Hemodynamic and metabolic effects of three times 4 min of oxygen deficiency were investigated in 18-month-old rats in comparison to 4-month-old Wistar rats. Left-ventricular isovolumic-pressure-generating capacity and dp/dtmax during isovolumic conditions and hemodynamic indices during intact circulation were determined in open-chest rats. Additionally, high-energy phosphates were measured at the end of the experiments after 20 min of postasphyxial recovery. Older rats had a significantly reduced isovolumic left-ventricular pressure generating capacity (236 +/- 9 vs 269 +/- 5 mm Hg; p less than 0.05) and a low cardiac index (55 +/- 9 vs 117 +/- 8 ml x min-1 x kg-1). The effects of the oxygen deficiency were comparable in both groups. The isovolumic pressure generating capacity was reduced for 11% vs 14%, and dp/dtmax for 13% vs 13%. The myocardial ATP-content was also decreased for the same extent in both groups (0.6 vs 1.0 mumol/gww). Both hemodynamic and biochemical results indicate that aged myocardium does not have a reduced tolerance to repeated periods of oxygen deficiency.

Adenine Nucleotides↗

PubMedDate not supplied

The role of autonomic nervous system in the action of verapamil on the sinus node in man.

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Adult↗

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High-energy phosphates, myocardial contractile function and material properties after short periods of oxygen deficiency.

To investigate myocardial performance and diastolic properties after repeated periods of oxygen deficiency auxotonic and isovolumic measurements were performed after three periods (4 min) of asphyxia in Wistar rats (n = 19). Additionally, the response of the peak isovolumic left ventricular pressure to postextrasystolic potentiation was measured. The hemodynamic results were compared to the levels of high-energy phosphates. Already after 15 min of recovery from asphyxia auxotonic measures of systolic function were completely normal compared to the control group (n = 19). Isovolumic measurements after 20 min of postasphyctic recovery, however, demonstrated a considerable reduction of the peak left ventricular pressure (226.5 +/- 7.5 mm Hg vs. 262.6 +/- 3.4 mm Hg in controls, mean +/- SEM (p less than 0.01) indicating persistence of decreased postischemic contractile performance. The relative effect of postextrasystolic potentiation was similar in both groups, but could not compensate for the reduced performance of the postasphyctic hearts: the absolute postextrasystolic peak isovolumic pressure of the postasphyctic hearts was lower than the value of the regular isovolumic peak pressure in the controls. Diastolic properties (pressure/volume and stress/strain relationships) of the postasphyctic myocardium remained unchanged. The total sum of the adenine-nucleotides decreased from 7.2 +/- 0.2 to 5.6 +/- 0.3 mumol/gww (p less than 0.01). ATP was reduced from 4.8 +/- 0.2 to 3.9 +/- 0.3 mumol/gww (p less than 0.01). Phosphocreatine was elevated to 7.0 +/- 0.6 mumol/gww, x +/- SEM (p less than 0.01). Our results demonstrated normal postasphyctic basal hemodynamics and material properties. Thus, the energy supply was sufficient to maintain steady state conditions - in spite of decreased overall adenine-nucleotide levels. Isovolumic measurements and postextrasystolic potentation tests, however, indicated that the contractile performance of the postischemic myocardium was still reduced. This functional limitation cannot be explained by altered material properties and is probably not causally related to the decreased overall ATP content.

Adenine Nucleotides↗

PubMedDate not supplied

Influence of drugs on the relationship between sinus node recovery time and calculated sinoatrial conduction time in man.

Sinus node recovery time (SRT), the pacing rate with the maximal SRT, and calculated sinoatrial conduction time (SACT) were studied by overdrive atrial pacing and programmed premature atrial stimulation in 78 patients before and after the application of several antiarrhythmic drugs or of atropine. The maximum SRT was usually observed at lower rates of atrial pacing after application of a drug that prolonged SACT, whereas the opposite behaviour was observed in the majority of cases in whom the drug tested shortened calculated SACT. However, this relationship was not observed in all cases which may be due to random changes of sinus node automaticity or sinoatrial conduction, or to the inability of programmed premature atrial stimulation to detect changes of SACT. The results of this study further substantiate the importance of the properties of sinoat;ial conduction for achieving a maximal depression sinus node activity during high rate atrial pacing.

Anti-Arrhythmia Agents↗

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

Comparison of the antiarrhythmic efficacy of disopyramide and mexiletine against stimulus-induced ventricular tachycardia.

Programmed ventricular stimulation was used to assess the effect of oral disopyramide (600 mg/day), mexiletine (600--1000 mg/day), and a combination of both drugs in a randomized cross-over study on 12 patients with documented ventricular tachycardia and/or fibrillation. In two cases, all three types of treatment were ineffective in that ventricular tachycardia could still be initiated under the same conditions. In four cases, disopyramide and mexiletine alone were ineffective or the change in inducibility was only slight. However, when both drugs were administered in combination, ventricular tachycardia was more difficult to induce or was no longer inducible. In two other cases, disopyramide was the more effective drug. In the remaining four patients, all three types of treatment were similarly effective. In patients whose ventricular tachycardia remained inducible its rate decreased from 188 +/- 45 bpm (control) to 170 +/- 40 bpm on disopyramide, 172 +/- 31 bpm on mexiletine, and 146 +/- 39 bpm on disopyramide plus mexiletine. Long-term therapy was based on the results of acute testing. Seven patients received both disopyramide and mexiletine and tolerated this therapy well during a follow-up of 42 +/- 23 weeks. Two sudden deaths occurred, one possibly due to dose reduction and one in a patient in whom short bursts of ventricular tachycardia remained inducible during acute testing. We conclude that the combined administration of disopyramide and mexiletine is effective and safe in patients with ventricular tachycardia. It is tolerated without major side effects even during long-term therapy.

Adult↗