“…The electrical activity of the pacemaker cells in the preparation was recorded with a fine suction electrode (tip diameter, about 0.2 mm) or a floating glass microelectrode (WOODBURY and BRADY, 1956) and displayed on an ink writing oscillograph. Surface electrograms of the preparation were also recorded with a unipolar Ag-AgCI electrode (tip diameter, about 0.5 mm).…”
To correlate changes in pacemaker frequency with those of length and tension in mammalian atrial tissues, a strip of the sinoatrial (SA) nodal tissue (about 10 mm in length and 4 mm in width) isolated from the rabbit heart was subjected to constant-length and constantload stretches, and the relation between the resulting pacemaker frequency changes and the segmental length changes of the preparation was examined by means of cinematographic recording of the preparation with carbon markers on its surface. The amount of stretch-induced length changes was larger in the perinodal tissue segments than in the SA nodal segments, indicating that the nodal area is less extensible than the perinodal area. The time course of stretch-induced length changes of one nodal segment (closer to the inferior versa cava) was found to roughly parallel that of pacemaker frequency changes, suggesting that the pacemaker frequency is primarily dependent on the length but not on the tension of the SA nodal area.
“…The electrical activity of the pacemaker cells in the preparation was recorded with a fine suction electrode (tip diameter, about 0.2 mm) or a floating glass microelectrode (WOODBURY and BRADY, 1956) and displayed on an ink writing oscillograph. Surface electrograms of the preparation were also recorded with a unipolar Ag-AgCI electrode (tip diameter, about 0.5 mm).…”
To correlate changes in pacemaker frequency with those of length and tension in mammalian atrial tissues, a strip of the sinoatrial (SA) nodal tissue (about 10 mm in length and 4 mm in width) isolated from the rabbit heart was subjected to constant-length and constantload stretches, and the relation between the resulting pacemaker frequency changes and the segmental length changes of the preparation was examined by means of cinematographic recording of the preparation with carbon markers on its surface. The amount of stretch-induced length changes was larger in the perinodal tissue segments than in the SA nodal segments, indicating that the nodal area is less extensible than the perinodal area. The time course of stretch-induced length changes of one nodal segment (closer to the inferior versa cava) was found to roughly parallel that of pacemaker frequency changes, suggesting that the pacemaker frequency is primarily dependent on the length but not on the tension of the SA nodal area.
“…Intracellular recordings using the floating micro-electrode technique developed by Woodbury & Brady (1956) with an electrode resistance of the order of 25 MQ were made. A Bak amplifier and a Tektronix 502A oscilloscope were used to record activity.…”
SUMMARY1. A study has been made on the responses of the plaice (Pleuronectes platessa) heart, isolated and in situ to differential vagal stimulation using intra-and extracellular recording electrodes. The effects of direct application of acetylcholine and catecholamines and their respective blocking agents are also reported.2. Vagal stimulation at 7 Hz totally inhibits heart beat whilst stimulation at 2-3 Hz accelerates it. Both these effects are blocked by atropine (10-g/ml.). Bretylium (10-5 g/ml.) and pronethalol (10-6 g/ml.) have no effect upon either response to vagal stimulation.3. On cessation of prolonged inhibitory vagal stimulation there is a marked increase in the heart rate, and in quiescent hearts one or two beats are initiated after stimulation. 4. Vagal stimulation gives rise to a hyperpolarization in atrial cells. It is proposed that all the excitatory effects of vagal stimulation are due to rebound excitation from an inhibitory hyperpolarization. At high frequencies the hyperpolarizations summate to give rise to total inhibition. At lower frequencies of stimulation the heart beat is increased to rates dependent on interaction between the time course of the hyperpolarization and the refractory period of the heart. Both effects are cholinergically mediated.5. The rebound excitation in response to vagal stimulation (post-vagal tachycardia) persists in response to stimulation of the atrial myocardium in the presence of atropine (10-6 g/ml.) and bretylium (10-5 g/ml.). It is therefore suggested that this is a response of the muscle cell membrane to vagal stimulation and is not nerve-mediated.
“…The method of mounting small lengths of taenia coli has been described previously (Biilbring, 1954(Biilbring, , 1953(Biilbring, , 1957. Lengths from 4 to 6 mm were mounted isometrically in an organ bath of 3 ml., made of Perspex, through which solution flowed continuously at the rate of 2-3 ml./min, at a constant temperature of 350 C. The membrane potential was measured with intracellular electrodes with a resistance between 20 and 40 mQ, by the 'floating' method described by Woodbury & Brady (1956). Tension was measured with a mechano-electronic transducer valve (RCA 5734) mounted in the manner described by Bulbring (1955).…”
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