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H C Strauss

Publications and source records attributed to H C Strauss.

At least 19 recordsLinked to original sources
PubMed1992

Regulation of extracellular calcium entry in endothelial cells: role of intracellular calcium pool.

We have investigated the role of the intracellular Ca2+ pool in regulating Ca2+ entry into vascular endothelial cells. The intracellular Ca2+ pool was mobilized using either thapsigargin (TG) or 2',5'-di(tert-butyl)-1,4-benzohydroquinone (BHQ), inhibitors of the endoplasmic reticulum Ca(2+)-adenosinetriphosphatase (ATPase). Mobilization of intracellular Ca2+ stores with either inhibitor depleted intracellular Ca2+ and greatly reduced subsequent mobilization of the inositol 1,4,5-trisphosphate (IP3)-sensitive intracellular Ca2+ pool by bradykinin. However, bradykinin-induced mobilization of the IP3-sensitive intracellular Ca2+ pool only partially reduced the subsequent response of cells to TG and BHQ. Mobilization of the intracellular Ca2+ pool by either TG or BHQ led to a concentration-dependent elevation of cytosolic Ca2+ concentrations ([Ca2+]i) without initiating inositol polyphosphate formation. In contrast to the rapidly developing, transient rise in Ca2+ concentration initiated by bradykinin, maximal concentrations of TG and BHQ stimulated a slowly developing, prolonged elevation of [Ca2+]i that required extracellular Ca2+ and could be blocked by extracellular Ni2+. Extracellular Ca2+ entered the cell through an activated cation entry pathway, since bradykinin, TG, and BHQ stimulated Mn2+ and 45Ca2+ entry. Bradykinin-stimulated 45Ca2+ uptake reached a peak within 2 min, whereas 45Ca2+ influx initiated by TG or BHQ continued for at least 8 min. Importantly, the [Ca2+]i response after low concentrations of BHQ was more transient than that seen after TG. The return of [Ca2+]i to basal values after low concentrations of BHQ was associated with reversal of Ca(2+)-ATPase inhibition and refilling of the IP3-sensitive Ca2+ pool. The continued elevation of [Ca2+]i and prolonged Ca2+ entry seen with TG was associated with continued Ca(2+)-ATPase inhibition and an empty IP3-sensitive Ca2+ pool. We conclude that mobilization of intracellular Ca2+ stores induces Ca2+ entry in endothelial cells which continues until the intracellular Ca2+ pool is refilled.

Animals↗
PubMed1979

Electrophysiologic effects of disopyramide phosphate on sinus node function in patients with sinus node dysfunction.

The electrophysiologic effects of intravenously administered disopyramide (2 mg/kg) on three parameters of sinus node function were examined in 16 symptomatic patients with sinus node dysfunction. Based on their ECG data before study, patients were subdivided into group A (n = 8), those with sinus pauses and/or sinoatrial (SA) exit block; and group B (n = 8), those with sinus bradycardia. Disopyramide shortened spontaneous cycle length in 10 of 16 patients and lengthened it in six--markedly so (91%) in one patient. Estimated SA conduction time decreased in seven of 14 patients and increased in seven. Two patients developed second degree SA exit block after disopyramide. Maximum sinus node recovery time was prolonged by disopyramide in 11 of 16 patients and markedly so in four. For the group as a whole there was no significant difference in spontaneous cycle length, maximum sinus node recovery time or estimated SA conduction time. P-wave and QRS durations and H-V intervals were significantly lengthened by disopyramide. Marked depression of the three parameters of sinus node function occurred in three group A patients and in one group B patient who had persistent severe sinus bradycardia. These four patients also had secondary pauses after termination of rapid atrial pacing under control conditions. Disopyramide should be administered cautiously to patients with sinus node dysfunction, particularly those with sinus pauses, SA exit block or secondary pauses.

Adult↗
PubMed1979

The estimation of sinoatrial conduction time in rabbit heart by the constant atrial pacing technique.

This study compared estimates of sinoatrial conduction time (SACT) obtained by constant atrial pacing (CAP) and premature atrial stimulation (PAS) with measured SACT in isolated rabbit right atrial preparations. Transmembrane potentials and surface electrograms were recorded from the sinus node and crista terminalis, respectively. The crista terminalis was paced 5, 10 and 15 beats/min faster than the spontaneous sinus rate with a train of eight pulses. Estimate of SACT by CAP was taken as the difference between the first atrial return cycle and the mean spontaneous cycle length. SACTs at 5, 10 and 15 beats/min faster were 76 +/- 10, 86 +/- 10 and 96 +/- 10 msec (mean +/- SEM; n = 12), respectively; correlation coefficients with the true SACT were 0.7, 0.54 and 0.4. Consecutive determinations of SACT by PAS and CAP in the same preparation (n = 6) at 10 beats/min faster gave SACTs of 86 +/- 13 and 79 +/- 14 msec, respectively, compared with true SACTs of 79 +/- 10 msec. Shortening of sinus node action potential, depression of automaticity and shifts in the site of the primary pacemaker contributed to the errors in both techniques. Estimation of SACT by CAP may be further complicated by failure of sinus node capture. Principles to minimize some of these errors are also presented.

Animals↗
PubMed1979

An analysis of the effects of acetylcholine on conduction and refractoriness in the rabbit sinus node.

The effects of acetylcholine (ACh) on sinus node automaticity, atrio-sinus conduction, and refractoriness were studied in 41 isolated rabbit right atrial preparations. Average control rate was 126 beats/min, and ACh 5 x 10(-8) M, 5 x 10(-7) M, and 5 x 10(-6) M significantly decreased heart rate by 7, 15, and 43%, respectively (P less than 0.01, 0.001, and 0.001). Atrio-sinus conduction time at a pacing cycle length of 400 msec did not significantly change during exposure to ACh 5 x 10(-8) and 5 x 10(-7) M. However, the mean effective refractory period (ERP) of the sinus node, at a pacing cycle length of 400 msec, increased from 183 +/- 16 msec to 210 +/- 24 msec during exposure to ACh 5 x 10(-7) M (P less than 0.025). The change in ERP followed the change in action potential duration. In contrast to the lack of effect of ACh 5 x 10(-7) M on atrio-sinus conduction time, ACh 5 x 10(-6) M caused 2:1 atrio-sinus block in 8 of 10 experiments. The site of block was identified using multiple microelectrode impalements, and occurred between the perinodal fibers bordering on the edge of the sinus node and the pacemaker area in the sinus node proper. When the pacing cycle length was increased and 1:1 atrio-sinus conduciton was present, conduction time did not significantly differ from control. At this longer pacing cycle length the mean ERP of the sinus node was 380 msec greater than control and lasted well after repolarization was completed. Thus, atrio-sinus block during exposure to ACh 5 x 10(-6) M resulted from a marked prolongation of refractoriness.

Acetylcholine↗
PubMed1979

Sinus node disease.

Sinus node dysfunction may be clinically asymptomatic or may lead to serious arrhythmias and sudden death. Symptomatology relates to the resulting brady- or tachyarrhythmias. Clinical and electrocardiographic assessements fail to identify the cause in many patients. Ambulatory electrocardiography establishes the diagnosis in a greater percentage of patients and permits the direct correlation of symptoms with rhythm disturbances. Functional electrophysiologic testing which examines the sinus node response to constant atrial pacing and premature atrial stimulation may be performed for further evaluation of these patients. Sensitivity and specificity of sinus node recovery times (SNRT) and sino- atrial conduction time (SACT) derived by functional testing vary markedly in different reports. This variation may relate to differences in patient population, limitations of testing procedures, and the uncertainties as to the normal limits of SNRT and SACT. As a result, the full value of these tests in diagnosis and in furthering our understanding of sinus node disease remains to be established. At present, permanent pacing remains the definitive treatment in symptomatic patients.

Animals↗
PubMed1978

Electrophysiologic testing in patients with sinus pauses and/or sinoatrial exit block.

28 symptomatic patients with documented episodes of sinus pauses and/or sinoatrial exit block underwent electrophysiologic study. Abnormal responses to electrophysiologic testing were observed in 23/28 patients (82%). Abnormal prolongation of the maximum sinus node recovery time (SNRT max) occurred in 17/28 (61%) patients, of postpacing cycles 2.10 (secondary pauses) occurred in 21/28 (75%), and of estimated sinoatrial conduction time occured in 15/28 (54%). The incidence of abnormal responses to rapid atrial pacing (prolonged SNRT max or secondary pauses) (22/28, 79%) was higher than the incidence of abnormal responses to premature atrial stimulation (15/28, 54%) (P less than 0.005). Life-threatening cardiac arrhythmias were observed, prior to electrophysiologic study, in 5 out of 28 (18%) patients. Symptomatic patients with sinus pauses and/or sinoatrial exit block frequently (23/28, 82%) showed abnormal responses to electrophysiologic testing and have a relatively high incidence of life-threatening arrhythmias.

Adult↗
PubMed1976

Electrophysiologic evaluation of sinus node function in patients with sinus node dysfunction.

Twenty patients of mean age 66.2 years, with suspected sinus node dysfunction, underwent extensive electrophysiologic study. Sinus bradycardia (18), sinus pauses (3), and sinoatrial block (1) were identified in their ECGs prior to study. Also 11 patients had some abnormality of atrioventricular nodal and/or intraventricular conduction prior to study. At the time of electrophysiological study, 10/20 patients (50%) had a mean cycle length exceeding 1000 msec, and mean P-V interval exceeded 210 msec in 7/20 (35%). The estimated "sinoatrial conduction time" exceeded 215 msec in 6/16 (38%) patients. The maximum first escape cycle following pacing at six different rates exceeded a value equal 1.3 X the mean value of the control cycle length + 101 msec (slope of regression line + Y intercept + 1 SD) in 13/9 (68%) patients. Nineteen patients received 1 mg atropine intravenously and mean cycle length decreased by 19%, from 891 +/- 175.8 msec to 718 +/- 182.9 msec. Graded infusion of isoproterenol was employed in 19 patients; four patients required an infusion rate greater than 28.3 ng/kg/min to produce a 20% decrease in spontaneous sinus cycle length. These data would indicate that a variety of interventions are required to characterize the disturbance of sinus node automaticiy and sinoatrial conduction in patients with sinus node dysfunction.

Adult↗
PubMed1976

Analysis of secondary pauses following termination of rapid atrial pacing in man.

The first ten cycles following cessation of atrial pacing were evaluated in 44 control subjects (mean age 52.9 +/- 14.88 yr) and 39 patients (mean age 62.9 +/- 15.41 yr) suspected of having sinus node dysfunction (SND). The maximal cycle length for each postpacing cycle following several pacing periods in each control subject was determined, and was normalized by dividing it by the subject's mean spontaneous control cycle length (SCL). Using the control group, a normalized maximal post-pacing response pattern (mean and SD) was derived. For each SND patient, a composite SD for each post-pacing cycle was calculated by adding the patient's SCL variance to the variance determined for each post-pacing cycle in the control group. Two composite SD above the mean value for each post-pacing cycle was selected as the upper limit of the normal recovery response and used to identify abnormal post-pacing responses in the 39 SND patients. Abnormally prolonged cycle lengths subsequent to the first escape cycle (secondary pauses) were found in 16/39 (41.0%) patients, of whom 11/39 (28.2%) had a prolonged SNRTmax. Of importance, 11/12 (91;7%) patients with documented SA block or sinus pauses prior to electrophysiologic study, demonstrated secondary pauses, while only 7/12 (58.3%) had a prolonged SNRTmax. Criteria are derived for the identification of secondary pauses during the postpacing period, and a close association between secondary pauses and the presence of spontaneous SA block or sinus pauses prior to electrophysiologic study is demonstrated.

Aged↗
PubMed1976

Electrophysiologic effects of propranolol on sinus node function in patients with sinus node dysfunction.

The electrophysiologic effects of intravenously administered propranolol (0.1 mg/kg) on three parameters of sinus node function were examined in ten symptomatic patients with sinus node dysfunction. The patients ranged in age from 26 to 79 years. Symptoms ranged from fatigue to frank syncope. Sinoatrial (SA) block and sinus pauses were observed in one patient; sinus pauses alone were observed in three patients. Five (5/10) patients had intraatrial block; three (3/10) patients had atrioventricular block; four (4/10) patients had an intraventricular conduction disturbance. At the time of electrophysiologic study, two patients had a control spontaneous sinus cycle length that exceeded 1000 msec. Following propranolol, the mean spontaneous cycle length increased by 17.4% (924 to 1085 msec, P less than 0.005) and spontaneous second degree SA block reappeared in the one patient. The maximum escape cycle ranged from 116% to 229% of the prepacing spontaneous cycle length and was considered to be prolonged in two of ten patients. Propranolol had no significant effect on the maximum escape cycle/prepacing cycle length X 100 (%). The estimated sinoatrial conduction time (SACT) was determined in seven patients and ranged in value from 120 to 238 mes. Propranolol increased the mean value of the estimated SACT from 179 to 213 msec, P less than 0.025. Propranolol may cause marked bradyarrhythmias in some patients with sinus node dysfunction, and should be used with caution in these patients.

Adult↗
PubMed1975

Sinus nodal function in the intact dog heart evaluated by premature atrial stimulation and atrial pacing.

Sinus nodal function was analyzed in 25 dogs by premature stimulation of the right atrium. The return (AT-AR) and post-return (AR-A) cycles were plotted as a function of the premature cycle, and four zones were identified. Zone I (compensatory zone) was observed during the last 4.8 percent (mean value) of the sinus cycle (A-A). Zone II was observed during 43.6 to 95.2 percent (mean value) of the sinus cycle. During the latter part of zone II, AT-AR was nearly constant and AR-A remained nearly equal to A-A during the last 29 percent (mean value) of the cycle. Earlier in zone II three distinct patterns of return cycle responses were observed whereas post-return cycles either remained nearly equal to A-A or showed progressive lengthening. Zone III (interpolation) was observed in 10 animals during 39.5 to 46.2 percent (mean value) of the sinus cycle. AR-A was nearly equal to A-A in zone III. Interpolation was incomplete late and complete early in the zone. Zone IV (echo zone) was seen in another 10 animals during 40.9 to 45.3 percent (mean value) of the sinus cycle and in this zone AR-A was greater than A-A. No significant difference in these zones was seen among the animals anesthetized with pentobarbital or alpha-chloralose, or given 6-OH-dopamine. The AR-A was important in the analysis of these zones and appears to be essential to the interpretation of data derived from premature atrial stimulation. Responses to premature atrial stimulation through a catheter electrode positioned against the sinus nodal region compared favorably with responses to direct epicardial stimulation. After periods of continuous right atrial pacing a vairety of patterns of sinus nodal depression were observed at different rates and durations of stimulation. The frequent occurrence of a short sinus escape cycle followed by the maximal pause observed during rapid pacing rates suggests sinus nodal entrance block. This may be an important factor to consider in determining an optimal pacing rate for assessing sinus nodal function.

Anesthesia, Intravenous↗