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Biomedical subjects

W J Lammers

Publications and source records attributed to W J Lammers.

32 records · Page 2Linked to original sources
PubMed1991

Motor responsiveness to stimuli presented during sleep: the influence of time-of-testing on sleep stage analyses.

The relationship between time-of-night of testing (circadian factors) and motor responsiveness to stimuli presented during different stages of sleep was examined. Nine males slept for two nonconsecutive nights in the laboratory. On Night 1, tympanic temperature was assessed at 30 min intervals. On Night 2, responsiveness was assessed with an incremental series of tones presented in sleep stages 2, 3/4, and REM throughout the night. Subjects were instructed to make a microswitch closure to the tones. Results showed that for all stages, responsiveness decreased across thirds of the night. Because the distribution of each sleep stage differed across the night, the effects on responsiveness due to time-of-testing and to sleep stage were confounded. When time-of-testing was held constant, responsiveness was greater in stages 2 and REM than in stage 3/4. When time-of-testing was not held constant, effects nearly opposite of the latter could be demonstrated.

Arousal↗
PubMed1991

Temperature, time-of-night of testing, and responsiveness to stimuli presented while sleeping.

The present study examined how time-of-night of testing and body temperature related to responsiveness to stimuli presented in sleep. Nine males slept for two nonconsecutive nights in the sleep laboratory. On Night 1, tympanic temperature was assessed at 30-min intervals. On Night 2, responsiveness was assessed with an incremental series of tones (5dB steps) presented in sleep stages 2, 3/4, and REM throughout the night (0030-0800 h). Subjects were instructed and given practice prior to sleep to make a microswitch closure to the tones. Results showed a curvilinear pattern of responsiveness across the night in that the intensity of tones required for a response increased until about 0530 h, then decreased thereafter. This pattern of responsiveness was positively related to the circadian rhythm of body temperature. A close correspondence was also found between the temperature trough and the performance trough (both occurred at about 0530 h). A greater emphasis on circadian factors may help understand previously reported but contradictory findings. The present results also suggest that measures of responsiveness follow a circadian pattern regardless of the sleep/wake state.

Adult↗
PubMed1990

Quantification of spatial inhomogeneity in conduction and initiation of reentrant atrial arrhythmias.

In isolated superfused left atria of the rabbit, inhomogeneity in conduction was quantified using the activation times measured with a high-density mapping system. At each recording site, the maximal difference with neighboring activation times (i.e., phase difference) was calculated. Local phase differences were plotted in a phase map, revealing the spatial distribution of inhomogeneities in conduction, and from each map a total index of inhomogeneity was calculated. During slow pacing (2 Hz) local differences in conduction velocity, depending on the direction of propagation, were found already. Inhomogeneity in conduction increased significantly during single early premature beats (inhomogeneity index increased from 2.3 to 3.1; P less than 0.001). The application of multiple premature beats further increased inhomogeneity in conduction, whereas rapid pacing induced the highest level of inhomogeneity (inhomogeneity index 5.3; P less than 0.001). An analysis of the spatial distribution of maximal phase differences revealed that during premature beats inhomogeneities in conduction were limited to an area of 6 mm around the point of origin of the premature impulse, whereas during rapid pacing inhomogeneities in conduction were found throughout the whole preparation. Phase maps constructed during the initiation of reentrant tachyarrhythmias showed that reentry occurred at sites with the highest phase differences. Quantification of spatial inhomogeneities in conduction is a useful tool to evaluate the vulnerability of the myocardial substrate for reentrant arrhythmias.

Animals↗
PubMed1989

Habituation of P300 to target stimuli.

Two experiments examined the effects on N100, N200, and P300 of 1) repeated target presentation, 2) interblock intervals, 3) knowledge of session end, and 4) reversal of targets and nontargets. In the first experiment, subjects (N = 40) performed an oddball task across six test blocks (35 targets per block). Statistical analyses showed that repeated target presentation resulted in P300 amplitude decreases (habituation) and P300 latency increases within and across test blocks (11.3 microV to 5.4 microV, 330 msec to 348 msec), and also resulted in N200 amplitude increases within blocks and N200 latency increases within and across blocks. Interblock intervals resulted in partial recovery of these habituation effects. Knowledge of session end increased P300 amplitude, while reversal of targets and nontargets had no effect. The latencies of N200 and P300 were positively correlated (r .55), while the amplitudes were not. The second experiment demonstrated P300 habituation at multiple scalp sites (Fz, Cz, Pz). Two factors that may relate to habituation of the P300 are decreased arousal level and degree of involvement in the task.

Adolescent↗
PubMed1988

An easy and direct approach to investigate conduction properties of the rabbit sinus node.

The sinus node is not only important for the generation of the cardiac impulse but also as conductor of this impulse from the site of origin toward the atrium. An easy method to investigate conduction properties of sinus nodal tissue directly is described. The isolated right atrium of the rabbit was divided--via an incision perpendicular to the crista terminalis--into two halves connected only by a bridge of sinus nodal tissue. By means of two atrial surface electrodes conduction through the sinus node bridge was monitored. It appeared that conduction in the sino-atrial border zone is many times slower than in the atrium and refractory period markedly longer. In the center of the sinus node conduction is again slower and refractory period longer than in the border zone. Validity of the method was tested by reconstruction of the conduction route of stimulated impulses using microelectrode recordings. Applications of the method were demonstrated by studying the effects of rate and rhythm, hypothermia, hypoxia, acetylcholine and norepinephrine as well as verapamil. The model is suitable for investigation of the effects of drugs and other interventions on impulse conduction in sinus nodal tissue.

Acetylcholine↗
PubMed1988

Reentrant and focal arrhythmias in low potassium in isolated rabbit atrium.

In isolated superfused left atria of the rabbit, tachyarrhythmias became highly inducible with a decrease of the extracellular potassium concentration to 2.0 mM. The nature of the arrhythmias was determined with a high-resolution mapping system. In several cases, abnormal impulse formation was found, but the majority of arrhythmias (75%) was caused by a circus movement of the impulse. Furthermore, circus-movement tachyarrhythmias often degenerated into fibrillatory activity, and activation maps revealed the presence of multiple wavelets during this chaotic rhythm. The occurrence of reentrant arrhythmias may be caused either by an increase in inhomogeneity in conduction or by a shortening of the wavelength in low potassium. Inhomogeneity in conduction was determined by calculating the difference in activation times between neighboring electrodes. In low potassium, premature activation significantly increased the inhomogeneity index compared with slow rhythm (from 2.2 to 3.9; P less than 0.001) but was not significantly different from the inhomogeneity measured at normal potassium concentrations. Low potassium, however, did shorten significantly the wavelength of the impulse by approximately 40%. The increased inducibility of reentry in low potassium is therefore caused by a reduction of the length of the excitation wave and not by an increase in inhomogeneity in conduction.

Animals↗
PubMed1988

Length of excitation wave and susceptibility to reentrant atrial arrhythmias in normal conscious dogs.

We calculated the wavelength of the atrial impulse in chronically instrumented conscious dogs by measuring both conduction velocity and refractory period: wavelength = refractory period X conduction velocity. Implantation of multiple stimulating and recording electrodes allowed wavelength determination at four different areas: the right and left parts of Bachmann's bundle and the free walls of the right and left atria. During programmed electrical stimulation, three types of arrhythmias were observed: rapid repetitive responses, atrial flutter, and atrial fibrillation. During normal rhythm, the wavelength of the atrial impulse varied between 14 and 18 cm. Premature beats had a shorter wavelength, depending on the degree of prematurity. Premature beats that evoked rapid repetitive responses showed a critical shortening of the wavelength below 12.3 cm. Episodes of atrial flutter were induced at a wavelength below 9.7 cm, while fibrillation occurred at wavelengths shorter than 7.8 cm. We correlated the induction of these arrhythmias with the values of refractory period, conduction velocity, and wavelength during control and during administration of several drugs. Intravenous administration of acetylcholine shortened the wavelength by 30-40%, mainly because of refractory period shortening. Both propafenone and lidocaine had strong but opposite effects on refractoriness and conduction and, consequently, little effect on the wavelength. Quinidine markedly prolonged the refractory period, but prolongation of wavelength was less because of a simultaneous decrease in conduction velocity. d-Sotalol also increased refractory period, but because it had no appreciable effect on conduction velocity, this drug was the most effective in prolongation of wavelength. Linear discriminant analysis of the data showed that the refractory period and the conduction velocity each were poor parameters to predict the occurrence of the different arrhythmias (predictive value 48% and 38%, respectively). The combination of both properties, however, as expressed in the wavelength, was a more reliable index that predicted the induction of the different arrhythmias correctly in 75% of the cases. We conclude that the wavelength is a useful parameter for evaluating antiarrhythmic drugs.

Acetylcholine↗
PubMed1987

The influence of the atrial myocardium on impulse formation in the rabbit sinus node.

In the isolated right atrium of the rabbit heart the influence of the atrial myocardium on impulse formation in the sinus node was investigated. Under normal conditions the pacemaker (earliest activation) was located in the center of the node where fibers with the highest rate of diastolic depolarization were found. After disconnection of the atrium from the sinus node spontaneous cycle length decreased from a mean of 348 ms to a mean of 288 ms (-18%) in all experiments (n = 15). This was accompanied by a shift of the pacemaker from the nodal center towards the border zone. By means of multiple microelectrode impalements changes in action potential configuration were studied. After disconnection of atrium and sinus node the rate of diastolic depolarization of fibers in the border zone was increased from a mean of 26 mV/s to a mean of 78 mV/s, whereas in the center of the sinus node no increase was found (mean: 52 mV/s). It was concluded that the fibers in the border zone of the sinus node are better pacemaker fibers than in the nodal center. However under normal conditions the intrinsic pacemaker properties of the border zone fibers are electronically depressed by the connected atrial myocardium.

Action Potentials↗
PubMed1986

A microcomputer system for haemodynamic measurements in isolated, working rat hearts.

This study describes the application of an Apple IIe microcomputer in combination with a pre-processor in the on-line calculation of haemodynamic variables of the isolated working rat heart and of relative rapid changes in these variables, induced by variations in left atrial filling pressure (preload) and end-diastolic aortic pressure (afterload). Variables such as heart rate, systolic and diastolic left ventricular pressure, the maximal positive and negative first derivative of the left ventricular pressure, systolic and diastolic aortic pressure and aortic flow were continuously calculated and printed at minimal intervals of 6 s. A newly designed procedure to detect the activation of the electrogram, which was necessary to start the detection of a new cardiac cycle, is described.

Animals↗
PubMed1986

The wavelength of the cardiac impulse and reentrant arrhythmias in isolated rabbit atrium. The role of heart rate, autonomic transmitters, temperature, and potassium.

We measured the wavelength of the cardiac impulse, defined as the distance traveled by the depolarization wave during the functional refractory period, in isolated narrow strips of rabbit atrium. During control, wavelength was 42 mm during pacing with 2 Hz, and was 28 mm at the maximum pacing rate; early premature beats had a wavelength as short as 23 mm. Administration of carbamylcholine (4 X 10(-7) g/ml) shortened the wavelength to 21 mm during 2 Hz, 18 mm at the maximum pacing rate Fmax, and 16 mm during an early premature impulse, respectively. The effects of epinephrine (6 X 10(-7) M) were strongly rate dependent. At slow heart rates, epinephrine clearly prolonged the wavelength (58 mm), whereas, during maximum pacing, wavelength remained unchanged (28 mm). Hypokalemia (2 mM) decreased the length of the impulse at all stimulation frequencies. Moderate hyperkalemia (5.6 and 7.0 mM) did not modify wavelength because refractoriness and conduction velocity were affected proportionally. Above 7.0 mM potassium, the wavelength became progressively prolonged because of the development of post-repolarization refractoriness. Cooling to 27 degrees C resulted in a slight lengthening of the impulse. At lower temperatures, however, wavelength prolonged significantly because of a relatively strong prolongation of the refractory period. In separate experiments in 15 X 20 mm segments of atrium, reentrant tachyarrhythmias were induced and the circuit size compared with the wavelength. The size of intraatrial circuits was similar to the magnitude of the measured wavelength during maximum pacing. Carbamylcholine and hypokalemia, both of which shorten the impulse length, also clearly decreased the size of reentrant circuits. Cooling to 27 degrees C, which affects both refractoriness and conduction velocity, only slightly prolonged the wavelength; accordingly, the size of reentrant circuits at 27 degrees C was only slightly longer than at 37 degrees C. These experiments emphasize the importance of the wavelength of the cardiac impulse in relation to the occurrence of intramyocardial reentry.

Animals↗
PubMed1984

Intra-atrial reentry as a mechanism for atrial flutter induced by acetylcholine and rapid pacing in the dog.

In the isolated blood-perfused canine heart we produced episodes of rapid atrial flutter by continuous infusion of acetylcholine and rapid pacing. The spread of excitation during atrial flutter was mapped with the aid of two endocavitary mapping electrodes containing 960 leads and recording from 192 different sites simultaneously. The flutter maps clearly showed that intra-atrial reentry was the mechanism responsible for the arrhythmia. However, the localization and size of the intra-atrial circuits differed from case to case even in the same heart. The orifices of the venae cavae or the atrioventricular ring did not serve as a central anatomic obstacle for circus movement. We also failed to identify a special role of the internodal pathways in the formation of the loop. Instead, the intra-atrial circuits could be found everywhere, provided sufficient atrial mass was available to accommodate the circuit. The diameter of the circuits varied between 1.5 and 3 cm at a cycle length between 65 and 155 msec. The average conduction velocity of the circulating impulse varied between 60 and 80 cm/sec. Spontaneous termination of atrial flutter frequently occurred and was based on local conduction block in a narrow part of the circuit. Another interesting aspect of these studies is the finding that during continuous circus movement of the impulse, the amount of myocardium that is activated may vary considerably. This marked periodicity in excited tissue mass during atrial flutter could adequately explain the continuously undulating baseline or typical sawtoothlike F waves as seen in the surface electrocardiogram during atrial flutter.

Acetylcholine↗
PubMed1980

The effect of ouabain on the isolated sinus node preparation of the rabbit studied with microelectrodes.

In 30 isolated, spontaneously beating right atrial preparations of the rabbit, the arrhythmogenic actions of ouabain were studied with microelectrodes. Ouabain (10(-6) M) uniformly produced the following events: (1) a gradual increase in sinus rate with periods of alternation of beta-to-beat atrial intervals, (2) a rapid rate and regular rhythm, (3) severe irregularity of rhythm, (4) total atrial arrest. Cycle length decreased from 394 msec +/- 43 (mean +/- SD) during control to 229 msec +/- 26 during the period of rapid rate and regular rhythm (P less than 0.001). Pretreatment with atropine or propranolol did not abolish this positive chronotropic action of ouabain. Maps of the spread of activation in the area of the sinus node in eight experiments revealed that the speeding up of rate is accompanied by a shift of dominant pacemaker site toward the sinoatrial border. In explanation, it is shown that sinoatrial border fibers develop strong diastolic depolarization, whereas dominant pacemaker fibers do so to a lesser extent or not at all. The atrial arrhythmias--best to be described as "digitalis-induced sinus tachycardia"--may represent the experimental counterpart of the so-called "paroxysmal atrial tachycardia with block" described as a common manifestation of digitalis intoxication in man.

Action Potentials↗
PubMed1978

Sinus node response to premature atrial stimulation in the rabbit studied with multiple microelectrode impalements.

In this study we investigated the response of the isolated rabbit sinus node to ectopic atrial premature beats elicited late in the atrial cycle. In three experiments the response of at least 45 different fibers of the sinus node was recorded, whereas, in other experiments, investigation was less extensive. In this way the spread of activation of the total pacemaker area could be mapped accurately both during spontaneous beating and the induction of ectopic atrial beats of different degrees of prematurity. We found that: (1) The conduction of an impulse from the dominant pacemaker area to the atrium during spontaneous rhythm (antegrade conduction) is slower than the conduction of an ectopic atrial impulse towards the center of the sinus node (retrograde conduction). (2) The action potential of the dominant pacemaker fibers in the sinus node is shortened because of premature activation caused by an ectopic impulse from the atrium. Late premature beats had no effect on diastolic depolarization. If the retrograde activation wave did not reach the area of the dominant pacemaker before the spontaneous discharge of these fibers, there was electrotonic influence demonstrable over a distance of about 0.5 mm. (3) Comparison of the true sinoatrial conduction time with the estimated sinoatrial conduction calculated indirectly from the length of the postextrasystolic atrial cycle revealed that, in the isolated rabbit heart, the calculated value is a serious underestimation of the true antegrade sinoatrial conduction time.

Action Potentials↗