Chronotrope Wirkung von Calcium und Magnesium am isolierten Hundeherzen

Schmidt, H. D.; Schmier, J; Schmitz, Stephan

doi:10.1007/bf00363240

Cited by 15 publications

(4 citation statements)

References 9 publications

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“…On the other hand, Seifen et al (1964a) reported that the effect of calcium on heart rate was not altered by prior administration of atropine, nor was it modified in the depletion of cardiac catecholamines by the treatment with reserpine . Schmidt et al (1965) obtained a similar result by pretreatment with reserpine . Seifen et al (1964b) examined effect of calcium on the SA node pacemaker fibers of the rabbit with the intracellular microelectrode technique and concluded as follows: An increase in calcium concentration of the bathing medium increased the rate of slow diastolic depolarization.…”

Section: Discussionmentioning

confidence: 55%

“…It has been known that magnesium slows the heart rate in the dog heart (Stanbury and Farah 1950;Schmidt et al 1965) and in the isolated guinea-pig atria (Schaer 1968). The negative chronotropic effect of magnesium was proportional to the increase in its concentration (Schaer 1968) and was not mediated by choliner gic transmitter (Schmidt et al 1965;Schaer 1968). Hoffman and Suckling (1956) reported that the change in the concentration of magnesium had little effect on the transmembrane potential of the Purkinje fibers of the dog heart when the calcium concentration was normal.…”

Section: Discussionmentioning

confidence: 99%

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Influence of Calcium and Magnesium Ions on the Sino-atrial Node Pacemaker Activity of the Canine Heart

Hashimoto

Suzuki

Chiba

1974

Tohoku J. Exp. Med.

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Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Influence of Calcium and Magnesium Ions on the Sino-atrial Node Pacemaker Activity of the Canine Heart

Hashimoto

Suzuki

Chiba

1974

Tohoku J. Exp. Med.

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“…Tetrodotoxin, which blocks fast Na channels (20), suppresses Purkinje fibers (15,21) but not sinus node cells (15,22,23). High Ca decreases the rate of spontaneous discharge of Purkinje fibers (24) but increases that of the sinus node (19,(25)(26)(27)(28)(29), even after abolition of autonomic influences (25,28,29). Although the slowing in Purkinje fibers is due to a shift in threshold (24), the acceleration in the sinus node is due to a steepening of diastolic depolarization (25,27).…”

Section: Discussionmentioning

confidence: 99%

Role of the Sympathetic Nervous System in the Sinus Node Resistance to High Potassium

Vassalle

Greineder

Stuckey

1973

Circulation Research

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The resistance of sinus node automaticity to high potassium (K) levels was studied in anesthetized dogs by perfusing the sinus node artery with oxygenated Tyrode's solution containing different K concentrations. The following results were obtained.(1) Sinus node automaticity persisted at a K concentration of 21.6 DIM, although the pacemaker site tended to shift in and out of the node at this concentration. (2) Sinus node dominance at high K concentrations was progressively lost as sympathetic influences were progressively eliminated. (3) Sinus node pacemaker activity was suppressed at a K concentration lower than 21.6 mM when calcium was omitted from the perfusion fluid. (4) The pacemaker site shifted consistently from the sinus node towards the atrioventricular node at high K concentrations after the elimination of sympathetic activity (5) The transient sinus tachycardia caused by high K concentrations persisted after bilateral vagotomy. It is concluded that catecholamines participate in the resistance of the sinus node to K, suggesting that the difference in resistance to high K concentrations between the sinus node and Purkinje fibers may, in part, result from the more abundant innervation of the sinus node. KEY WORDScatecholamines reserpine sympathectomy propranolol calcium dog• Ventricular Purkinje fibers perfused in vitro usually become quiescent when the potassium (K) content of Tyrode's solution is increased from 2.7 mM to 5.4 mM (1). In contrast, the sinus node continues to discharge spontaneously when K is increased to a concentration at which atrial fibers become inexcitable (2-6). The reason for the resistance of sinus node pacemaker activity to high K concentrations is not understood. It seems likely that this resistance to K reflects membrane characteristics peculiar to sinus node cells, but other factors cannot be excluded. One of these factors could be sympathetic innervation, since it has been shown that catecholamines counteract the depressant effect of K on cardiac excitability (4, 7). It does not seem unreasonable, therefore, to propose that catecholamines also counteract the depressant effect of K on automaticity. Sympathetic innervation of ventricular Purkinje fibers is sparse and that of the sinus node abundant (8) This work was supported in part by grants from the U. S. Public Health Service and the New York Heart Association. The work was carried out while Dr. Vassalle was the recipient of a Sinsheimer Award.A preliminary report has appeared in abstract form (Am J Cardiol 26:636, 1970).Received September 22, 1972. Accepted for publication January 11, 1973. reinforces the possibility that catecholamines play an important role in the difference in sensitivity between atrial and ventricular pacemakers to K.The aim of the present investigation was to study the effect of the sympathetic nervous system on the sinus node resistance to high K concentrations by perfusing the sinus node artery with a solution in which K content was varied. Autonomic denervation, catecholamine depletion...

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“…There is some evidence reported that hypermagnesemia could contribute to the depressed ventricular function that we observed, and even possibly to some of the electrocardiographic changes. Infusion of magnesium salts in intact dogs or isolated dog hearts is accompanied by tachycardia and decreased force of ventricular contraction [M axwell et al, 1965;Schmidt et «/., 1965;U chiyama, 1968] without changes in coronary flow. Ventricular action potentials in the dog are shortened and ST segment of the ECG is elevated [Uchiyama, 1968] [Regan et al, 1969], However, we observed increases in arterial as well as venous plasma [K+], but no consistent loss of myocardial K ' (table II).…”

Section: Discussionmentioning

confidence: 99%

Effects of DC Electric Countershock on Ventricular Function, Cation Balance and Endogenous Norepinephrine in the Dog Heart

et al. 1974

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Effects of DC electric countershock on cardiac function in thoracotomized dogs were evaluated from recordings of ECG, aortic pressure, left ventricular pressure and its first derivative, and coronary sinus flow. Samples of arterial and coronary venous plasma and left ventricular myocardium obtained before and after countershock at times corresponding to post-shock arrhythmias and recovery were analyzed for Mg⁺⁺, K⁺ and Ca⁺⁺, and norepinephrine. At 1 min after countershock, ECG changes included transient cardiac arrhythmias and ST segment alterations, accompanied by depressed ventricular function and decreased myocardial Ca⁺⁺ concentration. At 5 min post-shock, coronary venous Mg⁺⁺ and K⁺ concentrations had risen and ventricular function was still depressed. Function recovered within 10–20 min. There was no evidence of consistent loss of endogenous myocardial norepinephrine

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Chronotrope Wirkung von Calcium und Magnesium am isolierten Hundeherzen

Cited by 15 publications

References 9 publications

Influence of Calcium and Magnesium Ions on the Sino-atrial Node Pacemaker Activity of the Canine Heart

Influence of Calcium and Magnesium Ions on the Sino-atrial Node Pacemaker Activity of the Canine Heart

Role of the Sympathetic Nervous System in the Sinus Node Resistance to High Potassium

Effects of DC Electric Countershock on Ventricular Function, Cation Balance and Endogenous Norepinephrine in the Dog Heart

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