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A L Taylor

Publications and source records attributed to A L Taylor.

At least 55 records · Page 3Linked to original sources
PubMed1990

Differential enhancement of postischemic segmental systolic thickening by diltiazem.

Prolonged depression of segmental systolic thickening after brief coronary artery occlusion may result principally from events during reperfusion rather than during the ischemic interval. Thus, cellular calcium overload at reperfusion may be a mediator of contractile dysfunction after brief ischemia, and reduction of calcium entry by diltiazem, a calcium channel antagonist, may enhance recovery of systolic thickening after brief periods of ischemia. Thirteen awake unsedated dogs instrumented with hemodynamic catheters, left anterior descending coronary artery occluders and five to six pairs of intramyocardial sonomicrometers underwent two 15 min coronary artery occlusions with 24 h reperfusion. The order of infusion of diltiazem (15 micrograms/kg per min) or saline solution was alternated. Systolic thickening, hemodynamic variables and regional myocardial blood flow were measured serially over 24 h. Despite equally severe ischemic dysfunction during coronary occlusion, diltiazem-treated segments with systolic thinning during ischemia recovered control segmental thickening significantly earlier than saline solution-treated segments (at 30 versus 180 min of reperfusion). Blood pressure was mildly decreased during diltiazem treatment; therefore, a second group of 10 dogs underwent a similar occlusion and reflow period during infusion of nitroprusside to lower mean arterial pressure equivalently. Decreases in blood pressure in this group resulted in some improvement in segmental systolic function; however, this did not reach statistical significance at any time. Regional myocardial blood flows were similar in the saline solution- and diltiazem-treated groups during ischemia and reflow. Thus, it is concluded that 1) diltiazem infusion significantly enhanced recovery of segmental systolic thickening after 15 min of ischemia and 24 h of reperfusion; 2) the enhancement in segmental systolic function could not entirely be attributed to decreased mean arterial pressure; 3) improvement in postischemic segmental ventricular function was seen only in those segments with systolic thinning during ischemia; thus, segments with the most severe ischemic dysfunction benefited most; and 4) there were no important differences in regional myocardial blood flow during ischemia and reperfusion between saline- and diltiazem-treated animals.

Animals↗
PubMed1990

Aortic valve morphology: an important in vitro determinant of proximal regurgitant jet width by Doppler color flow mapping.

In vitro and in vivo studies suggest that proximal aortic regurgitant jet width on Doppler color flow mapping predicts severity of aortic regurgitation. The influence of aortic valve morphology on proximal regurgitant jet width has not been studied. Despite equal cross-sectional area, differences in aortic valve morphology may influence regurgitant jet width and thus estimates of severity of aortic regurgitation. Aortic valve simulations representing degenerative, rheumatic and bicuspid valves as well as a circle in two cross-sectional areas (0.2 cm2 and 0.7 cm2) were placed in a flow model using two gradients (50 and 100 mm Hg) to produce simulated aortic regurgitant jets. Flow maps were obtained from parasternal and apical positions with color gain, frames per second, low velocity reject and depth held constant. The mean of three regurgitant jet widths for each shape, size and gradient were compared by three factor analysis of variance. Aortic valve morphology significantly affected regurgitant jet width in both parasternal and apical views (p = 0.0001 by analysis of variance) with bicuspid shapes producing regurgitant jet widths significantly different from all other shapes. Valve area also consistently significantly influenced proximal regurgitant jet width (p = 0.0001) in both views. Initial pressure gradient was less important. It is concluded that in an in vitro flow model aortic valve morphology introduces significant variability in the measurement of proximal regurgitant jet widths independent of orifice cross-sectional area. Estimates of severity of aortic regurgitation may therefore be influenced considerably by aortic valve morphology.

Analysis of Variance↗
PubMed1990

Entrainment onset in a pacemaker model of reentrant ventricular tachycardia: insight into localization of critical elements of a reentrant circuit.

We investigated entrainment in a pacemaker model of reentrant ventricular tachycardia (VT) created in the intact dog heart using a VAT pacemaker with both electrodes on the ventricular epicardium. This produced an incessant wide QRS tachycardia originating from the pacing site with a cycle length equal to the conduction time between the sensing and pacing site plus the pacemaker AV delay. The conduction time between entrainment sites and the critical elements of the reentrant pathway (sensing and pacing sites) was determined by pacing at a comparable cycle length during sinus rhythm. Entrainment was achieved in 12 tachycardias with pacing at 1-4 sites at cycle lengths 10-100 msec shorter than tachycardia and confirmed by constant QRS fusion, progressive QRS fusion, and coupling of the first nonpaced QRS or intracardiac electrogram at the entraining cycle length. By least squares regression, the timing of entrainment onset (first reset of pacing or sensing site electrogram) measured by the prematurity of the local electrogram at the entraining site was highly correlated to the shortest conduction time between the entraining site and the circuit (F value of 84.7 and R = 0.752 [P less than 0.001]). Therefore, the timing of entrainment onset maybe useful in predicting the conduction time from the entraining site to critical elements of a reentrant circuit and may assist in localization of the reentrant pathway.

Animals↗
PubMed1990

Potentiation of reperfusion-associated ventricular fibrillation by left ventricular hypertrophy.

Important electrophysiological alterations that may predispose hearts to arrhythmias have been described for hypertrophied myocytes, and hypertrophy coupled with ischemia has been associated with an increased incidence of sudden death; however, an influence of hypertrophy on reperfusion arrhythmias has not been previously described. We hypothesized that reperfusion-associated arrhythmias would be potentiated by left ventricular hypertrophy. After induction of renovascular hypertension, 37 awake, unsedated dogs (17 with left ventricular hypertrophy and 20 without hypertrophy) underwent 15 minutes of coronary artery occlusion and reperfusion. All dogs were pretreated with lidocaine bolus injections and with lidocaine by continuous infusion during coronary occlusion and reperfusion. Reperfusion-associated ventricular fibrillation occurred in seven of 17 dogs with left ventricular hypertrophy versus one of 18 dogs without hypertrophy (p less than or equal to 0.05). The presence of hypertension was not significantly associated with an increased incidence of reflow ventricular arrhythmias. Neither QT interval nor area-at-risk was different between the dogs with and without reperfusion ventricular fibrillation; however, increased heart rate just before reperfusion did correlate with an increased incidence of ventricular fibrillation at reperfusion. Thus, 1) left ventricular hypertrophy was associated with a significantly increased incidence of reperfusion-induced ventricular fibrillation after 15 minutes of ischemia, 2) this increased incidence was independent of the presence of hypertension, and 3) lidocaine protected control and hypertrophied hearts against ventricular fibrillation during ischemia but was ineffective in protecting hypertrophied hearts against reperfusion-induced ventricular fibrillation.

Animals↗
PubMed1989

Day to day variability of Doppler color flow jets in mitral regurgitation.

Doppler color flow mapping offers the potential to assess serial changes in mitral regurgitation associated with therapeutic interventions such as surgical valve repair or after-load reduction. However, the day to day variability of color flow jets in mitral regurgitation must be established to distinguish therapeutic responses from random variation. Therefore, 14 patients with mitral regurgitation were each studied on 5 sequential days by color flow velocity mapping. Instrument settings were kept constant for each patient, and no patient had a significant change in heart rate, blood pressure, left ventricular end-diastolic dimension or circumferential wall stress between studies. To assess day to day variability, the area of the Doppler color flow map was carefully measured in multiple views by an experienced echocardiographer. Mitral regurgitant jet area by color flow mapping tended to be greater from apical rather than parasternal views (5.6 +/- 4.0 versus 2.9 +/- 2.1 cm2, respectively, p less than 0.03). The maximal jet area in any view ranged from 0.4 to 15.0 cm2 in individual subjects. Variability of maximal jet area within subjects was not statistically significant by repeated measures analysis of variance (F = 1.88, p = 0.13); however, the coefficient of variation was approximately 15%. Thus, a reduction in jet area of greater than or equal to 30% would be needed to predict a therapeutic response at the 95% confidence level. These data have important implications regarding the use of color flow mapping to assess the efficacy of therapeutic interventions in mitral regurgitation.

Adult↗
PubMed1989

Local platelet activation causes vasoconstriction of large epicardial canine coronary arteries in vivo. Thromboxane A2 and serotonin are possible mediators.

The goal of the present study was to demonstrate that intracoronary platelet deposition may trigger intense vasoconstriction of large epicardial coronary arteries in vivo and that this is largely mediated by thromboxane A2 and serotonin released by activated platelets. Cyclic flow variations (progressive declines in blood flow followed by sudden restorations of flow) due to recurrent intracoronary platelet activation and thrombus formation were induced by damaging the endothelium and placing a cylindrical constrictor on the left anterior descending coronary artery (LAD) in open-chest, anesthetized dogs. Coronary diameters were measured in vivo by means of ultrasonic crystals sutured on the LAD immediately distal to the constrictor (LAD1) and 1 cm below (LAD2) and on the circumflex coronary artery (Cx). Coronary artery diastolic diameters were measured continuously before and during cyclic flow variations and after they were abolished by administration of LY53857, a serotonin-receptor antagonist (group 1, n = 7), or SQ29548, a thromboxane-receptor antagonist (group 2, n = 7). During cyclic flow variations, at the nadir of coronary flow, LAD1 (a site of maximal platelet accumulation) cross-sectional area decreased by 52 +/- 10% and 38 +/- 6% in group 1 and 2 animals, respectively (p less than 0.001 compared with values recorded during a brief LAD occlusion obtained by a suture snare), whereas LAD2 (a site of minimal or no platelet accumulation) cross-sectional area did not differ from that recorded during the brief LAD occlusion. SQ29548 abolished cyclic flow variations in seven of seven dogs and LY53857 in six of seven, but they affected the increased coronary vasoconstriction differently: LAD1 cross-sectional area increased by 32 +/- 6% of the control value in SQ29548-treated animals, whereas it returned to baseline dimension values in the LY53857-treated group as these interventions also abolished the cyclic flow variations. We conclude that a marked coronary vasoconstriction may be triggered by local platelet deposition and that thromboxane A2 and serotonin are mediators of this vasoconstriction.

Animals↗
PubMed1988

Effect of increasing heart rate on left ventricular performance in patients with normal cardiac function.

The influence of an increase in heart rate on left ventricular (LV) contractile performance was assessed in patients with normal LV function. In 19 patients (3 men, 16 women) ages 55 +/- 9 years (mean +/- standard deviation) with normal global and segmental LV function and normal coronary arteries, LV dP/dt max was measured at baseline heart rate and during atrial pacing at baseline +5, baseline +25 and baseline +45 beats/min. In 10 of the patients, intravascular volume was not altered during pacing and, as a result, echocardiographically measured LV end-diastolic dimension decreased (5.4 +/- 0.4 at baseline vs 4.9 +/- 0.5 cm at baseline +45 beats/min, p less than 0.05). In these patients, LV dP/dt max increased modestly (1,571 +/- 237 at baseline vs 1,760 +/- 199 mm Hg/s at baseline +45 beats/min, p less than 0.05). In the other 9 patients, intravascular volume was expanded rapidly (by saline infusion) during pacing and, as a result, LV end-diastolic dimension was held constant (5.2 +/- 0.6 at baseline vs 5.1 +/- 0.6 cm at baseline +45 beats/min, difference not significant). In these patients, LV dP/dt max increased substantially with pacing (1,505 +/- 228 at baseline vs 2,050 +/- 258 mm Hg/s at baseline +45 beats/min, p less than 0.05). Thus, an increase in heart rate induces a modest increase in LV dP/dt max in patients in whom LV preload (as reflected by end-diastolic dimension) is allowed to decrease; in contrast, it causes a marked increase in LV dP/dt max in those in whom LV preload is maintained constant.

Adult↗
PubMed1988

Left ventricular dysfunction due to chronic right ventricular pressure overload. Resolution following percutaneous balloon valvuloplasty for pulmonic stenosis.

Left ventricular dysfunction due to chronic right ventricular pressure overload is well documented in experimental animals, but is controversial in humans. Whether left ventricular dysfunction resolves following the relief of chronic right ventricular pressure overload has not been studied. In this report, rapid improvement in both right and left ventricular function following successful percutaneous balloon valvuloplasty is described in a patient with severe isolated valvular pulmonic stenosis and biventricular dysfunction. It appears that: (1) geometric distortion played a major role in his reversible left ventricular dysfunction, and (2) severe biventricular dysfunction should not be a contraindication to valvuloplasty for valvular pulmonic stenosis.

Adult↗
PubMed1987

Cooperative mediation by serotonin S2 and thromboxane A2/prostaglandin H2 receptor activation of cyclic flow variations in dogs with severe coronary artery stenoses.

We have reported previously that thromboxane A2/prostaglandin (PG)H2 and serotonin independently mediate the occurrence of cyclic flow variations (CFVs) in a canine preparation of severe coronary artery narrowing. This may be due to an effect of these substances on platelets and/or the vascular wall. We tested the hypothesis that there is a cooperative effect between thromboxane A2/PGH2 and serotonin receptor stimulation in the development of CFVs in this animal preparation. After placement of a hard plastic cylindrical constrictor around the left anterior descending coronary artery, CFVs develop and are characterized by repetitive cycles of declines in coronary blood flow and abrupt increases in flow. In a control group of dogs, CFV frequency (cycles/hour) and severity (lowest coronary blood flow just before its restoration) did not change significantly over a 3 hr interval. In a second group of dogs, CFVs were established after constrictor placement, abolished with the serotonin (5HT2) receptor antagonist ketanserin, and reestablished by the continuous infusion of serotonin into the left atrium. Serotonin-induced CFVs were then abolished with a thromboxane A2/PGH2 receptor antagonist, SQ29,548, or a thromboxane synthetase inhibitor, dazoxiben (UK37,248). The relative specificity of the respective antagonists, SQ29,548 and ketanserin, was determined in canine platelets and rat aortic vascular strips. No significant cross-reactivity between ketanserin and SQ29,548 was found. Thus, the data obtained in these studies demonstrate a cooperative interaction between thromboxane A2/PGH2 and serotonin S2 receptors that contributes to the development of CFVs in this experimental preparation.

Animals↗
PubMed1987

Extreme bradycardia during sleep apnea caused by myxedema.

A 52-year-old man with myxedema was evaluated for anterior chest pain that was considered to be compatible with myocardial ischemia. The night after admission he developed extreme bradycardia, hypotension, and apneic episodes lasting up to 25 s. Continuous positive airway pressure and administration of medroxyprogesterone acetate prevented further episodes and relieved much of the somnolence and lethargy that had contributed to the evidence for myxedema. Alveolar hypoventilation caused by decreased sensitivity to carbon dioxide, inadequate central neural drive, peripheral muscle force, and obesity all may have contributed to the apnea. Chest pain has not recurred, and results of electrocardiography have remained normal following full thyroid hormone replacement. The early recognition of myxedema causing sleep apnea will allow specific treatment to avoid the cardiovascular risks related to prolonged apnea and will help avoid confusion with other etiologies of cardiovascular abnormalities.

Bradycardia↗
PubMed1986

Inhibition of cyclic flow variations in stenosed canine coronary arteries by thromboxane A2/prostaglandin H2 receptor antagonists.

We tested the hypothesis that thromboxane A2 and thromboxane A2/PGH2 receptor occupation are important in mediating cyclical reductions in coronary blood flow (CFVs) in concentrically narrowed canine coronary arteries. Two potent and selective thromboxane A2/PGH2 receptor antagonists, SQ29,548 and SQ28,668 eliminated CFVs and restored a normal pattern of blood flow through the severely narrowed vessels in 77 and 75% of the dogs, respectively. CFVs were eliminated within several minutes of an intravenous bolus injection of SQ29,548 or SQ28,688. A continuous infusion of SQ29,548 (0.2 mg/kg X min) prevented the recurrence of CFVs throughout the duration of its infusion. Left atrial infusion of the thromboxane A2 mimetic, U46619, restored CFVs in 5 of 8 SQ29,548-treated and in 5 of 7 SQ28,668-treated dogs. Circulating concentrations of the stable metabolites of TxA2 and PGI2, TxB2 and 6-keto-PGF1 alpha, respectively, were unaffected by administration of SQ29,548. However, stenosed vascular segments of the left anterior descending coronary artery (LAD) of SQ29,548-treated dogs produced significantly less thromboxane A2 than comparable segments from untreated dogs. Morphologic studies showed that stenosed coronary arteries in which CFVs had been abolished by either SQ29,548 or SQ28,668 had relatively few adherent platelets, whereas comparable coronary segments removed from untreated animals had relatively large, platelet-rich mural thrombi. SQ29,548 did not alter the synthesis of TxB2 by platelets. 6-keto-PGF1 alpha concentrations in the stenosed LAD and nonstenosed circumflex coronary arteries were not altered by SQ29,548 administration. These data suggest that the thromboxane A2/PGH2 receptor antagonists, SQ29,548 and SQ28,688, inhibit cyclic reductions in coronary blood flow in this model by preventing the accumulation of platelets at the site of a critical coronary arterial stenosis. The data also suggest that TxA2 is important in mediating the interaction between platelets and the constricted coronary artery that is responsible for the development and maintenance of CFVs in this experimental model.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1986

Transient myocardial ischemia: experimental echocardiographic demonstration and evaluation of myocardial contraction abnormalities.

A continuing theme in our laboratory has been the use of echocardiographically-measured systolic myocardial wall thickening to demonstrate and evaluate the consequences of regional myocardial ischemia. This presentation focuses on two areas: the immediate mechanical consequences of induced myocardial ischemia in two experimental models: canine and human; the correlation between persistent regional myocardial dysfunction and morphologic infarction after sequences of coronary artery occlusion and reperfusion. Many experiments using animal models have demonstrated that acute myocardial ischemia produces almost immediate replacement of normal systolic myocardial wall thickening by systolic thinning. Less is known about the immediate mechanical response of human myocardium to acute ischemia. This was studied in 5 open-chest humans undergoing various cardiac operations. Wall thickening was continuously displayed by a 7 MHz M-mode echocardiographic transducer coupled to the epicardium by suction to maintain constant position. Coronary flow velocity was displayed by a pulsed Doppler device coupled to an epicardial coronary artery by suction. Ischemia was induced by the surgeon who manually occluded the coronary artery with a soft-tipped Kitner dissector or vascular forceps for 30 seconds. It was found that cessation of coronary flow was accompanied by reductions in normal systolic thickening but systolic thinning or expansion only rarely occurred. In contrast, when the identical techniques were used in 5 dogs, systolic thinning always occurred immediately after coronary arterial occlusion. This suggests that there are important species differences between canine and human myocardium in the immediate mechanical response to myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Artifactual regional gray level variability in contrast-enhanced two-dimensional echocardiographic images: effect on measurement of the coronary perfusion bed.

The purpose of this study was to determine the extent of regional variability of image echocardiographic amplitude (expressed as gray level variability) in contrast-enhanced two-dimensional echocardiographic images, and to assess the effect of such baseline gray level variability on quantitation of the coronary perfusion bed. In 10 anesthetized closed chest dogs, short-axis papillary muscle echocardiographic images were obtained during control preinjection conditions and during injection of three contrast agents into the left main coronary artery with and without circumflex artery occlusion. Regional echocardiographic amplitude variation was measured by computer-based videodensitometric analysis of mean gray levels in four myocardial regions after cavity (background) gray level subtraction. To determine the effect of regional gray level variability on quantitation of the coronary perfusion bed, the contrast-enhanced left anterior descending artery perfusion bed was measured by two methods. The circumferential method ignored myocardial contrast inhomogeneity by measuring the circumferential extent of contrast enhancement, whether or not the enhancement by contrast medium extended transmurally. The exact method measured only the area of myocardium actually enhanced by contrast medium, which often did not extend transmurally. The perfusion beds determined by the two echocardiographic methods were compared with the anatomic perfusion bed determined by postmortem barium-gelatin coronary arteriography. Regional gray levels varied qualitatively and quantitatively in the control state (before contrast injection), with lateral regions being less bright than axial regions. After injection of contrast medium, brightness increased in all regions, the axial regions brightening most.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Host DNA replication forks are not preferred targets for bacteriophage Mu transposition.

Bacteriophage Mu DNA integration in Escherichia coli strains infected after alignment of chromosomal replication was analyzed by a sandwich hybridization assay. The results indicated that Mu integrated into chromosomal segments at various distances from oriC with similar kinetics. In an extension of these studies, various Hfr strains were infected after alignment of chromosomal replication, and Mu transposition was shut down early after infection. The positions of integrated Mu copies were inferred from the transfer kinetics of Mu to an F- strain. Our analysis indicated that the location of Mu DNA in the host chromosome was not dependent on the positions of host replication forks at the time of infection. However, the procedure for aligning chromosomal replication affected DNA transfer by various Hfr strains differently, and this effect could account for prior results suggesting preferential integration of Mu at host replication forks.

Amino Acids↗
PubMed1985

Echocardiographically detected dyskinesis, myocardial infarct size, and coronary risk region relationships in reperfused canine myocardium.

After permanent coronary artery occlusion, the extent of two-dimensional echocardiographically detected dyskinesis correlates well with infarct size. Reperfusion after coronary artery occlusion decreases infarct size; however, contractile function of myocardium salvaged in this way may remain depressed for several weeks. The purpose of this study was to explore the relationship between echocardiographically detected dyskinesis and infarct size in reperfused myocardium. We hypothesized that after transient coronary artery occlusion, the relationship between dyskinesis and infarct size would be altered because of the prolonged depression of contractile function after reperfusion so that dyskinesis would not predict infarct size. We also wanted to explore two related questions: (1) Does inotropic stimulation of reperfused myocardium result in improved systolic function in segments that are dysfunctional but not necrotic? (2) Does the relationship between infarct size and coronary risk region, which is linear in myocardium subjected to permanent coronary occlusion, remain linear in myocardium subjected to a sequence of occlusion and reperfusion? Thirty-seven sedated dogs with preplaced circumflex occluders underwent 1 or 2 hr of coronary artery occlusion, then 2 or 10 days of reperfusion. The percentage of the left ventricle that was dyskinetic was estimated from short-axis two-dimensional echocardiograms at the chordal and papillary muscle level obtained at control, after 1 or 2 hr of occlusion, after 20 min of reperfusion, and after 2 or 10 days of reperfusion. At 2 or 10 days of reperfusion, echocardiograms were also obtained during infusion of dobutamine. Area at risk was determined from postmortem barium-gelatin angiography and infarct size was determined at pathologic examination. We found a significant linear correlation between infarct size and risk region size in reperfused myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗