Biomedical subjects

J G Ochs

Publications and source records attributed to J G Ochs.

5 recordsLinked to original sources

PubMed1995

[Chronic frequency-adaptive pacemaker therapy in patients with heart failure].

Twenty patients (complete AV block n = 13, sick sinus syndrome n = 4 (replacement of a VVI system), bradyarrhythmia n = 3) with rate-adaptive pacemakers (respiration volume guided n = 10, QT-driven n = 1, dual sensor (QT/activity) system n = 9) were randomly assessed by ergospirometry after 4 weeks of VVI- (70 bpm), VVIR1-(70-110 bpm, low upper rate) and VVIR2-pacing (70-130 bpm, high upper rate). Oxygen uptake (VO2), work load (W), and heart rate were determined at peak exercise (max) and at the anaerobic threshold (AT). In the whole population, rate adaptation led to a significantly higher VO2-max than VVI-pacing for both VVIR1- (15.5 +/- 5.1/12.6 +/- 4.1 ml/kg/min, 28 +/- 37%, p < 0.01) and VVIR2-pacing (14.8 +/- 4.4/12.6 +/- 4.1 ml/kg/min, 20 +/- 23%, p < 0.01). At the AT, however, VO2 was significantly improved only by the VVIR1 mode (low upper rate, 9.8 +/- 2.5/8.0 +/- 2.1 ml/kg/min, 28 +/- 36%, p < 0.01). Regarding only patients with moderately limited exercise capacities (Weber class C, n = 11), rate adaptive VVIR1 and VVIR2 pacing could not produce a significant increase of VO2-max and VO2-AT. In contrast, patients with severely reduced exercise capacities (Weber class D, n = 9) significantly profited from the rate adaptation, but only in the VVIR1 mode (VO2-max 48 +/- 45%, VO2-AT 51 +/- 38%, p < 0.01). Thus, in the whole population an increase of oxygen uptake and of exercise workload at the anaerobic threshold could only be achieved by pacing with the low upper rate of 110 bpm. By this, particularly patients with heart failure and a severely limited exercise tolerance (Weber D) had a significant benefit. Therefore, the upper rate should be programmed in a lower range in patients with heart failure, at least for rate-adaptive ventricular pacemaker systems.

Aged↗

PubMed1995

Carmoxirole inhibits platelet aggregation in vitro and ex vivo.

The influence of carmoxirole, a new antihypertensive DA2-agonist on human platelet aggregation was studied in vitro and ex vivo. In an open study 15 patients with essential hypertension received 3 doses of carmoxirole, 0.5, 1 and 2 mg daily, each for a 2-week period, following a 2-week placebo phase. At the end of each 2-week period blood pressure, platelet aggregation, plasma carmoxirole and plasma catecholamines were measured. Preliminary experiments in vitro showed that 10 microM carmoxirole inhibited the adrenaline induced aggregation velocity by 10%: Increasing the carmoxirole concentration caused dose dependent inhibition which was complete at 1 mM. Carmoxirole itself caused a weak aggregating effect on human platelets in vitro. Blood pressure was reduced from 163 +/- 11/103 +/- 3 before treatment to 155 +/- 11/97 +/- 4, 148 +/- 11/93 +/- 4 and 143 +/- 11/90 +/- 6 mmHg following 2 weeks of 0.5, 1 and 2 mg oral carmoxirole, respectively. Carmoxirole plasma levels 2 1/2 h after the last capsule administration were 0.37 +/- 0.612, 0.95 +/- 1.045 and 3.69 +/- 2.570 ng/ml following treatment with 0.5, 1 and 2 mg carmoxirole, respectively. No influence of carmoxirole on plasma catecholamines could be established. Compared to 100% before treatment, the 5-hydroxytryptamine induced platelet aggregation velocity ex vivo decreased to 70%, 38% and 69% after the administration of 0.5, 1 and 2 mg carmoxirole, respectively. The adrenaline induced aggregation velocity was reduced in the same manner. These results show that carmoxirole is an antihypertensive agent with antithrombotic potential.

Blood Pressure↗

PubMed1994

[Increasing physical endurance with salmeterol].

10 patients with mild to moderate chronic obstructive pulmonary disease were assessed by lung function tests at rest and spiroergometry before and 1 resp. 7 hours after inhalation of 50 micrograms salmeterol. The parameters changed as follows: Forced exspiratory volume in 1 second: +16% +/- 6% after 1 resp. +13% +/- 5% after 7 hours; airway resistance: -43% +/- 11% resp. -43 +/- 9%. Work capacity at the anaerobic threshold (AT): +44% +/- 17% resp. +37% +/- 16%, oxygen consumption at the AT (VO2AT): +53% +/- 18% resp. +54 +/- 23%, ventilation at the AT (VEAT): +31% +/- 11% resp. 30% +/- 7%. Maximum work capacity: +14 +/- 5% resp. +22 +/- 7%, maximum oxygen consumption (VO2max) +58 +/- 24% resp. 64 +/- 22%, maximum ventilation (VEmax) +33 +/- 10% resp. + 46 +/- 11%. In conclusion, salmeterol leads to a long lasting improvement of exercise capacity. This is related to the improvement of the ventilation caused by salmeterol. Significant changes of heart rate or blood pressure were not observed.

Administration, Inhalation↗

PubMed1992

[Physical exercise tolerance in chronic obstructive emphysematous bronchitis and coronary heart disease under antiobstructive therapy].

19 consecutive patients (18 men, one woman, mean age 61.4 [49-73]years) with chronic obstructive airways disease (bronchitis and emphysema) together with angiographically confirmed coronary heart disease were studied to investigate their cardiopulmonary exercise tolerance and the effects of bronchodilators on their myocardial ischaemia. Because they were receiving drug therapy for angina or because they had previously undergone aortocoronary bypass operation or balloon dilatation, the patients were symptom-free. In three cases slight ischaemia was demonstrable during maximal exertion. Aerobic and anaerobic exercise capacity was determined by spiroergometry after inhalation of salbutamol (S, 0.2 mg) alone or in combination with oxitropium bromide (O, 0.2 mg). The supplementary effect of oral theophylline (T, 15 mg/kg.day) was studied in 13 patients. In terms of maximal aerobic exercise tolerance the following improvements were noted: energy output (watts): S: + 6.3%; S and O: + 12.3% (P < 0.05); S, O and T: + 14.0% (P < 0.01). Oxygen uptake (ml/min): S: + 8.2% (P < 0.05); S and O: + 18.2% (P < 0.01); S, O and T: + 35.4% (P < 0.01). Maximum exercise capacity was not significantly improved, although maximum oxygen uptake was significantly increased by the two-drug combination by 16.9% (P < 0.05) and by the three-drug combination by 19.2% (P < 0.05). Maximum minute volume and tidal volume rose significantly, though respiratory rate was unchanged. Heart rate and blood pressure remained practically unaffected by the treatment, both at rest and during exertion. There was no evidence of significant aggravation of ventricular arrhythmias or of ischaemia during ergometric testing.

Albuterol↗

PubMed1990

Effects of urapidil on 5-hydroxytryptamine induced platelet aggregation and on 14C-5-hydroxytryptamine uptake in platelets.

Urapidil inhibits the 5HT induced human platelet aggregation and the 5HT uptake by platelets in vitro and ex vivo. The aggregation was inhibited with a KI-value of 8.8 microM and the 5HT uptake in a noncompetitive way with KI1 = 15.3 microM and K12 = 10.6 microM. In vivo, the 5HT induced platelet aggregation was increased 4 h after oral administration of 60 mg urapidil. Subsequently, the aggregation decreased and reached a minimum at various times in the different volunteers. Eight h after oral administration of 60 mg urapidil, the 5HT uptake velocity was reduced approximately 40%.

Administration, Oral↗