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Biomedical subjects

V Kühlkamp

Publications and source records attributed to V Kühlkamp.

83 records · Page 5Linked to original sources
PubMed1989

[Heart arrhythmia following surgery of congenital heart defects].

As a result of the intraoperative trauma sinus node dysfunction and AV conduction defects have been observed. In addition bifascicular block (RBBB with LAH) may occur after repair of a ventricular septal defect. This electrocardiographic pattern indicates a high risk of developing a trifascicular block only in those patients with reversible AV block in the early postoperative period. After closure of an atrial septal defect, atrial fibrillation can develop as well as ventricular tachycardia and fibrillation after repair of a ventricular septal defect. The latter seems to be the underlying mechanism of sudden cardiac death occurring late after operation, especially in patients with Fallot tetralogy. In addition to the scar, persistent structural myocardial changes seem to be an important factor. Electrophysiological investigation is indicated in all symptomatic patients especially for detection and treatment of ventricular tachyarrhythmias. However, there is yet no proof that sudden death can be prevented by antiarrhythmic treatment of all ventricular premature beats in the endangered patients.

Arrhythmias, Cardiac↗
PubMed1988

[Flecainide-induced hepatitis].

Flecainide was given to a patient in a dose of 150 mg twice daily to convert a newly developed atrial fibrillation; concomitant therapy was unchanged. After the fourth dose the patient complained of upper abdominal pain and nausea. GOT and GPT, normal at admission to the hospital, became markedly elevated and reached a maximum of 960 IU/I (GOT) and 993 IU/I (GPT) one day later, although the enzymes which indicate cholestasis remained at a normal level or did not increase. On the assumption of a drug-induced allergic reaction, flecainide was withdrawn, after which liver enzymes rapidly returned to control values. Although neither a reexposition with flecainide nor a liver biopsy was obtained, a flecainide-induced hepatitis seems probable.

Aortic Valve Stenosis↗
PubMed1988

[Electrophysiologic effects of betaxolol on conduction properties of the antegrade and retrograde pathway in patients with typical atrioventricular node reentry tachycardia following intravenous and oral administration].

The electrophysiologic effects of the beta-1 selective beta adrenergic blocking drug Betaxolol were investigated after intravenous (0.15 mg/kg body weight) and oral (20 mg/day) administration in 11 patients with atrioventricular-nodal reentrant tachycardia. Betaxolol significantly (p less than 0.01) prolonged cycle length, sinus node recovery time, AH-interval, as well as the antegrade functional refractory period of the slow and fast AV-nodal pathway. The effective refractory period of the fast AV-nodal pathway was also markedly increased (p less than 0.05). In only six patients could the effective refractory period of the slow AV-nodal pathway be determined; in the other patients, it was shorter than the effective refractory period of the atrium. The effective refractory period of the atrium and the ventricle was not significantly altered by Betaxolol. Intravenous administration of Betaxolol suppressed induction of tachycardia in eight patients, whereas after oral Betaxolol, tachycardia was not inducible in ten patients. Betaxolol prevented induction of tachycardia in two patients by prolonging antegrade conduction over the slow AV-nodal pathway. The retrograde fast AV-nodal pathway was blocked in eight patients. Presumably the increased effectiveness of oral Betaxolol can be attributed to higher Betaxolol plasma concentrations, reached after oral treatment (58 +/- 38 ng/ml), as compared to intravenous administration (40 +/- 40 ng/ml). There were no false positive results after intravenous testing of Betaxolol.

Administration, Oral↗
PubMed1988

[Effect of a new class I anti-arrhythmia agent cibenzoline in patients with therapy refractory, sustained ventricular tachycardias].

The effectiveness of Cibenzoline was assessed by means of programmed ventricular stimulation in 13 patients with sustained, drug refractory ventricular tachycardia. Besides Cibenzoline, an average of 3.5 antiarrhythmic drugs were tested, or were clinically ineffective. Cibenzoline was applied, i.v., in a dose of 1.5 mg/kg within 10 min. Cycle length was significantly shortened (p less than or equal to 0.05) while increases were noted for effective refractory period of the right ventricle (p less than or equal to 0.05), intranodal (AH-interval) and infranodal (HV-interval) conduction time (p less than or equal to 0.01), QRS-duration (p less than or equal to 0.001), QT-interval corrected for frequency (p less than or equal to 0.001) as well as cycle-length of the tachycardia (p less than or equal to 0.05). After i.v. Cibenzoline, induction of tachycardia was more difficult in two patients and unchanged in five patients. Spontaneous occurrence of the tachycardia was noted in three patients, and in one patient tachycardia was sustained by atrial stimulation. Cibenzoline i.v. prevented tachycardia in two patients respectively induction of tachycardia was not reproducible. It is concluded that Cibenzoline may be effective in individual patients with sustained ventricular tachycardia unresponsive to other antiarrhythmic drugs.

Adult↗
PubMed1987

Calcitonin gene-related peptide stimulates rat gastric somatostatin release in vitro.

The influence of rat calcitonin gene-related peptide (rCGRP) on the secretion of gastric somatostatin and gastrin was studied in vitro using the isolated, vascularly perfused rat stomach preparation. rCGRP stimulated somatostatin secretion dose-dependently reaching 3-fold stimulation at 1 microM. The kinetics of somatostatin response were characterized by a sharp increase in the initial phase of rCGRP perfusion followed by sustained elevated levels. Gastrin secretion was moderately suppressed at 1 nM to 100 nM CGRP. Somatostatin responses to half-maximal stimulation with 100 nM CGRP were not affected by concomitant perfusion of atropine, propranolol, and tetrodotoxin. It is concluded that increases in somatostatin release in response to CGRP are probably due to a direct effect on the gastric somatostatin-producing D-cell and may be important for the potent acid-inhibitory activity of CGRP.

Animals↗
PubMed1987

Muscarinic receptors mediate negative and positive inotropic effects in mammalian ventricular myocardium: differentiation by agonists.

The concentration-dependence of the negative and positive inotropic effect of choline esters and of oxotremorine was studied in isometrically contracting papillary muscles of the guinea-pig. The preparations were obtained from reserpine-pretreated animals and were electrically driven at a frequency of 0.2 Hz. In the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methyl xanthine (IBMX, 100 mumol l-1), choline esters and oxotremorine produced concentration-dependent negative inotropic effects. Oxotremorine exhibited the highest negative inotropic potency (with a half-maximal effective concentration, EC50, of 20 nmol l-1) followed by carbachol (139 nmol l-1), methacholine (490 nmol l-1), acetylcholine in the presence of 10 mumol l-1 physostigmine (1.36 mumol l-1) and bethanechol (10 mumol l-1). Atropine was a competitive antagonist of the negative inotropic effects. Carbachol and oxotremorine decreased Vmax, overshoot and duration of slow Ca2+-dependent action potentials which had been elicited in the presence of 100 mumol l-1 IBMX. Choline esters produced a concentration-dependent positive inotropic effect. With an EC50 of 32 mumol l-1, carbachol was the most potent compound, followed by methacholine (35 mumol l-1), acetylcholine in the presence of 10 mumol l-1 physostigmine (46 mumol l-1) and bethanechol (142 mumol l-1). Compared to carbachol and methacholine which increased force by 100% of control, the increase induced by acetylcholine and bethanechol was only 64 and 58%, respectively. Atropine shifted the concentration-effect curves of all choline esters to higher concentrations. Choline esters caused intracellular Na+ activity to increase in the quiescent papillary muscle. This effect was reversed by atropine. Oxotremorine produced a small concentration-dependent positive inotropic effect (about 30% of the maximal effect of carbachol) which was resistant to atropine. Oxotremorine was a potent inhibitor of the positive inotropic effect of choline esters, and did not cause an increase in intracellular Na+ activity in the quiescent papillary muscle. The results show that muscarinic receptors of the ventricular myocardium mediate two inotropic effects, which are opposite in direction and differ in their concentration-dependence by a factor of 100. Although agonists differentiate between both inotropic effects, it is unknown whether the receptors involved represent receptor states or separate receptor subpopulations. The negative inotropic effect of choline esters and of oxotremorine can be best explained by adenylate cyclase inhibition. While stimulation of phosphoinositide hydrolysis might have been responsible for the positive inotropic effect of choline esters via modulation of cation-fluxes across the cell membrane, such a mechanism was not involved in the positive inotropic effect of oxotremorine.

1-Methyl-3-isobutylxanthine↗
PubMed1986

The reaction of ouabain with the sodium pump of guinea-pig myocardium in relation to its inotropic effect.

[3H]ouabain binding (1.85-500 nmol/l) was evaluated in resting guinea-pig papillary muscles at 1.2-12 mmol K/l. The time course of binding was biphasic. This finding excluded a homogeneous population of non-interacting binding sites of ouabain, even though the identical susceptibility of both phases to K suggested the occupation of similarly operative receptors. Concomitant with ouabain binding, intracellular Na ion activity (aiNa) increased in the presence of 2.4 or 12 mmol K/l. Occupation of the receptor molecule by ouabain, therefore, conformed to Na-pump inhibition. Although K antagonized both ouabain binding and its effect on aiNa, the antagonistic effect on aiNa was more pronounced. The reduction of passive Na influx with depolarization as well as the stimulation of the Na pump by K presumably contributed to the antagonistic effect of K. The decrease in aiNa from 8 to 5 mmol/l, when in the absence of ouabain K was raised from 2.4 to 12.0 mmol/l, confirmed the relevance of Na fluxes. Simultaneous changes in aiNa and in the force of rested-state contractions were apparent upon addition of ouabain. At 2.4 mmol K/l, increase in aiNa raised the force of contraction by constant proportions. At 12 mmol K/l, the inotropic effect produced at comparable values of aiNa was approximately tenfold higher and was susceptible to a change in extracellular Ca concentration. Increase in aiNa, however, was differently effective on force of contraction of low as compared with high values of aiNa. The influence of resting membrane potential on electrogenic Na-Ca exchange is supposed to interfere with the inotropic effectiveness of aiNa after the cell membrane depolarized from -102 mV to -65 mV with the increase of K from 2.4 to 12 mmol/l. In view of the role of both membrane potential and aiNa not just a single mechanism appeared to be involved in the control of force of contraction.

Animals↗
PubMed1985

Muscarinic receptor-mediated increase of intracellular Na+-ion activity and force of contraction.

The aim of the present study was to determine the mechanism of the positive inotropic effect of carbachol on ventricular myocardium. Carbachol produced a concentration-dependent (0.1 to 300 mumol/l) increase in contraction force on the catecholamine-depleted papillary muscle of the guinea pig without affecting the normal action potential or the slow action potential evoked in 24 mmol/l K+. Since atropine prevented the inotropic effect of carbachol, muscarinic receptors were involved. Carbachol (300 mumol/l) produced an increase in intracellular Na+-ion-activity, aiNa, by about 3 mmol/l in the quiescent muscle, and the time course of the aiNa change corresponded with the development of the positive inotropic effect as determined in the stimulated preparation (0.2 Hz). The effect of carbachol on force of contraction and on aiNa was diminished by reducing [Ca2+]0. The positive inotropic effect of carbachol was dependent on repetitive activity and was markedly enhanced in the presence of dihydro-ouabain. The results are consistent with the hypothesis, that carbachol increases the Na+ permeability of the sarcolemma via muscarinic receptors, and enhances force of contraction by stimulating the Na+-Ca2+-exchange.

Action Potentials↗
PubMedDate not supplied

Variable responsiveness of anterograde and retrograde fast pathway conduction to adenosine in patients with typical AV-nodal reentry tachycardia.

Adenosine is known as a substance which depresses predominantly the slow pathway of the av-node. However, the effect of adenosine on the anterograde and retrograde fast pathway (FP) has not been studied in a large patient population. Ninety-one patients with inducible typical av-nodal reentrant tachycardias (AVNRT) were included. The clinically used dosage of 12 mg adenosine was administered subsequently as bolus injection during a constant atrial and ventricular pacing (500 ms) in all patients. Electrophysiological av-nodal parameters were determined. A higher responsiveness of the anterograde compared to the retrograde FP was observed: the majority of patients (76%) blocked anterogradely and 55% blocked retrogradely within the FP after the administration of 12 mg adenosine. Thirty-six percent of all patients revealed a differential behaviour to adenosine. Sixteen percent of all patients were completely resistant to adenosine (P=0.012). Electrophysiological parameters did not predict the responsiveness of the FP to adenosine. In patients with typical AVNRT the anterograde FP shows a higher sensitivity than the retrograde FP to adenosine. This might reflect an anatomical and/or functional distinction between anterograde and retrograde FP. The variable response to adenosine could be due to individual anatomical and electrophysiological heterogenity of the perinodal tissue and the av-node.

Adenosine↗
PubMedDate not supplied

Anxiety in patients with an automatic implantable cardioverter defibrillator: what differentiates them from panic patients?

OBJECTIVE: Anxiety seems to be a frequent problem in patients with an automatic implantable cardioverter defibrillator (AICD). Distressing experiences before or after AICD implantation such as resuscitation, or AICD shocks are suspected as causes for enhanced anxiety levels. A closer examination of the level and structure of anxiety in AICD patients and a comparison with panic patients might help to examine additionally both conditioning and cognitive models of anxiety. METHODS: There were 61 AICD patients examined with a specifically designed AICD questionnaire and standardized anxiety and depression questionnaires. Subgroups of AICD patients without, with some, and with definite anxiety related to AICD shocks were compared with panic patients and healthy control subjects. RESULTS: Although fear of dying was greatly reduced by AICD implantation, approximately one third of the AICD patients, especially patients with definite anxiety related to AICD shocks, were characterized both by enhanced anxiety levels and avoidance behavior. These patients were comparable with panic patients in most questionnaire scores. Anxiety levels were not associated with objective AICD shock experiences or medical variables. CONCLUSIONS: Anxiety in AICD patients seems to be unrelated to traumatic experiences, a finding that casts doubt on pure conditioning models of anxiety. Presumably, a life-threatening cardiac disorder increases the likelihood for catastrophic interpretations of bodily signs, especially in anxiety prone AICD patients. In accordance with cognitive models of panic disorder, this cognitive dysfunction could lead to anxiety and depression levels comparable with those of panic patients.

Adult↗