摘要:

The pathogenesis of histamine-induced coronary spasm was examined angiographically and morphometrically in Gbttingen miniature pigs. In five of 36 consecutive pigs that were 4 to 5 months of age, coronary spasm was provoked by the intracoronary administration of histamine, and the left coronary arteries were examined histologically without endothelial denudation (group 1). Endothelial balloon denudation of the major branch of the left coronary artery was performed in 31 of 36 pigs and five died during the procedure. The remaining 26 pigs were randomly allotted to one of two groups, one fed a cholesterol-supplemented (group 2, n = 13) and one fed a regular low-cholesterol diet (group 3, n = 13). After 3 months, serum cholesterol increased significantly from 57 ± 6 to 222 ± 27 mg/dl (p < .01) in group 2, but remained unchanged (48 + 5 to 55 6 mg/dl) in group 3. Percent narrowing of the coronary diameter induced by 10 μ/kg ic histamine after administration of the H2 blocker cimetidine (60 mg/kg iv) was 39 ± 3% and 24 ± 2% (p < .05 between groups 2 and 3) at the nondenuded site and 78 ± 3% and 74 ± 4% at the denuded site in groups 2 and 3, respectively (p < .01 between nondenuded and denuded sites). Histamine-induced percent narrowing of the coronary diameter after cimetidine in group 1, 2, and 3 pigs correlated well with the degree of intimal thickness on an exponential curve (r = .92, p < .001). Since percent narrowing at the intact site was 27% (n = 19) in all three groups, predicted histamine-induced percent narrowing at the spastic site, applying the geometric theory, was 33 ± 3%. Accordingly, enhanced constriction of the coronary artery with intimal thickening in response to histamine can largely be explained by the acquired hyperresponsiveness of the vascular wall to autacoids. This phenomena, not related to the level of serum cholesterol, may be uniquely linked to the basic pathology of evolution of atherosclerosis.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The existence of significant synergism between tissue-type plasminogen activator (t-PA) and single-chain urokinase-type plasminogen activator (scu-PA), and between t-PA and urokinase in thrombolysis in vivo is described. In a quantitative preparation of thrombolysis, consisting of rabbits in which a blood clot was induced in the jugular vein with125I-labeled fibrin, intravenous infusion over 4 hr of t-PA, scu-PA, or urokinase in amounts of 0.5, 1.0, or 2.0 mg/kg body weight resulted in significant thrombolysis (30% to 60%). The simultaneous infusion of t-PA and scu-PA or of t-PA and urokinase had a significantly greater (p < .001) thrombolytic effect than could be anticipated on the basis of the added effects of each agents alone. However, no synergism was observed between scu-PA and urokinase. The observed a2-antiplasmin consumption and fibrinogen breakdown after urokinase at higher doses did not occur with the equivalent thrombolytic combinations of t-PA and urokinase. The combined use of synergic thrombolytic agents in patients may permit a significant reduction in total administered doses, probably with elimination of the systemic activation of the fibrinolytic system and the concomitant fibrinogen breakdown that is unavoidable with the currently used thrombolytic doses of each agent.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Although augmentation of flow does not improve the performance of normal myocardium, the hyperemic response after brief coronary occlusion is associated with transient hyperfunction in the previously ischemic region. In this study we assessed the effect of vasodilator-enhanced coronary blood flow on the systolic function of postischemic stunned myocardium. In 18 open-chest, anesthetized dogs the anterior descending artery was occluded for 5 min, followed by a 10 min period of reflow, repeated 12 times with a final 90 min recovery period. After the recovery period, either 0.06 mg/min dipyridamole (n = 6), 1 mg/min papaverine (n = 6), or 1.5 μ/kg/min nitroglycerin (n = 6) was infused intravenously for 15 min. Regional myocardial blood flow, which had returned to normal before administration of vasodilator, was increased 150% above baseline by dipyridamole and 80% by papaverine, but was unchanged by nitroglycerin. Segmental shortening decreased after repeated occlusions: from 17.5% to 0.9% in the group later treated with dipyridamole, from 18.6% to 6.7% in the papaverine group, and from 19.2% to - 1.9% in the nitroglycerin group (p < .005 for all groups). Segmental shortening increased to 8.8% after dipyridamole, 13.6% after papaverine, and 5. 1% after nitroglycerin (p < .05 for all groups), although the load-independent end-systolic pressure-length relationship (ESPLR) showed a significant shift to the left, reflecting enhanced performance, only after dipyridamole and papaverine. For all dogs combined, the percent improvement in ESPLR was correlated with the percent increase in flow (R = -.73, p < .001). Performance was unchanged in the control region despite similar augmentation of flow. This study demonstrates that the function of postischemic myocardium can be selectively enhanced by augmentation of coronary blood flow to levels greater than normal.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

To evaluate the potential advantages of thallium-201 (201T1) single-photon emission computerized tomography (SPECT) to assess myocardial infarct size in the experimental animal, six normal dogs and 14 dogs with 6 to 8 hr closed-chest coronary occlusion (eight left anterior descending and six left circumflex) were studied. Ten minutes after intravenous administration of 2 mCi of201T1, 30 projections were obtained over 180 degrees. The dogs were killed and their hearts sliced and stained by triphenyl tetrazolium chloride (TTC). Pathologic infarct size was calculated for each slice and for the entire left ventricular myocardium as percent weight. Tomograms were quantified by automatically generating maximum-count circumferential profiles, which were compared with normal limit profiles derived from the six normal dogs. Tomographic infarct size was defined as the percentage of circumferential points falling below normal for each tomogram. SPECT and TTC infarct size on 71 slices correlated highly (mean SD 27.9 ± 23.4% and 26.7 25.3%, respectively; r = .93, p < .001, SEE = 9.4%). To determine SPECT infarct size as percent total left ventricular myocardial weight, infarct sizes from each slice were added to one another after each was multiplied by a coefficient that reflected the contribution of that slice to the total left ventricular weight. SPECT and TTC infarct size for the entire left ventricle correlated closely (mean ± SD 20.5 ± 7.6% and 19.3 ± 8.3%, respectively; r = .86, p < .001, SEE = 4.5%). It is concluded that 201T1 SPECT is a valid method for the noninvasive assessment of experimental myocardial infarct size.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

To guide surgical therapy for ventricular tachycardia by preoperative endocardial catheter mapping, accurate anatomic localization of arrhythmogenic sites is mandatory. For this reason we developed a mathematical cineradiographic method to compute left ventricular sites relative to three anatomic reference points: the centers of aortic and mitral valve ostia and the left ventricular apex. To validate the method 14 epicardial left ventricular markers were implanted in four dogs to simulate arrhythmogenic sites. Distances between markers and the anatomic references were calculated and the results were compared with postmortem measurements. The difference between calculated and measured distances was 0.5 ± 3. 1 mm (mean ± SD), confirming accurate localization of anatomic marker sites. However, in surgery the results have to be displayed in a practically applicable, unambiguous way. Therefore, wire skeletons were constructed to represent calculated endocardial marker sites relative to the anatomic reference points. To validate this approach, 14 markers were implanted in the left ventricular subendocardium in four dogs. Wire skeletons were constructed, one for each marker site, and inserted postmortem into the left ventricular cavity via a 2 cm incision. In all cases the correct indication of a marker site by the corresponding wire skeleton was confirmed by fluoroscopic inspection in multiple projections. This wire skeleton technique may enhance the practical usefulness of preoperative endocardial catheter mapping.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Postganglionic stimulation of vagal terminals (PGVS) in the isolated rabbit heart atrioventricular (AV) node was used to study the effects of cholinergic influence on AV nodal conduction. Standard microelectrode techniques were used to record action potentials, predominantly from cells located in the N region of the AV node. In addition, programmed stimulation was used in conjunction with PGVS to initiate or terminate AVN reentry. The introduction of a single short burst of PGVS (total duration 50 to 100 msec, impulse duration 1 msec, and interimpulse interval 6 msec) with subthreshold amplitude for AV node fibers caused reproducible disorganization of the prevailing excitation front. This was manifest as local nonuniform depression of conduction, hump formations in the action potentials, and alteration in the sequence of depolarization. The introduction of repetitive bursts of PGVS revealed a triphasic time course of changes in AV nodal conduction time, representing initial maximal prolongation, relative shortening, and secondary inhibition. It was found that these phases corresponded to vagally induced initial disorganization and a subsequent rebound process. Vagally induced disorganization of the sequence of action potential depolarization was also a triggering mechanism for concealed as well as manifest AV nodal reentry. In the latter case the reentry circuit usually involved the AN region and perinodal atrial tissue. PGVS-induced depression of the N region was also able to block the retrograde wavefront, thereby terminating reentry. The possible relationship of PGVS-induced disorganization of conduction and the inhomogeneous structure of AV node are discussed. The present results provide additional information for better understanding of the AV nodal conduction abnormalities observed clinically and particularly those related to AV node-vagus interaction.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Doxorubicin, in concentrations that have no effect on fast or slow response action potentials, has been shown to suppress ouabain-induced delayed afterdepolarizations. In this study, we used standard microelectrode techniques to determine the effects of doxorubicin on isolated canine Purkinje fibers. We studied automaticity induced at normal and low membrane potentials, conduction in normal and K'-depolarized Purkinje fibers, and triggered activity induced by ouabain and by experimental myocardial infarction. Doxorubicin, 50, μM, suppressed the triggered activity and the delayed afterdepolarizations that induced it, but had no effect on the other variables. We then studied the effects of intravenous doxorubicin, 16 to 64 mg/m2 body surface area, on ouabain-induced ventricular tachycardia and the ventricular tachycardia that occurs 24 hr after ligation of the left anterior descending coronary artery in the intact dog. There was no effect on the infarct-induced arrhythmia, but concentrations of doxorubicin that had no other effect on the electrocardiogram suppressed those ouabain-induced arrhythmias that appeared to have been triggered. The automatic arrhythmias induced by ouabain were not affected. Both the latter mechanisms were verified in studies of isolated Purkinje fibers that were obtained on completion of the intact animal experiments. These results indicate that agents having high selectivity for specific arrhythmogenic mechanisms can be useful adjuncts in discriminating among the mechanisms responsible for arrhythmias in intact animals.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Precise determination of left and right ventricular stroke volumes is limited with conventional imaging techniques. We determined whether right and left ventricular stroke volumes could be precisely measured with cine computed tomography (CT). Cine CT enables simultaneous imaging of the right and left ventricles at an 8 mm slice thickness with a maximal scanning rate of 17 frames/sec (50 msec acquisition intervals). In eight dogs, true right ventricular and left ventricular stroke volumes were determined by dividing thermodilution cardiac output by heart rate and/or with the use of an aortic electromagnetic flow probe implanted over a long term. After at least 5 sec of suspended respiration, cine CT images were acquired during central venous injection of a nonionic contrast agent. Multiple perturbations in stroke volume were induced in each dog by the administration of dobutamine, sodium pentobarbital, or sodium nitroprusside or by coronary artery occlusion. Right and left ventricular stroke volumes were obtained by Simpson's reconstruction of end-diastolic and end-systolic short-axis tomograms from apex to base. The cine CT left ventricular stroke volume (range 1 1 to 45 ml) correlated highly with the true left ventricular stroke volume (r = .99, slope - 1.01, y intercept = - 0.2 ml, SEE = 1.5 ml, n = 25). The cine CT right ventricular stroke volume (range 11 to 34 ml) also correlated highly with the true right ventricular stroke volume (r - .98, slope = 0.9, y intercept = 2.2 ml, SEE = 1.7 ml, n = 15). In 12 studies, the mean difference between nearly simultaneous right and left ventricular stroke volumes by cine CT was 1.1 ml (range 0.1 to 3.2 ml). Calculation of right and left ventricular stroke volumes from data from cine CT were highly reproducible. Intraobserver variability in measurements of right ventricular stroke volume (r = 1.0, slope = 0.99, y intercept = 0. 19 ml) and left ventricular stroke volume (r 1.0, slope = 1.02, y intercept = - 0.21 ml) was minimal. Interobserver variability in measurements of right ventricular stroke volume (r = .98, slope = 0.90, y intercept = 1.66 ml) and left ventricular stroke volume (r - .99, slope = 0.97, y intercept = - 0.02 ml) was likewise minimal. Thus, precise and highly reproducible measurements of right and left ventricular stroke volumes can be obtained with cine CT.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Postsystolic myocardial segment shortening (PSS) has been observed in dogs and humans by means of ultrasonic crystals but has never been studied specifically. In this study, both subendocardial and subepicardial regional function in the basal circumflex and midventricular anterior myocardium (LAD) was studied during late systole and early diastole with ultrasonic crystals. Fifteen open-chest dogs were instrumented with electrocardiographic leads; Millar catheters for measurement of left ventricular pressure, left ventricular dP/dt, and aortic blood pressure; flow probes for determination of aortic and mitral blood flow; and subendocardial and subepicardial crystal pairs to measure subendocardial segment length shortening velocity (dL/dt). Crystal pairs were placed in the subendocardial left oblique mode and the extreme subendocardial right oblique mode (-50 and + 50 degrees from equator) in the lateral basal (circumflex, n = 9) and anterior midventricular myocardium (LAD, n = 6). Subendocardial segments showed PSS averaging 34 7% of the total shortening distance in the circumflex bed and 21 ± 2% in the LAD bed (p = NS). The rate of subendocardial segment shortening during PSS increased 273 42.6% (p < .05) relative to the rate of segment shortening during ejection in the circumflex bed and 126 40% (p < .05) in the LAD bed (p = NS). The most rapid diastolic increase in subendocardial length (peak + dL/dt) occurred immediately after subendocardial PSS. Subendocardial diastolic peak + dL/dt occurred after the onset of mitral inflow during the acceleration limb of the rapid ventricular filling phase. Overlying subepicardial segments began lengthening 82 ± 12 msec before onset of subendocardial segment lengthening in the circumflex bed and 63 ± 9 msec before subendocardial lengthening in the LAD bed (p < .05), indicating that the subepicardial segment had begun to lengthen while subendocardial segment shortening continued after end-systole. Onset of early segmental subepicardial lengthening varied with respect to the point of endsystole. Early segmental subepicardial lengthening with subendocardial PSS may be a mechanism by which the rapid filling phase of the left ventricle is actively potentiated by storing potential energy released as early diastolic elastic recoil.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID