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Biomedical subjects

D E Euler

Publications and source records attributed to D E Euler.

72 records · Page 4Linked to original sources
PubMed1981

Sinoatrial node artery distribution and its relation to hierarchy of cardiac automaticity.

The sinoatrial node (SAN) artery (SANA) was cannulated in dogs anesthetized with chloralose (7 dogs) or pentobarbital (1 dog). Intra-SANA injection of acetylcholine (ACh) with edrophonium (EPh) produced a transient junctional rhythm (JR) when the cannula tip lay near SANA origin. However, when ACh-EPh was injected while the cannula tip lay within SAN region, a slower P wave rhythm, rather than a JR, developed. To determine visually the injected ACh-EPh distribution, an equal volume of dye was injected under similar conditions. Dye-distribution patterns were consistent in all atria. These averaged 44 +/- 2% of the total endocardial surface, indicating that SANA distribution is not discrete, but widespread. Dye extended cranially, caudally, and laterally and included documented subsidiary pacemaker sites. Dye approached, but never trespassed, the coronary sinus ostium. Results suggest that cholinergic drug injection into the proximal SANA may suppress not only the SAN, but subsidiary atrial pacemakers as well. In this situation, junctional pacemakers probably emerge, not because of inherently greater automaticity, but after default of subsidiary atrial pacemakers.

Acetylcholine↗
PubMed1981

Autonomic control of ventricular refractoriness.

The effects of vagal and sympathetic stimulation on canine ventricular refractoriness were studied in vivo. Sympathetic stimulation reduced the left ventricular refractory period to an extent linearly related to the logarithm of nerve stimulation frequency. Vagal stimulation had no effect in the absence of sympathetic stimulation but produced a frequency-dependent attenuation of sympathetic effects when the two systems were stimulated simultaneously. The effects of combined vagal and sympathetic stimulation were best described by a multilinear regression model using the logarithm of vagal and sympathetic frequency as covariates. The magnitude of vagal attenuation of sympathetic effects did not show any regional variation at the five widely spaced sites (2 right ventricular, 3 left ventricular) studied.

Animals↗
PubMed1980

Continuous fractionated electrical activity after stimulation of the ventricles during the vulnerable period: evidence for local reentry.

Ventricular multiple extrasystoles and fibrillation were induced in open chest dogs by the delivery of either a single electrical pulse or a train of pulses to the right ventricle during the vulnerable period of the cardiac cycle. Bipolar epicardial electrodes delivered current while bipolar plunge electrodes recorded the activation complexes at various distances from the stimulation site. At stimulus intensities below the threshold for multiple ventricular responses, the electrograms recorded from muscle adjacent to the stimulation site showed fragmented activation complexes that lasted considerably longer than the control complexes. At stimulus intensities that evoked multiple ventricular extrasystoles or fibrillation, the fragmented electrical activity became continuous and bridged the diastolic interval between successive ectopic complexes. The continuous fractionated electrical activity that preceded the appearance of multiple extrasystoles and fibrillation was recorded only from electrodes placed within a few millimeters of the stimulating electrodes and could be evoked only by stimulation during the vulnerable period. Disappearance of the fractionated local electrical activity during a run of extrasystoles was followed immediately by the resumption of a normal rhythm. In addition, the fractionated continuous electrical activity that appeared after delivery of a single stimulus during the vulnerable period could be abolished by the delivery of a second stimulus during the protective zone. The presence of continuous local electrical activity before the development of multiple extrasystoles and fibrillation provides strong evidence that the ventricular fibrillation threshold technique operates by producing local reentrant activity.

Animals↗
PubMed1980

Norepinephrine release by ventricular stimulation: effect on fibrillation thresholds.

In adult dogs anesthetized with pentobarbital sodium, ventricular fibrillation thresholds determined by scanning the vulnerable period with a train of 14 pulses (4 ms, 100 Hz) were significantly less (P less than 0.01) than fibrillation thresholds determined by scanning the vulnerable period with a single 10-ms stimulus. Following beta-adrenergic blockade with propranolol, the relative increase in the fibrillation thresholds measured with trains was about seven times greater than the relative increase in the single-stimulus threshold (P less than 0.01). In a group of animals subjected to chronic cardiac denervation, fibrillation thresholds measured with trains were about three times greater than in a group of shamthoracotomized animals (P less than 0.01). Furthermore, the train fibrillation thresholds of the catecholamine-depleted hearts were not significantly different from the train thresholds of beta-blocked innervated hearts. These data, coupled with the finding that trains of stimuli produced a marked augmentation in local myocardial contractile force, suggest that locally released norepinephrine during a fibrillation-threshold determination may exert a profound influence on the level of current necessary to evoke fibrillation.

Animals↗
PubMed1980

Atrial ectopic foci in the canine heart: hierarchy of pacemaker automaticity.

The sinoatrial node (SAN) and adjacent tissue of the sulcus terminalis were surgically excised in sequential multiple sections to study the location and intrinsic rate of emerging pacemakers in the acute open-chest dog. Under chloralose anesthesia total of 17 ectopic atrial pacemakers emerged in 12 dogs ranging in location from the anterior interatrial band, midsulcus terminalis, and junction of the inferior vena cava-inferior right atrium. Four AV junctional and one idioventricular pacemakers also emerged in these experiments. Each successively inferior focus had a slower rate than the SAN. The average heart rate of the atrial ectopic pacemakers was 73 +/- 4% of the SAN but that the AV junctional pacemakers was 56 +/- 4% of the SAN (P less than 0.05). The greatest reductions in rate were achieved with total excision of the SAN and entire sulcus terminalis, but in only 50% of the animals did this result in a junctional rhythm. The location and rate of atrial ectopic foci support the notion that the AV junctional region is not the fastest pacemaker in the absence of the classically defined SAN and suggest that atrial ectopic pacemakers are intermediate in the hierarchy of cardiac pacemakers in the dog.

Action Potentials↗
PubMed1980

Release of autonomic neuromediators by local ventricular electrical stimulation.

Trains of electrical stimuli were applied to the ventricular epicardium in pentobarbital-anesthetized dogs. The trains, delivered during the absolute refractory period via Walton-Brodie strain gauge arches, resulted in a highly localized potentiation of ventricular contractile force. The magnitude of the potentiation was directly related to the intensity of the trains. The positive inotropic response of either ventricle to trains of stimuli was abolished following chronic cardiac denervation or beta-adrenergic blockade with tolamolol, indicating that the response was probably mediated by the excitation of local sympathetic nerve fibers. Following the elimination of adrenergic influences, a slight negative inotropic response to trains of stimuli was observed in some animals. Administration of atropine blocked the negative inotropic response. When the adrenergic system was intact the administration of atropine resulted in a significant augmentation of the positive inotropic response of both ventricles to trains of stimuli. Thus in addition to norepinephrine release, it also appeared that electrical stimulation of the ventricles resulted in activation of local parasympathetic fibers with subsequent release of acetylcholine.

Animals↗
PubMed1980

Cardiac arrhythmias after chronic embolization of the sinus node artery: alterations in parasympathetic pacemaker control.

Embolization of the sinus node artery was accomplished in dogs by injecting rapidly hardening vinyl latex into the sinus node artery. Embolization immediately shifted the pacemaker to a junctional focus; however, with time postoperatively, the pacemaker shifted to an atrial site. Variable episodes of pacemaker failure, sinoatrial block, junctional rhythm, wandering atrial pacemaker and idioventricular escape rhythms were commonly observed on Holter monitor in isolation but only rarely when the dog was in the laboratory. Severe bradycardia (38.9 +/- 3.7 beats/min) was the predominant rhythm by 3-6 months postoperatively. In addition, these same dogs had a greater overall increase in heart rate after atropine than normal dogs (17.5 +/- 13.5 vs 116.6 +/- 15.9 beats/min above control; p less than 0.02). Responses to vagal stimulation in this group were abnormal, as long periods of asystole and bradycardia were observed after stimulation was terminated. These data suggest an alteration in parasympathetic pacemaker control after chronic embolization of the sinus node artery.

Animals↗
PubMed1979

Role of skin temperature in the control of sweating.

In five male subjects tympanic membrane temperature (Tty), rectal temperature, skin temperatures at 12 sites were simultaneously recorded. Local sweating rate was measured at six sites using resistance hygrometry. After steady-state sweating was established, the lower body was heated at ambient temperatures of 50, 60, 70, and 80 degrees C or cooled at an ambient temperature of 29 degrees C while the upper body remained at a constant ambient temperature. During lower body heating or cooling, Tty was maintained constant by the drinking of cold (10 degrees C) or warm (45 degrees C) water. Sweating rate on both upper and lower body surfaces was proportional to lower body skin temperature. The regression coefficients for sweating rate versus mean lower body skin temperature varied from 0.03 to 0.09 mg/cm2.min. degrees C between subjects, but were not significantly different from each other (P greater than 0.05). This study demonstrates an influence of cutaneous thermoreceptors on sweating rate under steady-state conditions.

Humans↗
PubMed1979

Supraventricular pacemaker underdrive in the absence of sinus nodal influences in the conscious dog.

The ability to reduce and maintain heart rate by electrical stimulation (underdrive) was tested in three groups of chronically instrumented dogs: sinoatrial node intact, ectopic atrial pacemaker produced by injection of rapidly hardening latex into the sinoatrial nodal artery, and idioventricular pacemaker produced by injection of formalin into the atrioventricular node. In the conscious unsedated state, underdrive of sinoatrial or idioventricular pacemakers resulted in competition between driven and intrinsic foci. However, the cycle length of ectopic atrial pacemakers could be increased by 148.4 +/- 30.7 msec (P less than 0.001) and maintained at that value. Cessation of underdrive resulted in a period of pacemaker suppression similar to that produced following overdrive. Single premature stimuli produced marked cycle length prolongations in dogs with ectopic atrial foci. Total autonomic blockade had no significant effect on the production of underdrive. Thus, the results of the present experiments provide evidence for maintained capture of cardiac pacemakers at rates significantly below intrinsic control and indicate that underdrive varies as a function of pacemaker site. Underdrive may explain the failure of junctional escape in the presence of slower atrial rhythms.

Animals↗
PubMed1978

Comparison of SA nodal and subsidiary atrial pacemaker function and location in the dog.

A 3-4 cm length of sulcus terminalis tissue including the sinoatrial node (SAN) was excised from 14 dogs. After an initial junctional rhythm with SAN excision a P wave emerged within days to weeks in 12 animals. Maximum heart rates of the SAN (preoperative) in response to exercise (276 +/- 15 beats/min), isoproterenol infusion in conscious animals (272 +/- 11 beats/min), and stellate stimulation during anesthesia (273 +/- 9 beats/min) were significantly greater than subsidiary pacemakers (postoperatively) for exercise (219 +/- 9 beats/min), isoproterenol (226 +/- 8 beats/min), and stellate stimulation (197 +/- 9 beats/min). During a final experiment, electrophysiological mapping of the area of earliest epicardial activation (pacemaker location) was carried out. By use of a suction electrode in reference to plunge electrodes located in the anterior interatrial band (AIB), eustachian ridge of the coronary sinus, and limbus of the fossa ovalis, the pacemaker was located at the inferior vena cava-inferior right atrial junction in 80% of the animals mapped. During isoproterenol infusion the foci shifted to regions of the AIB in 70% of the animals mapped. The concept of pacemaker hierarchy is discussed.

Animals↗
PubMed1976

Cardiac dysrhythmias in the conscious dog after surgically induced autonomic imbalance.

The ventrolateral cardiac nerve in the dog is a primary branch of the left sympathetics and represents a direct neural link between the central nervous system and the heart. Its electric excitation elicits characteristic shifts in pacemaker and tachydysrhythmias related to its explicit innervation of the inferior atrial, atrioventricular (A-V) junctional and ventricular tissues. Total denervation of the canine heart, sparing the ventrolateral cardiac nerve, produced a long-term model in which only these portions of the heart retained their sympathetic innervation. The trained unanesthetized model dog was subjected to severe exercise in order to determine the effects of elevated levels of sympathetic tone upon these important regions of the conduction system. Reproducible tachydysrhythmias were elicited in all six animals completing the regimen of periodic testing over a period of 136 to 378 days after operation. The abnormal rhythms consisted of shifting cardiac pacemakers and supraventricular A-V junctional and ventricular tachycardias with frequent premature systoles. Comparable abnormalities were not observed in a similarly tested sham-operated animal or in dogs with a totally denervated heart. The exercise-induced dysrhythmias gradually disappeared with time, presumably in relation to autonomic reinnervation of the heart. The characteristic patterns of ventrolateral cardiac nerve and upon its presumed influence upon Purkinje fiber and A-V nodal automaticity and temporal dispersion of refractoriness in myocardial tissues.

Animals↗
PubMed1976

Autonomic neural control of cardiac rhythm: the role of autonomic imbalance in the genesis of cardiac dysrhythmia.

Cardiac dysrhythmias result from abnormalities in rate, regularity, or sequence of cardiac activation, and because of direct actions of the autonomic nervous system upon each of these properties, imbalance in this system may play an important role in the genesis of cardiac dysrhythmia. A canine model has been developed in which the extrinsic innervation of the heart is ablated with the exception of the ventrolateral cardiac nerve. This nerve is distributed primarily to the inferior atrial, AV junctional, and ventricular tissues. Following recovery from surgery, the animal is placed on a treadmill and required to perform strenuous exercise. In all of six animals which sustained repeated exercise testing over periods of 4-12 months, dysrhythmias of varying complexities were elicited. None appeared in parallel experiments conducted in control or sham-operated animals. The dysrhythmias consisted of supraventricular, AV junctional, or ventricular tachycardias with occasional premature atrial or ventricular systoles. The dysrhythmias were not influenced by atropine but were generally controlled by propranolol.

Animals↗