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Biomedical subjects

W Meesmann

Publications and source records attributed to W Meesmann.

At least 19 recordsLinked to original sources
PubMed1988

Prophylactic lidocaine: concentrations in plasma and myocardial tissue and antifibrillatoric efficacy during early ischemia in dogs and pigs.

We investigated the antifibrillatoric efficacy of lidocaine and the time courses of lidocaine concentrations in plasma and nonischemic (NIM) and ischemic myocardium (IM) during early myocardial ischemia in anesthetized dogs and pigs. Lidocaine (2 or 3 mg/kg bolus + 50, 100, 150, or 500 micrograms/kg.min) was administered over 30 min to 29 dogs and 15 pigs. The left anterior descending coronary artery (LAD) was occluded 2 min after bolus application. Blood and myocardial biopsies were sampled for analysis by high-performance liquid chromatography (HPLC) up to 40 min. In 19 dogs and 6 pigs, we determined the ventricular fibrillation threshold (VFT) with and without lidocaine during acute LAD occlusion for 7-13 min. Dosages leading to therapeutic plasma levels (1.6-4.2 micrograms/ml) resulted in lidocaine concentrations always highest in the IM (IM greater than NIM greater than plasma). Under identical dosages, all lidocaine levels were higher in pigs than in dogs. The IM concentrations decreased less in the pigs. Lidocaine prevented the ischemic drop in VFT and spontaneous fibrillation only at persistent IM concentrations greater than 8 micrograms/g. With therapeutic dosages, this was achieved only in pigs, occluding the LAD as early as 2 or 10 min after bolus application. Lidocaine prophylaxis with clinically recommended dosages in humans will hardly result in myocardial concentrations sufficiently high to be antifibrillatorically effective during early acute ischemia.

Animals↗
PubMed1985

Antiarrhythmic effect of regional myocardial chemical sympathectomy in the early phase of coronary artery occlusion in dogs.

To investigate the importance of local noradrenaline (NA) release in initiating early ventricular extrasystoles (VES) and primary ventricular fibrillation (VF) after acute myocardial ischemia, a special form of regional myocardial chemical sympathectomy (RMCS) has been performed in dogs. After RMCS the tissue content of NA within the denervated region was reduced below 1.5% of normal, whereas the residual myocardium retained its functional state almost unchanged. After acute left circumflex coronary artery (LCX) occlusion (30 min), all control animals with normal circumflex circulation and without functionally effective collaterals died of VF. In contrast, after RMCS none of the dogs had VF and very few had VES. After RMCS the rise in myocardial extracellular K+ activity ([K+]e) during coronary occlusion is slightly slower, but the same [K+]e are reached at 8 min of occlusion. Therefore, the effect of RMCS cannot be explained by changes in myocardial K+ liberation. These results, obtained from RMCS experiments, are supported by the preliminary results of experiments using a special perfusion technique to wash out blood from the acutely occluded myocardial region, and show an ischemia-induced raise of the locally released NA in the early arrhythmic phase 1a with a further increase in phase 1b.

Animals↗
PubMed1979

Construction and function of a new hydraulic cuff occluder.

The construction of a new type of vascular cuff occluder for use in conscious animals is described. This occluder has the following features: 1. Safe complete vessel occlusion. 2. Occlusion at a definite cuff pressure with extrathoracally pressure control behind the cuff. 3. Long term implantability. 4. Possibility of multiple usage and sterilization.

Animals↗
PubMed1979

Prophylaxis of ventricular fibrillation after acute experimental coronary occlusion by chronic beta-adrenoceptor blockade with atenolol.

Acute occlusions of the left circumflex coronary artery were performed in open-chest dogs. A control group (n = 19) was compared with three groups (total n = 17) pretreated once daily with different doses of the cardioselective beta-blocking drug atenolol (ICI 66 082) given by mouth for 5 days. Only animals without coronary collateral vessels were examined, having a mortality rate of 100% in the control group. Arrhythmias and ventricular fibrillation during the first 30 min after coronary occlusion showed a biphasic distribution in time (phase 1a and 1b). A lower degree of beta-adrenoceptor blockade reduced the incidence of arrhythmias and ventricular fibrillation in phase 1a, but fibrillation occurred in all animals during phase 1b. A higher dose of the beta-blocking drug protected the animals from ventricular fibrillation, and arrhythmias in phase 1a were greatly reduced. At all times the ventricular fibrillation threshold in the group pretreated with atenolol was significantly higher than in the control group. In both groups a significant decrease in ventricular fibrillation threshold was found only during phase 1a. The greater sensitivity of phase 1a arrhythmias to beta-blockade and the lack of a decrease in ventricular fibrillation threshold during phase 1b might indicate differences in the genesis of arrhythmias and fibrillation in phases 1a and 1b.

Animals↗
PubMed1979

Extracellular potassium activity changes in the canine myocardium after acute coronary occlusion and the influence of beta-blockade.

Extracellular potassium activity before and after coronary occlusion was measured in the canine heart by means of potassium-selective surface electrodes. In the ischaemic myocardium potassium activity rapidly increased from a preocclusion value of 3.2 +/- 0.3 mmol.litre-1 to 10 +/- 0.6 mmol.litre-1 within the first 5 min and to about 11.3 +/- 0.5 mmol.litre-1 after 10 min of ischaemia (range from 9.5 to 14.5 mmol.litre-1). Following the initial 10 min of ischaemia no further increase was measured. In the non-ischaemic area potassium activity remained constant. Acute beta-blockade significantly attenuated the initial rate of increase in potassium activity; however, beta-blockade did not influence maximal values of extracellular potassium activity measured after occlusion. Lowering of heart rate by vagal stimulation did not modify the pattern of increase in potassium during acute ischaemia. Following ventricular fibrillation, a slow but continuous rise in potassium activity was found. These results demonstrate that extracellular potassium activity in the acutely ischaemic myocardium is considerably higher than indicated by the technique of coronary vein sampling and is in the range necessary for the development of re-entrant arrhythmias in the early phase after coronary occlusion.

Animals↗
PubMed1976

Time course of changes in ventricular fibrillation threshold in myocardial infarction: characteristics of acute and slow occlusion with respect to the collateral vessels of the heart.

The time course of the changes in ventricular fibrillation threshold (VFT) was determined in 28 dogs by means of electrical stimulation, triggered from the R wave, with DC square wave pulse series (of 140 ms duration) inserted into the vulnerable period of the cardiac cycle. After acute coronary occlusion there was a sudden decrease in the VFT followed by a slow increase such that 30 min after the ligation pre-occlusion values of VFT were reached. The magnitude of the decrease in VFT depended upon the collateral blood supply. There were no other changes in VFT during the remaining course of the experiment. Following slow coronary occlusion the first arrhythmic phase was not detectable. Any decreases in VFT that occurred were smaller and of shorter duration than those occurring after acute occlusion and were independent of the extent of the collateral blood supply.

Angiocardiography↗
PubMed1976

[Acute myocardial infarct and pindolol. Effect of a beta sympatholytic with intrinsic sympathomimetic activity on hemodynamics and contractility].

After acute circumscribed myocardial infarction the effects of the beta-sympatholytic agent 1-(indol-4-yl-oxy)-3-isopropyl-amino-propan-2-ol (pindolol; Visken) on hemodynamics and contractility were examined. Hemodynamic changes after application of pindolol are of small extent only. Heart rate shows a rising tendency whereas systolic and diastolic aortic pressure decreases only after higher doses. Left ventricular end-diastolic pressure (LVEDP) does not change remarkably. Cardiac output is reduced by small doses of pindolol and reaches starting values again before the administration of higher doses. Changes of the contractility parameters (dp/dt)max, t-(dp/dtmax, and PEP in the sense of a beta-sympatholysis appear only in the lower range of the doses given. Thus maximum decrease of contractility is 20% measured at (dp/dt)max, which consequently reaches the starting value again. The other contractility parameters change accordingly. These typical dose-response relations between pindolol and contractility parameters are considered to be due to lacking cardiac depressive properties combined with significant so-called positive intrinsic activity. Our results show that no contraindication can be derived from the small influence of pindolol on contractility in acute myocardial infarction.

Animals↗
PubMed1976

[Contractility, pressure and volume reserve of pressure-hypertrophied hearts in situ].

In 18 adult mongrel dogs (24.6 kg) a statistically significant left ventricular hypertrophy (LVH) was induced by chronic aortic coarctation (180 days). In 12 anesthetized dogs (LVH 1) the effect of increasing doses of catecholamines on maximum contractility, expressed by (dp/dt)max, Vpm, t-(dp/dt)max was determined in comparison to a control group (KO 1; N = 6). There was no depression of the acute maximum contractility of hypertrophied hearts compared with the controls, also in respect to other haemodynamic parameters (SV/10 kg, HR, LVEP). In 6 other LVH-dogs (LVH 2) the maximum reached left ventricular pressure - obtained by complete clamping of the ascending aorta - was significantly higher. Either pressure per 100 g left ventricle did not differ significantly.

Animals↗