Biomedical subjects

J Morlans

Publications and source records attributed to J Morlans.

4 recordsLinked to original sources

PubMed1989

Effects of manganese chloride, verapamil, and hypoxia on the rate-dependent increase in internal longitudinal resistance of rabbit myocardium.

The effects of high rates of stimulation on the internal longitudinal restivity (Ri) and conduction velocity (theta) were studied on rabbit papillary muscle preparations using a silicon-oil chamber. Increasing the rate from 75 to 150/min caused Ri to rise and theta to decrease. The maximum rate of depolarization and action potential duration were also decreased. At a rate of 300/min the effects were more pronounced. Blockade of the slow inward current (Isi) and of the Na-Ca exchange by MnCl2 (5 mmol/L) did not prevent rate-induced changes in these variable. Verapamil (0.02 mmol/L) was also ineffective. Hypoxia (PO2 = 5.3 kPa) at 75/min induced changes in Ri and theta which were similar to those recorded at 150/min under aerobic conditions. The effects of high rates of stimulation were potentiated under hypoxia. From the present results it is suggested that Isi and the Na-Ca exchange are not the main determinants of the rate-induced increase in Ri, which could be determined by other intracellular Ca-release mechanisms or by a decrease in myoplasmic pH.

Animals↗

PubMed1979

Rate-dependent action potential changes in rat atrium.

Experiments in isolated left atria from rat hearts were performed in order to study the effects of stimulation rate on the transmembrane action potential. 1. Two components (fast and slow) of the action potential upstroke could be differentiated by adding MnCl2 to the perfusion solution. 2. With the increase in rate of stimulation over the control cycle length (500 msec), amplitude, Vmax and action potential duration at 80% of repolarization (D80) diminished in normal Krebs. In Mn-containing Krebs, only a slight reduction in amplitude was recorded. Resting potential and action potential duration at 20% (D20) and 50% (D50) of repolarization were only slightly affected in normal Krebs and not at all in Mn-Krebs. 3. Low rates of stimulation in normal Krebs increased D50 only slightly; however, D80 increased significantly while other parameters remained constant. No effects were seen in Mn-Krebs. 4. The results with Mn-Krebs indicate the importance of slow inward current on changes induced by stimulation rates. A possible mechanism relating intracellular calcium concentration and the outward K current, depending on the rate of stimulation, is discussed.

Animals↗

PubMed1978

Effects of atrial premature stimulation on sinus node function in isolated rabbit atria.

The effects of premature atrial depolarizations (PADs) on the sinus node function were studied in isolated rabbit atria by using simultaneous intracellular recordings in the sinus node and adjacent regions. Late PADs (test cycle 85% or more of the basic cycle) did not capture the sinus node, blocking somewhere between this structure and the crista terminalis, inducing however a shortening of action potential, an increased rate of rise (Vmax) and amplitude of phase 0, and a variable depression of phase 4 depolarization on sinus node fibres. These effects were attributed to electrotonic interactions. Earlier PADs (test cycle 45--85% of the basic cycle) penetrated and captured the sinus node, changing its action potential shape, depending on the prematurity of the response. Two major effects were demonstrated: 1) a reduction in the maximum diastolic potential; 2) a linearly-related (p less than 0.001) decrease of the slope of phase 4 depolarization. These effects resulted in a depression of sinus node automaticity that was inversely-related to the test cycle length. Dominant pacemaker shifts within the sinus node were frequently observed with early as well as with late PADs resulting in a change of the basic cycle by as much as 90 msec. It is concluded that the use of the technique of premature atrial stimulation may not permit precise evaluation of sinoatrial conduction time.

Action Potentials↗

PubMed1975

Genesis of arrhythmias and mechanism of electrical defibrillation of the heart.

Atrial arrhythmias were induced in experiments on dogs by electrical stimulation or by local application of aconitine and methacholine to the atrium. The action of the defibrillator discharge on these arrhythmias was studied. The defibrillator discharge abolished the arrhythmias maintained by the circus movement of the excitation wave over the atria but did not abolish sinus tachycardia or ectopic aconitine tachysystoles. The threshold of the defibrillating effect depends on the existence of micro-or macro-reentries. Thmechanism of defibrillation consists of excitation of the atrial myocardium with a consequent decrease in the pathway for the circulation of excitation to below the critical size for maintaining the circus movement of the excitation wave. The axtion of the defibrillator does not inihibit the automatism of the nomotopic and heterotopic cardiac pacemakers.

Aconitum↗