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Biomedical subjects

W Schmitz

Publications and source records attributed to W Schmitz.

At least 199 records · Page 11Linked to original sources
PubMed1985

Evidence for adenosine receptor-mediated isoprenaline-antagonistic effects of the adenosine analogs PIA and NECA on force of contraction in guinea-pig atrial and ventricular cardiac preparations.

The effects of the adenosine agonists (-)-N6-phenylisopropyladenosine (PIA) and 5'-N-ethylcarboxamideadenosine (NECA) on force of contraction, adenylate cyclase activity and normal as well as slow action potentials were studied in guinea-pig isolated atrial (left auricles) and ventricular preparations (papillary muscles). In auricles PIA and NECA exerted concentration-dependent negative inotropic effects with similar potencies (mean EC50:0.05 mumol l-1 for PIA and 0.03 mumol l-1 for NECA). Similar results were obtained in the presence of isoprenaline. In papillary muscles PIA and NECA alone had no effect on force of contraction but produced negative inotropic effects in the presence of isoprenaline (mean EC50:0.19 mumol l-1 for PIA and 0.10 mumol l-1 for NECA). In both preparations, the negative inotropic effects of PIA and NECA in the presence of isoprenaline were antagonized by the adenosine receptor antagonist 8-phenyltheophylline. In both preparations, PIA and NECA did not affect adenylate cyclase activity, both in the absence and presence of isoprenaline. In auricles the negative inotropic effects of both nucleosides were accompanied by a shortening of the action potential. This effect was also observed in the presence of isoprenaline. In papillary muscles the adenosine analogs did not detectably alter the shape of the normal action potential. Ca2+-dependent slow action potentials elicited in potassium-depolarized preparations also remained unaltered in the presence of PIA or NECA alone. However, the isoprenaline-induced enhancement of the maximal rate of depolarization of slow action potentials was attenuated by PIA or NECA.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1985

Effects on transmembrane action potential, slow inward current and force of contraction in ventricular cardiac muscle of BRL 31660, a new antiarrhythmic drug with class I and class IV activity.

The effects of 1-30 mumol l-1 BRL 31660 on transmembrane action potential and force of contraction were investigated in guinea-pig electrically driven papillary muscles. Lidocaine was studied for comparison. BRL 31660 depressed Vmax of the action potential without changing the resting potential, decreased the force of contraction and decreased the action potential duration. Similar effects were obtained with lidocaine. BRL 31660 inhibited the recovery of Vmax from inactivation, the time constant of which was estimated to be about 1,100 ms in the presence of 10 mumol l-1 BRL 31660. The depressive effect on Vmax was particularly pronounced at low (less negative) membrane potentials. BRL 31660 can thus be classified as a class I antiarrhythmic agent of the lidocaine type. Additional voltage-clamp experiments in cow ventricular trabeculae provided evidence that BRL 31660 also depressed the slow inward current at concentrations similar to those producing the effects on the transmembrane action potential. BRL 31660 thus exerted an additional class IV action. This effect was not shared by lidocaine. It is concluded that BRL 31660 is a new antiarrhythmic agent which depresses both the fast and slow inward current at similar concentrations. The dual effects of BRL 31660 conceivably contribute to its antiarrhythmic activity, but the clinical relevance of these results remains to be elucidated.

Action Potentials↗
PubMed1985

Late pulmonary embolization of a retained pacemaker electrode fragment after attempted transatrial extraction.

Embolization of pacemaker electrode fragments into the pulmonary circulation is a rare complication following transvenous pacemaker implantation. One such case is reported here. In a 67-year-old patient, a battery pocket infection developed after transvenous pacemaker implantation and subsequent surgical revision. After removal of the pacemaker and ventricular pacing lead, the atrial lead broke within the superior vena cava when prolonged traction was applied after frustrating attempts to extract the electrode. Attempts to extract the fragment transvenously using endoscopic forceps were unsuccessful. Due to firm fixation of the electrode by extensive fibrous scar tissue in the atrial wall, a further attempt to remove the retained electrode fragment by atriotomy also failed. On the first postoperative day, the fragment migrated to the left pulmonary artery, from where it was successfully extracted by means of a Dormier basket.

Aged↗
PubMed1985

Reduction of postoperative donor blood requirement by use of the cell separator.

In a prospective, randomized study of 20 patients undergoing elective open-heart surgery, up to c. one-third of the total intraoperative and postoperative transfusion requirement could be provided by autologous centrifuged blood. Retransfusion of washed, packed red blood cells freed from cellular debris, heparin and activated clotting factors significantly reduced blood loss during and after surgery. The cell separator is a valuable aid in autotransfusion technique.

Adult↗
PubMed1985

Cardiac effects of adenosine and adenosine analogs in guinea-pig atrial and ventricular preparations: evidence against a role of cyclic AMP and cyclic GMP.

The effects of adenosine, the Ri site adenosine receptor agonist (-)-N6-phenylisopropyladenosine (PIA), the Ra site agonist 5'-N-ethylcarboxamideadenosine (NECA) and the P site agonist 2',5'-dideoxyadenosine (DIDA) on force of contraction, cyclic AMP (cAMP) and cyclic GMP (cGMP) content and on transmembrane action potential were studied in isolated electrically driven left auricles and papillary muscles from guinea pigs. Furthermore, the effects on adenylate cyclase activity in a particulate membrane preparation were investigated. In the auricles, adenosine, PIA and NECA had negative inotropic effects which were accompanied by a shortening of the action potential. Theophylline antagonized these effects which are likely mediated by R site adenosine receptors. DIDA was ineffective. Except for a small positive inotropic effect of adenosine the analogs were ineffective in the papillary muscles. None of the mechanical effects was accompanied by a change in cAMP and cGMP content in the intact preparations. In the broken cell preparation PIA and NECA had no effect on adenylate cyclase activity. Adenosine and DIDA inhibited the enzyme. The latter effects can be classified as P site-mediated effects. In conclusion, distinct mechanical, i.e., negative inotropic effects of adenosine and its analogs in the heart are observed in auricular preparations only. These effects are unlikely to be related to the cAMP and/or cGMP system. Instead, they are probably due to a direct shortening of the action potential which, in turn, is conceivably due to an increase in K+ outward current and a secondary decrease in Ca++ inward current. This effect is apparently mediated by cardiac R site adenosine receptors which are not detectably coupled to adenylate cyclase.

Adenosine↗
PubMed1985

[Aortic ring abscess following bacterial endocarditis of the aortic valve and aortic valve replacement].

Valve replacement was performed in a 30-year-old male patient with acute aortic insufficiency due to bacterial endocarditis. During a routine examination three months later, an aortic ring abscess was found by echocardiography. In the following night, the patient was readmitted with acute anterior myocardial infarction. Coronary angiography showed a compression of the left coronary artery by the large ring abscess of the aortic valve. 48 hours after surgical revision of the aortic valve prosthesis and the ring abscess, the patient died due to pump failure.

Abscess↗
PubMed1984

Negative inotropic effects of aldosterone antagonists in isolated human and guinea-pig ventricular heart muscle.

The effects of K+-canrenoate (Aldactone pro inj.) and its metabolite canrenone on isometric force of contraction were measured in isolated guinea-pig and human papillary muscle preparations driven electrically at a frequency of 1 Hz. In guinea-pig hearts both substances exerted a concentration-dependent negative inotropic effect; the IC50 of K+-canrenoate and canrenone were 129 +/- 22 mumol l-1 (n = 5) and 85 +/- 11 mumol l-1 (n = 12), respectively. At the maximally tested concentration canrenone (250 mumol l-1) and K+-canrenoate (1,000 mumol l-1) reduced force of contraction by 68 +/- 4% (n = 12) and 83 +/- 3% (n = 5), respectively. The negative inotropic effects of canrenone and K+-canrenoate were not affected by 10 mumol l-1 atropine. The negative inotropic effect of canrenone was also not affected by 14 mumol l-1 aldosterone, but canrenone (10 mumol l-1 diminished the maximal positive inotropic effect of dihydro-ouabain from 554 +/- 75% (n = 4) to 269 +/- 39% (n = 4) of the predrug value. In human heart muscles K+-canrenoate and canrenone also exerted a concentration-dependent negative inotropic effect. K+-canrenoate (1,000 mumol l-1) and canrenone (250 mumol l-1) reduced force of contraction by 57 +/- 7% (n = 8) and 67 +/- 2% (n = 6), respectively. A positive inotropic effect of both substances was never observed. It is concluded that the improvement of cardiac performance after application of aldosterone antagonists observed in patients cannot be explained by a direct effect on the heart. K+-canrenoate and canrenone are devoid of any direct cardiotonic action. Instead, K+-canrenoate and canrenone have direct negative inotropic effects at high concentrations.

Animals↗
PubMed1984

Alpha-adrenoceptor-mediated positive inotropic effect of phenylephrine in isolated human ventricular myocardium.

In isolated human ventricular myocardium the alpha-adrenoceptor agonist phenylephrine had a positive inotropic effect in preparations from 9 of 14 patients. This effect was seen in the presence of the beta-adrenoceptor-blocking agent propranolol but was nearly abolished by the alpha-adrenoceptor blocking agent prazosin. In contrast to the beta-adrenoceptor-mediated positive inotropic effect, the effect of phenylephrine was accompanied by a prolongation of the isometric contraction. The results suggest that alpha-adrenoceptors exist in human ventricular myocardium.

Adult↗
PubMed1984

Positive inotropic effects of digitoxin- and digoxin-glucuronide in human isolated ventricular heart muscle preparations.

The effect on force of contraction of human isolated ventricular heart muscle preparations was studied with the 16'-glucuronides of digitoxin (dt-gluc) and digoxin (dg-gluc). The parent compounds digitoxin (dt) and digoxin (dg) were studied for comparison and all compounds were also investigated in guinea-pig isolated papillary muscles. All compounds increased myocardial force of contraction in human preparations in a concentration-dependent manner. The positive inotropic effect of dt-gluc and dg-gluc began at 0.1 mumol 1(-1) and was maximal at 1 mumol 1(-1). The metabolites were slightly less potent but, on the other hand, slightly more effective than the parent compounds dt and dg. The positive inotropic effects of all compounds peaked after about 60 minutes. In contrast, the decline of the positive inotropic effect upon washing was about twice as fast in the case of the hydrophilic metabolites. Similar results were obtained in guinea-pig papillary muscles. It is concluded that the glucuronides of digitoxin and digoxin are biologically active in the human heart. This may be of clinical importance with respect to the positive inotropic action and the plasma level determination of the cardiac glycosides.

Animals↗
PubMed1984

Effects of (-)-phenylephrine on force of contraction in the presence of cocaine and hydrocortisone in cat papillary muscle.

The positive inotropic effect of (-)-phenylephrine, in the presence of propranolol, was studied after inhibition of neuronal and extraneuronal uptake in isolated papillary muscles from reserpine-pretreated cats. An inhibition of extraneuronal uptake with hydrocortisone influenced the effect of (-)-phenylephrine neither when present alone nor in the presence of cocaine (additional inhibition of neuronal uptake). An inhibition of neuronal uptake with cocaine caused a small but significant increase in the potency of (-)-phenylephrine. We conclude that in cat ventricular cardiac muscle the extraneuronal compartment is apparently neither a "site of loss" nor a "site of gain" for (-)-phenylephrine with respect to force of contraction.

Animals↗
PubMed1984

Adenosine and adenosine analogs inhibit phosphodiesterase activity in the heart.

Adenosine and its analogs (-)-N6-phenylisopropyladenosine and 5'-N-ethylcarboxamideadenosine inhibit cAMP and cGMP phosphodiesterase activity in guinea-pig atrial and ventricular preparations at concentrations of 100 mumol l-1 and higher. These effects are probably unrelated to the inotropic effects of these substances. However, inhibition of cAMP breakdown may compensate for the adenosine-induced inhibition of adenylate cyclase and may thus at least partially explain why with this drug no changes in cAMP or cGMP content have previously been observed in intact cardiac tissue.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1984

Adenosine inhibition of catecholamine-induced increase in force of contraction in guinea-pig atrial and ventricular heart preparations. Evidence against a cyclic AMP- and cyclic GMP-dependent effect.

The antagonism between adenosine and isoprenaline on force of contraction, cyclic AMP (cAMP) and cyclic GMP (cGMP) content, adenylate cyclase activity and transmembrane action potential in isolated electrically driven atrial and ventricular muscle preparations from guinea-pig hearts was investigated. In atrial preparations adenosine added 5 min after isoprenaline decreased force of contraction. Adenosine abolished completely the positive inotropic effect of isoprenaline. Similarly, adenosine prevented the positive inotropic effect of isoprenaline when both substances were added simultaneously. In ventricular preparations adenosine also decreased the isoprenaline-induced increase in force of contraction. The effect was much smaller than it was in the atria. Adenosine reduced the isoprenaline-induced increase in force of contraction only by about 60%. Adenosine did not at all influence the positive inotropic effect of isoprenaline when both substances were added simultaneously. In both preparations the isoprenaline-induced increase in cAMP content of the intact contracting preparations was not diminished by adenosine. cGMP content remained unchanged too. Adenosine inhibited adenylate cyclase activity in broken cell preparations from both tissues. In atrial preparations the decrease in force of contraction of adenosine in the presence of isoprenaline was accompanied by a shortening of the action potential duration. In ventricular preparations adenosine failed to shorten the action potential. In conclusion, the effects of adenosine to inhibit the stimulatory action of isoprenaline on myocardial force of contraction are not due to changes in the cAMP and/or cGMP content. Instead, adenosine may inhibit a step beyond an increased cAMP level, e.g., may exert an inhibition of protein kinases. However, in the atria, but not in the ventricles, an additional direct effect of adenosine on transmembrane ion currents, most likely an increase in potassium conductance, probably is of even greater importance.

Adenosine↗
PubMed1983

[Inverted urothelial papilloma].

A case of an inverted urothelial papilloma is presented and the cases published so far are summarized. As it easily can be mixed up with a transitional cell carcinoma, the cystoscopic appearance and the histology are of special importance. To know the microscopic pattern and the clinical parameter is mandatory for urologist and pathologist, since the prognosis of the inverted urothelial papilloma following endoscopic resection seems to be very good. In case of obstructive symptoms, as seen in prostatic hypertrophy, an inverted papilloma should be considered.

Female↗
PubMed1982

Effect of vanadium in the +5, +4 and +3 oxidation states on cardiac force of contraction, adenylate cyclase and (Na+ + K+)-ATPase activity.

The influence of vanadium in the nominally +5 (NH4VO3; referred to as V5+), +4 (C10H14O5V and VOSO4; V4+) and +3 oxidation states (VCl3; V3+) on cardiac force of contraction, adenylate cyclase and (Na+ + K+)-ATPase activity was investigated in order to determine which form of vanadium mediates the cardiac effects. V5+, V4+ and V3+ (300 microM each) increased the force of contraction of isolated electrically driven cat papillary muscles by about 100%. In the presence of the reducing agent ascorbic acid (5 mM) none of the three compounds led to any distinct increase in force of contraction. On the particulate adenylate cyclase preparation from feline right ventricles only V5+ stimulated the enzyme activity by about 100%, whereas V4+ and V3+ were ineffective. In the presence of 5 mM ascorbic acid all three compounds were ineffective. In contrast, in the presence of the oxidizing agent diamide (azodicarboxylic acid-bis-dimethylamide; 1 mM) all three compounds became stimulatory. On the isolated (Na+ + K+)-ATPase V5+ (500 microM) alone reduced the basal activity by about 95%. In the presence of ascorbic acid the inhibitory effect of V5+ was greatly diminished. Similar results were obtained with V4+, V3+ (100 microM) alone inhibited (Na+ + K+)-ATPase activity only by about 40%. In the presence of ascorbic acid V3+ was ineffective. From the results it is concluded that positive inotropism, stimulation of adenylate cyclase and inhibition of (Na+ + K+)-ATPase by vanadium compounds likewise result from an action of vanadium in the +5 oxidation state.

Adenylyl Cyclases↗
PubMed1982

Stimulatory (insulin-mimetic) and inhibitory (ouabain-like) action of vanadate on potassium uptake and cellular sodium and potassium in heart cells in culture.

(1) The influence of vanadate (Na3VO4) on sodium and potassium uptake as well as on cellular ion contents of sodium and potassium has been studied in heart muscle and non-muscle cells obtained from various species. An ouabain-like inhibition of potassium uptake (up to 50%), combined with a decrease of cellular potassium (up to 20%) has been observed by vanadate (10(-4)-10(-3) M) in heart non-muscle cells obtained from neonatal guinea pigs and chick embryos. In heart muscle and non-muscle cells prepared from neonatal rats, as well as in Girardi human heart cells, a vanadate-induced stimulation of potassium uptake (up to 100%), combined with a rise in cellular potassium (up to 20%) and without significant alteration of cellular sodium, has been found. A slight increase of 22Na+ influx can be measured in rat heart muscle cells and in Girardi human heart cells in the presence of vanadate (10(-4)--10(-3) M). (2) In beating rat heart muscle cells in culture, detrimental effects of serum deprivation--concerning beating properties, potassium uptake and cellular potassium--can at least in part be overcome by addition of vanadate. Furthermore, this compound prevents ouabain-induced signs of toxicity (contractures) in these cells. (3) The stimulatory effects of vanadate on potassium can be mimicked by insulin (1-10 mU/ml). Furthermore, vanadate produces an insulin-like stimulation of 2-deoxy-D-glucose uptake in rat heart muscle and non-muscle cells as well as in Girardi human heart cells. (4) The experimental data demonstrate an ouabain-like inhibition as well as an insulin-mimetic stimulation of potassium-uptake in various heart cells. The reason for this antagonistic mode of action may be due to the different capabilities of the heart cell types to reduce vanadium in the V-valence state of vanadium in the IV-valence state, thereby favouring either ouabain-like inhibition (vanadium V) or insulin-mimetic stimulation (vanadium IV) of potassium transport.

Animals↗
PubMed1982

The effect of aortic valve replacement on survival.

We retrospectively studied 252 operated and 47 unoperated patients with isolated aortic valve disease. Aortic valve replacement (AVR) was recommended to all patients based on clinical and hemodynamic data. Preoperative hemodynamic and angiographic data were similar in operated and unoperated cohorts. Seventy-one percent of patients received a Björk-Shiley prosthesis. Operative mortality was 7% for the entire surgical series. For patients with predominant aortic stenosis (AS), survival at 3 years was 87% in operated and 21% in unoperated patients (p less than 0.001). For patients with predominant aortic insufficiency (AI), the 5-year survival rate was 86% in operated and 87% in unoperated patients (NS). AVR improved long-term survival in patients with AS who had normal or impaired left ventricular (LV) function. In patients with AI and normal LV function, survival was not improved after AVR, but those with LV dysfunction who were operated on tended to survive longer (NS). Long-term survival of unoperated patients with AI was better than that in unoperated patients with AS. We conclude that AVR improves long-term survival in patients with AS who were normal or abnormal LV function, and that AVR does not change long-term survival in patients with AI, although those with LV dysfunction tended to survive longer.

Adult↗