain reaction-restriction fragment length polymorphism and allocated to defined haplotypes *1 (55L/192Q), *2 (55L/192R), and *3 (55M/192Q). Frequency of PON1 genotypes without any mutation (PON1*1/*1, wild-type) in CAD cases was 16.9% versus 17.1% in control individuals. PON1*2/*2 showed a frequency of 6.6% versus 7.3% (P = 0.68 compared to wild-type), and PON1*3/3 occurred in 11.8% in CAD cases versus 10.3% among control individuals (P = 0.40). There was also no difference in the distribution of carriers heterozygous for *2 or *3 among cases and control individuals. A haplotype containing both mutations 55M and 192R was not observed. None of the investigated genotypes demonstrated association with early manifestation, severity of disease, acute coronary syndromes, or myocardial infarction. Logistic regression analysis with adjustment for age, gender, diabetes, hypertension, hypercholesterolemia and smoking revealed no evidence of increased coronary risk associated with PON1 genotypes. These results suggest that PON1 polymorphisms are not major genetic determinants of CAD.

Alleles↗
PubMed1999

Automatic and efficient R wave discrimination in the right atrium using a two-state hidden Markov model.

INTRODUCTION: Discrimination of far-field R waves from atrial events in atrial electrograms (EGMs) is problematic in present implantable pacing systems. Adjustments of atrial refractory periods and sensitivity settings are the only options, and they will not provide optimal performance in many patients. The reliable detection or rejection of R waves in atrial EGMs would avoid problems of atrial undersensing or oversensing, thus benefiting DDD patients by providing more reliable and specific atrial arrhythmia detection. In addition, detection of far-field R waves could allow a measurement of AV conduction time in AAI and aid in discrimination of supraventricular tachyarrhythmia from ventricular tachyarrhythmia. METHODS AND RESULTS: Both atrial and ventricular unipolar EGMs were collected from 25 patients undergoing pacemaker implant or replacement. An average of 141 seconds of intrinsic or VVI paced EGMs was recorded and post analyzed. A new two-state hidden Markov model (HMM) was developed specifically for far-field R wave and P wave discrimination in the atrium. The recorded patients' EGMs were analyzed using this model, and the sensitivity and positive predictivity of far-field R wave detection were evaluated. The collected atrial EGMs were visually examined and marked as the control for verification of the detection analysis. Far-field R wave detection using this model had an overall sensitivity of 94% +/- 9.4% and a positive predictivity of 98.3% +/- 4.4%; and the far-field R wave rejection using the same model had a sensitivity and a positive predictivity of 98.8% +/- 3.8% and 99.1% +/- 1.7%, respectively. CONCLUSION: Far-field R wave detection in the right atrium by the two-state HMM is reliable and accurate, and can significantly improve atrial arrhythmia management for patients.

Adolescent↗
PubMed1998

Arrhythmogenic effects induced by coronary conversion of pulmonary big endothelin to endothelin: aggravation of this phenomenon in heritable hyperlipidemia.

OBJECTIVES: We investigated whether endogenous pulmonary big endothelin has arrhythmogenic properties under normal conditions and in heritable hyperlipidemia. BACKGROUND: Endothelin (ET), one of the most potent vasoconstrictors, is known to induce ventricular arrhythmias. It is unclear, however, whether its precursor, big endothelin, released from the lung, contributes to arrhythmogenesis. METHODS: In a lung-heart model in which a Langendorff heart is serially perfused with the effluent from the isolated lung of the same animal, we evaluated arrhythmias in control and in Watanabe heritable hyperlipidemic (WHHL) rabbits. RESULTS: In both controls (n=12) and WHHL (n=8), serial perfusion evoked a decrease in coronary flow (controls, -11+/-3%; WHHL, -25+/-6%) and a fourfold increase of ventricular extrasystoles (VES) (controls, 40.7+/-8; WHHL, 40.2+/-5 VES/40 min, p < 0.05). However, WHHL developed more and longer nonsustained ventricular tachycardias (VT) compared with controls (incidence, 1.38+/-1.1 vs. 0.33+/-0.5 VT/40 min, p < 0.05; length, 14.36+/-3.1 vs. 7.25+/-1.5 beats/VT, p < 0.05). Arrhythmias were not ischemia-induced because corresponding mechanical flow reduction had no arrhythmogenic effect (n=6 in controls and WHHL). Although vasoconstriction disappeared entirely, arrhythmias were only partly suppressed by ET(A) antagonists (BQ-123, 2 micromol/liter; A-127722, 20 micromol/liter). The ET-converting enzyme inhibitor phosphoramidon (50 micromol/liter) completely suppressed arrhythmias and vasoconstriction. The ET(B) antagonists (IRL-1038, 4 micromol/liter; IRL-1025, 5 micromol/liter) had no effect (n=6). CONCLUSIONS: Endogenous pulmonary big ET produces arrhythmogenic effects that are aggravated in heritable hyperlipidemia. These effects, requiring coronary conversion of big ET into ET, are partly ET(A)-mediated and ET(B)-independent.

Animals↗
PubMed1998

Fibrinogen breakdown, long-lasting systemic fibrinolysis, and procoagulant activation during alteplase double-bolus regimen in acute myocardial infarction.

Recent clinical studies comparing accelerated versus bolus administration of alteplase tissue plasminogen activator (t-PA) suggest similar thrombolytic efficacy, but reveal higher bleeding complications among older patients during the double-bolus regimen. The objective of the present study was to characterize the hemostatic profile of t-PA administered as double-bolus doses of 50 mg, at intervals of 30 minutes. Among 50 patients with acute myocardial infarction treated by double-bolus t-PA thrombolysis, coagulation and fibrinolysis parameters, as well as t-PA levels, were monitored. Monitored t-PA levels peaked at 5 and 35 minutes and were detectable within the therapeutic range even after 90 minutes. Marked systemic fibrinolytic activation was indicated by 75% depletion of both plasminogen and fibrinogen, as well as by 19-fold and 300-fold increases of fibrin degradation and fibrinogen degradation products. Plasminogen-activator inhibitor activity was completely suppressed. Pronounced procoagulant activation was reflected by a 3.4-fold increase of both factor XIIa and prothrombin fragment 1+2, and by a threefold increase of thrombin-antithrombin complex. Independent of t-PA weight dosage, fibrinolytic activation was more pronounced among older patients (> or = 63 years). We conclude that t-PA after bolus administration has a long half-life. Double-bolus regimen leads to a long-lasting systemic fibrinolytic state, which is even more remarkable among older patients--a fact that may explain the higher bleeding complications reported for this age group.

Aged↗
PubMed1998

Coronary constriction and consequent cardiodepression in pulmonary embolism are mediated by pulmonary big endothelin and enhanced in early endothelial dysfunction.

OBJECTIVES: Myocardial ischemia plays a central role in the development of right ventricular failure after acute pulmonary embolism. This study investigates whether pulmonary mediators act specifically on coronary tone and cardiac contractile function in acute pulmonary microembolization and whether such effects are altered in the case of early systemic atherosclerosis. We employ a novel model of serial perfusion in which an isolated rabbit heart is perfused with the effluent of the same animal's isolated lung. DESIGN: Controlled experiment using isolated organs. SETTING: Experimental laboratory. SUBJECTS: Male New Zealand White rabbits (controls). Age-matched, male Watanabe rabbits (hypercholesterolemic, development of accelerated atherosclerosis). INTERVENTIONS: Seven isolated control and seven isolated Watanabe hearts were perfused with the saline effluent of the same animal's isolated lung. After the assessment of the baseline data, the lungs were gradually embolized with glass beads measuring 100 microm in diameter to induce an increase in mean pulmonary arterial pressure from 6 to 8 mm Hg, at baseline, up to 25 mm Hg. MEASUREMENTS AND MAIN RESULTS: Pulmonary embolization to 25 mm Hg evoked a coronary constriction, measured as coronary flow decrease to 89 +/- 7% of the baseline value in controls. In the Watanabe group, coronary constriction was significantly enhanced, compared with controls, with coronary flow decreasing to 76 +/- 6% of the baseline value. In both groups, coronary constriction was followed by a deterioration in cardiac contractile performance. This cardiodepression was significantly deeper in Watanabe hearts with respect to both maximum ventricular pressures and maximum rates of pressure development and decline. Coronary constriction and cardiodepression were prevented by coronary infusion of the nonselective endothelin antagonist PD-145065, the endothelinA antagonists A-127722 and BQ-123, and the endothelin-converting enzyme inhibitor phosphoramidon. Concentration of big endothelin in pulmonary effluent increased from 5.6 +/- 0.3 pmol/L in controls and 5.6 +/- 0.2 pmol/L in the Watanabe group, at baseline, to 8.8 +/- 0.4 pmol/L in controls and 8.9 +/- 0.4 pmol/L in the Watanabe group, at 25 mm Hg pulmonary arterial pressure. Endothelin was not detectable at any time during the experiment in pulmonary effluent. The coronary gradient, calculated as a difference in concentration between coronary and pulmonary effluent, was negative for big endothelin and positive for endothelin in both groups. CONCLUSIONS: We have demonstrated that an increase in pulmonary release of big endothelin occurs during lung embolism, which, in turn, results in coronary constriction and consequent cardiodepression. This action of big endothelin is based on its local coronary conversion into endothelin. In addition, coronary endothelial dysfunction, attributed to early systemic atherosclerosis, was shown to represent a specific risk factor in these events.

6-Ketoprostaglandin F1 alpha↗
PubMed1998

Electrogram signals recorded from acute and chronic pacemaker implantation sites in pacemaker patients.

Electrogram signals recorded from typical pacemaker implantation sites may be useful for a variety of pacemaker system functions including pacemaker follow-up, atrial and ventricular sensing (event detection), and triggered electrogram storage. We quantified the electrical characteristics of pacemaker pocket electrograms using a subcutaneous electrode array (SEA) in a population of 48 patients undergoing initial or replacement pacemaker implantation. SEA recorded intrinsic R wave amplitudes measured peak to peak averaged 118 microV and 65 microV for the two recorded SEA electrograms and were significantly different (P < 0.001); paced R wave amplitudes averaged 180 microV and 110 microV. P wave amplitudes averaged 39 microV and 26 microV. No statistically significant difference in amplitudes were observed between acute versus chronic pacemaker pocket or indication for pacing (AV block, sick sinus syndrome). Signal to noise ratios, using R wave amplitude as signal, were lower in the SEA electrogram on average (11 dB) compared to the intracardiac electrogram (27 dB), but sufficient for diagnostic assessment. R wave/P wave ratios for SEA signals were lower than surface and intracardiac values 3.1 and 2.7 compared to a range of 6.2-9.8, indicating a relative enhancement of P waves to R waves in SEA signals. In summary, SEA electrograms are of sufficient amplitude and signal quality (signal to noise ratio) to hold promise for future implantable device features such as electrogram telemetry, enhanced sensing, and diagnostic data storage.

Adult↗
PubMed1998

Autonomic effects of dipyridamole stress testing on frequency distribution of RR and QT interval variability.

Transient myocardial ischemia and associated changes in the autonomic nervous system may influence heart rate and ventricular repolarization to variable degrees. This study evaluated the effect of dipyridamole (DIP) induced ischemia on the autonomic balance by spectral analysis of RR and QT intervals variability. Patients with coronary artery disease undergoing DIP stress echocardiography were studied. From high resolution ECG recordings, RR and QT interval measurements were performed by a dynamic template-matching algorithm. A time-variant analysis was used to estimate power in the LF (0.05-0.15 Hz) and in the HF (0.15-0.4 Hz) band of RR and QT interval spectra. Patients were grouped in ischemic and nonischemic subgroups based on the echocardiographic detection of wall-motion abnormalities. In patients without ischemia (n = 28), DIP caused a decrease in LF power and an increase in HF power of the RR and QT interval variability, indicating concordant changes of both intervals. In contrast, patients with inducible ischemia (n = 11) showed a decrease in HF power of the RR interval spectra and an increase of HF power of QT interval spectra. Furthermore, LF power was increased for RR but decreased for QT interval spectra. Our study suggests that DIP induced ischemia causes a loss of autonomic coupling between heart rate and ventricular repolarization for sympathetic and parasympathetic activities. This lability in ventricular repolarization may constitute an arrhythmogenic substrate during acute ischemia in patients with coronary artery disease.

Algorithms↗
PubMed1998

Superiority of ibutilide (a new class III agent) over DL-sotalol in converting atrial flutter and atrial fibrillation. The Ibutilide/Sotalol Comparator Study Group.

OBJECTIVE: To compare the efficacy and safety of a single dose of ibutilide, a new class III antiarrhythmic drug, with that of DL-sotalol in terminating chronic atrial fibrillation or flutter in haemodynamically stable patients. DESIGN: Double blind, randomised study. SETTING: 43 European hospitals. PATIENTS: 308 patients (mean age 60 years, 70% men, 48% with heart disease) with sustained atrial fibrillation (n = 251) or atrial flutter (n = 57) (duration three hours to 45 days) were randomised to three groups to receive a 10 minute infusion of 1 mg ibutilide (n = 99), 2 mg ibutilide (n = 106), or 1.5 mg/kg DL-sotalol (n = 103). Infusion was discontinued at termination of the arrhythmia. MAIN OUTCOME MEASURE: Successful conversion of atrial fibrillation or flutter, defined as termination of arrhythmia within one hour of treatment. RESULTS: Both drugs were more effective against atrial flutter than against atrial fibrillation. Ibutilide was superior to DL-sotalol for treating atrial flutter (70% and 56% v 19%), while the high dose of ibutilide was more effective for treating atrial fibrillation than DL-sotalol (44% v 11%) and the lower dose of ibutilide (44% v 20%, p < 0.01). The mean (SD) time to arrhythmia termination was 13 (7) minutes with 2 mg ibutilide, 19 (15) minutes with 1 mg ibutilide, and 25 (17) minutes with DL-sotalol. In all patients, the duration of arrhythmia before treatment was a predictor of arrhythmia termination, although this was less obvious in the group that received 2 mg ibutilide. This dose converted almost 48% of atrial fibrillation that was present for more than 30 days. Concomitant use of digitalis or nifedipine and prolongation of the QTc interval were not predictive of arrhythmia termination. Bradycardia (6.5%) and hypotension (3.7%) were more common side effects with DL-sotalol. Of 211 patients given ibutilide, two (0.9%) who received the higher dose developed polymorphic ventricular tachycardia, one of whom required direct current cardioversion. CONCLUSION: Ibutilide (given in 1 or 2 mg doses over 10 minutes) is highly effective for rapidly terminating persistent atrial fibrillation or atrial flutter. This new class III drug, under monitored conditions, is a potential alternative to currently available cardioversion options.

Adult↗
PubMed1997

Pulmonary big endothelin affects coronary tone and leads to enhanced, ET(A)-mediated coronary constriction in early endothelial dysfunction.

BACKGROUND: Lung tissue produces a variety of mediators; however, little is known regarding how these mediators affect coronary regulation and myocardial contractility. In a novel rabbit lung-heart model, we investigated the possible influence exerted by pulmonary mediators on coronary tone both under normal conditions and in early endothelial dysfunction. METHODS AND RESULTS: In our model, the effluent from the isolated lung is used to serially perfuse the coronary vessels of the isolated heart of the same animal. Compared with the hearts of control rabbits, isolated hearts of Watanabe rabbits revealed pharmacological evidence of endothelial dysfunction and a significant steeper decrease of coronary flow during serial perfusion of the coronary vessels with lung effluent (75+/-6% versus 89+/-3%). This decline in coronary flow was prevented by the nonselective endothelin (ET) antagonist PD-145065, the ET(A) antagonists BQ-123 and A-127722, and the endothelin-converting enzyme inhibitor phosphoramidon. The concentration of big ET in lung effluent ranged from 5.5 to 5.8 pmol/L in both control and Watanabe groups, with levels in corresponding coronary effluent falling to 0.9 to 1.1 pmol/L in controls and to 1.0 to 1.2 pmol/L in the Watanabe group. In either group, ET was not detected in lung effluent, but it rose significantly in coronary effluent during serial perfusion. CONCLUSIONS: Pulmonary big ET, locally converted into ET during coronary passage, causes an ET(A)-mediated elevation in coronary tone under basal conditions as well as an enhanced coronary constriction when early endothelial dysfunction is present.

Acetylcholine↗
PubMed1994

[Therapy of cardiogenic shock].

Cardiogenic shock is a syndrome of different etiologies resulting in the inability of the heart to provide adequate O2 delivery to peripheral organs and tissues with or without signs of severe pulmonary congestion or pulmonary edema. Clarification of the underlying etiologies is essential for prognosis and therapy. Depending on the various etiologies, the therapeutic procedure may be totally different. Furthermore, it is decisive to differentiate between an acute shock (e.g., acute myocardial infarction) and the development of a cardiogenic shock state on the basis of preexisting chronic congestive heart failure (e.g., congestive cardiomyopathy). Whenever possible the underlying disease should be treated causally (e.g., PTCA or thrombolytic therapy in AM, lysis in acute pulmonary embolism) in addition to symptomatic pharmacologic treatment with vasodilators and/or inodilators. In myogenic cardiogenic shock, the treatment with inotropic drugs (with and without vasodilatory potency) and, if necessary, in combination with additional vasodilators may be life-saving. At present, there is no alternative to catecholamines in the acute state with apparent hemodynamic instability. Catecholamines still represent the initial first line treatment. A Swan-Ganz catheter is mandatory in such situations. In view of the rapid beta 1-receptor down-regulation induced by endogenous catecholamines, long-term administration of exogenous catecholamines (adrenalin, dopamine, dobutamine), seems essentially problematic, since these compounds intensify and accelerate this process.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1991

Sex hormone concentrations in men with angiographically assessed coronary artery disease--relationship to obesity and body fat distribution.

The relationship between circulating sex hormone levels and the occurrence of coronary artery disease (CAD) was studied in a group of 274 men undergoing coronary angiography. Hormone levels in men with CAD (n = 200) were compared to those in men found to be free of coronary lesions (n = 74). No significant differences were found for serum concentrations of estradiol, total testosterone, sex-hormone-binding globulin, free androgen index, dehydroepiandrosterone sulfate, or cortisol between the two groups. Serum androgens were negatively correlated to age in both groups, whereas estradiol was weakly associated with total cholesterol in the group of men without CAD. No consistent associations were detected between sex hormone levels and the degree of obesity or the distribution of body fat, the latter being assessed by the ratio of waist-to-hip circumferences. The results of this study do not support a significant role of sex steroid hormones in coronary artery disease in men.

Adult↗