ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTWe studied automaticity, triggered activity, and responses to a- and β-adrenergic stimulation in subendocardial Purkinje fibers overlying healed infarct scars (infarct preparation) and from remote normal zones (noninfarct preparation) of cat left ventricles. The preparations were studied 2 to 4 months after ligation of multiple distal tributaries of the left anterior descending and circumflex arteries. Subendocardial Purkinje fibers from corresponding areas of normal hearts served as control samples (control preparation). Transmembrane action potential characteristics and rates of automaticity (spontaneous phase 4 depolarization) did not differ among control, noninfarct, and infarct preparations. However, overdrive at cycle lengths of less than 400 msec suppressed automaticity to a greater degree in Purkinje fibers of infarct preparations than those of control and noninfarct preparations. Changes in automatic rate during superfusion with isoproterenol (10-10M to 10-6M) were not different among the three groups of preparations, but exposure to phenylephrine (10-9M to 10-5M) in the presence of 5 × 10-7M propranolol reduced the automatic rate to a greater degree in Purkinje fibers of infarct preparations than those of control or noninfarct preparations. Triggered activity arising from delayed afterdepolarizations was recorded in 10 of 29 infarct preparations (34%), but not in 12 control and 10 noninfarct preparations. These afterpotentials were augmented by increasing extracellular Ca++concentration, 10-7M isoproterenol, and 10-5M phenylephrine in the presence of 5 × 10-7M propranolol. We conclude that Purkinje fibers overlying healed infarct scars have altered physiology of spontaneous automaticity, enhanced responses to a-adrenergic interventions, and a tendency to triggered activity, and that both α- and β-adrenergic effects may result in worsening of arrhythmias by augmentation of afterpotentials in healed myocardial infarction.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTWe have previously demonstrated that the beneficial effect of cardioselective 13-blockade on exercise-induced ischemia is due entirely to negative chronotropism. Therefore we studied the effect of a new bradycardiac agent (UL-FS 49) in 10 dogs with chronic coronary artery stenosis produced by an ameroid constrictor. Regional myocardial function (sonomicrometers, wall thickness) and blood flow (microspheres) were measured during a control treadmill exercise bout and an identical run 3 hr later after the administration of UL-FS 49 (1.0 mg/kg iv). In the control run, heart rate increased from 114 ± 20 to 230 ± 19 beats/min and systolic wall thickening (%WT) in the poststenotic myocardium decreased from 23.3 ± 5.2% at rest to 9.3 ± 5.0%, a 60% reduction. Subendocardial blood flow in the ischemic area decreased from 1.04 ± 0.30 to 0.55 0.40 ml/min/g, blood flow per beat decreased from 9.1 × 10-3to 2.5 × 10-3ml/g, and mean transmural flow failed to increase (1.06 + 0.30 vs 1.08 ± 0.39 ml/min/g). During exercise with UL-FS 49, heart rate increased from 89 10 to only 139 ± 10 beats/min. End-diastolic left ventricular pressure was increased compared with that during the control run (35.7 ± 3.0 vs 28.9 ± 5.5 mm Hg) but left ventricular peak systolic pressure and dP/dt were unchanged. %WT in the ischemic zone did not change significantly during exercise with UL-FS 49 (23.3 ± 7.9% at rest, 21.5 ± 8.4% during the run), and in the nonischemic zone it increased to the same extent as during the control run. Absolute subendocardial blood flow (0.75 ± 0.32 ml/min/g) and flow per beat (5.3 ± 2.0 × 10-3ml/g) were significantly increased compared with those during the control run (p > .05), and transmural blood flow per beat increased to 9.8 ± 1.7 × 10-3ml/g (p > .01). These data demonstrate that UL-FS 49 is an effective bradycardiac agent that can markedly attenuate exercise-induced ischemic dysfunction and improve regional perfusion without compromising contractile function of nonischemic areas or global left ventricular contractility.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

ABSTRACTWe studied the effects of the pericardium on diastolic left coronary pressure-flow relationships in heart-blocked and isolated canine preparations. In these preparations, the left and right coronary arteries were dilated with adenosine and perfused by means of a pressurized arterial reservoir. The diastolic left heart pressure (LHP) was controlled by the height of a reservoir connected to the left atrium and left ventricle. The right atrial and ventricular pressure i.e., coronary outflow pressure, was kept constant at 0 mm Hg. Before and after pericardiectomy, diastolic coronary pressure-flow relationships were obtained at three values of LHP (0, 15, and 30 mm Hg) with driving pressure decreasing (2 mm Hg/sec or less) from approximately 60 mm Hg to the actual zero-flow pressure (Pf = 0) during a single long diastole induced by cessation of ventricular pacing. The slopes of the coronary pressureflow relationships were approximated by a linear regression analysis in which the correlation coefficients were greater than .98 in all cases. Before pericardiectomy, with LHP increasing from 0 to 15 and 30 mm Hg, the value of Pf = 0 significantly increased from 7 + 1 to 16 ± 1 (p > .01) and 28 + 2 mm Hg (p > .01 ), respectively. After pericardiectomy, it increased from 7 + 1 to 14 + 1 (p > .01 ) and 17 ± 2 mm Hg (p > .01), respectively. When LHP was at 0 and 15 mm Hg, the pericardiectomy had no effect on the value of Pf = 0. However, pericardiectomy lowered the value of Pf = 0 (p > .01) when LHP was at 30 mm Hg. On the other hand, the slopes of the regression lines were not significantly changed by either an increase in LHP or by pericardiectomy. From these results, we conclude that the pericardium plays an important role in regulating the coronary circulation by changing the effective back pressure, i.e., Pf = 0, when the intracardiac pressure increases beyond a certain degree.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID