ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The effects of lidocaine and quinidine on rabbit cardiac Purkinje fibers were compared at 37 °C, using action potential and voltage clamp measurements. At therapeutic concentrations (5 μg/ml), lidocaine shortened the duration of the action potential while quinidine lengthened it. When membrane potential was held constant between −151;40 and −151;50 mV by the application of the two-microelectrode voltage clamp, holding current consistently became more outward with lidocaine (+2.3 ± 0.7 nA, mean ± SEM,n= 5), but it either did not change or became more inward with quinidine (−2.1 ± 1.4 nA,n= 5). Both drugs reduced the outward tails generally associated with deactivation of the delayed rectifier current, ix. The depression of delayed rectification by quinidine (−151;68 ± 6%,n= 5) was greater than that produced by lidocaine (−151;12 ± 4%,n= 5), and can explain the observed prolongation of the action potential. To evaluate the possibility that lidocaine blocks steady state sodium channels, experiments were performed with tetrodotoxin (TTX), a specific blocker of sodium channels in a variety of excitable membranes. TTX at concentrations of 0.1–5 μM shortened the action potential, reducing its duration to 50% of control at 1.6 μM. Voltage clamp experiments revealed a small TTX-sensitive component of steady state current flowing at membrane potentials positive to −151;80 mV. In the presence of 10 μM TTX, lidocaine failed to produce additional steady outward membrane current. These data suggest that (1) lidocaine and quinidine differ substantially in their modification of membrane channels, with quinidine having a strong effect on delayed rectification, (2) a TTX-sensitive “window” current exists in the rabbit Purkinje fiber and helps maintain the action potential plateau, and (3) the effect of lidocaine on the cardiac action potential results primarily from block of TTX-sensitive sodium channels, rather than from an enhancement of potassium conductance.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

This study was undertaken to determine whether coronary blood flow can be regulated in response to coronary arterial occlusions briefer than a single diastole. The possible involvement of metabolic vs. myogenic mechanisms in such regulation was investigated. Eleven conscious dogs with experimentally produced complete heart block, chronically implanted electromagnetic flow probes, and pneumatic occluders on the left circumflex coronary artery were studied. Diastolic coronary occlusions lasting 100 to 400 msec were performed at paced heart rates of 40, 60, and 120 beats/min. At a heart rate of 60 beats/min, a 200-msec occlusion was sufficiently long to produce a significant reactive hyperemic response; 400-msec occlusions resulted in larger responses, while 100-msec occlusions did not generate a discernible response. The onset of reactive hyperemia was delayed from the end of the occlusion until the first post-occlusion systole. The length of this delay could be altered by changing the heart rate or occlusion duration, but no significant response was detected before the first post- occlusion systole. This characteristic of the data is more consistent with a metabolic than with a myogenic mechanism. If the response is metabolic, the data demonstrate that autoregulation of coronary flow by such a mechanism is very rapid, occurring during the first systole in which a flow deficit is detected by the myocardium.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

This study was undertaken to determine if coronary blood flow can be regulated in response to a transient increase in cardiac metabolic demand. Eight conscious dogs with experimentally produced complete heart block, a chronically implanted electromagnetic flow probe on the left circum- flex coronary artery, and fluid-filled catheters for measurement of left ventricular and aortic pressures were studied. At a paced heart rate of 60 beats/min, a single ventricular extra-stimulus was introduced with a delay of 150–200 msec from the preceding R-wave. The extra-stimulus produced a ventricular extra-activation, but not a discrete mechanical extra-systole. The ensuing beats exhibited systolic potentiation, manifest by a 50 ± 8% increase from control in maximum left ventricular dp/dt in the first potentiated beat, presumably accompanied by increased myocardial oxygen demand. In the diastole immediately following the first potentiated systole, the coronary vascular resistance index (mean aortic pressure/mean coronary flow in that diastole) fell significantly from control by 12 ± 2%. The results indicate that a transient increase in cardiac metabolic demand is followed immediately by a compensatory coronary vasodilation that occurs within the same cardiac cycle.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Body surface potential maps of human His bundle activity have been difficult to produce for two reasons: (1) The peak surface potentials are often less than 5 μv, and (2) the simultaneous atrial repolarization potentials frequently exceed 100 μv. We have therefore amplified surface signals 25 times the standard gain of 1000, and then removed by cross-correlation the static pattern of atrial repolarization for serial 1-msec maps of the P-R segment in five normal men. A consistent finding emerged: a positive anterior chest peak appeared 40 msec before QRS onset, and then-within 10 msec-spread out into a long, low transverse mound before disappearing in 5 more msec. The map data were analytically converted to serial electrical sources: the center of electrical activity moved first slightly down, then directly forward, before retracing its path and disappearing. The retrace and accompanying surface spread-out strongly suggests diverging dipolar sources. Thus the data fit a simple heart source which moves anteriorly and then breaks into two (right and left)-as expected from activation of the bundle of His and its bifurcation into left and right bundle branches.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Impaired coronary reserve in animals and patients with left ventricular hypertrophy (LVH) might be expected to augment infarct size following coronary occlusion (CO). To test this hypothesis, the circumflex coronary artery was acutely occluded in 30 control dogs and in 28 renal hypertensive (HT)-LVH dogs during the conscious state. Hemodynamics and regional myocardial flow (microspheres) were measured. After 48 hours of CO, we assessed infarct size pathologically and area at risk by postmortem coronary angiography. Mean arterial pressure (130 ± 5 mm Hg) and LV:body weight ratio (6.1 ± 0.1 g/kg) in HT-LVH dogs were about 35% greater than in control dogs (P< 0.05). During the 48 hours following CO, mortality rate was markedly increased in HT-LVH (54%) compared to control (17%) (P< 0.01). We performed a linear regression analysis of the relationship between area at risk (AR; % of LV mass) and infarct size (IS; % of LV mass); control, IS = 1.20AR - 25.6 (r = 0.96); HT-LVH, IS = 1.19AR - 16.3* (r= 0.95) (*P< 0.05 vs. control). Although the slopes of these relationships were similar, the intercepts were different. Consequently, the minimal AR associated with infarction was 35% smaller in HT-LVH (15 ± 2% of LV mass) than in control (22 ± 1%), and over the entire range of AR, the IS was increased in HT-LVH. The distance between the lateral extent of infarct size and area at risk in different layers of LV was measured. The increase in infarct size in the HT-LVH group reflected primarily an increase in midwall layer infarction. Increase in collateral flow to the risk area was attenuated in HT-LVH. In conclusion, infarct size relative to the area at risk is increased significantly in HT-LVH. This interaction between LVH and myocardial ischemia may significantly influence the outcome of myocardial infarction in patients with hypertension and LVH.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The sum of total left ventricular heat loss and left ventricular mean total external power was compared with the product of oxygen consumption and its energy equivalent. Myocardial blood flow, measured with 15 ± 3 μm radioactive microspheres, was multiplied by the transcoronary arteriovenous temperature difference and by oxygen content difference to obtain coronary heat loss and oxygen consumption, respectively. Since only part of the heat is carried away by the coronary system, a thermodilution technique was used to obtain the ratio between the heat removed by the coronary system and the external heat loss. A correction was made for the endothermic reactions of hemoglobin deoxygenation and carbon dioxide reactions with blood. Left ventricular oxygen consumption corresponded to 2.26 ± 0.66 W/100 g, and for the sum of total left ventricular heat loss and external power, 2.09 ± 0.51 W/100 g was found (n = 14). In a second series, the measured transmyocardial temperature distribution was compared with the calculated temperature distribution, assuming that heat production in the myocardium is uniform and that heat is lost by coronary flow and diffusion. When thoracic and luminal myocardial surface temperatures were about equal, blood flow was found to be about the same in the various layers of the heart, whereas myocardial temperature was found to be highest near the middle of the wall (0.36 ± 0.07 °C warmer than luminal temperature (n = 6)). When thoracic surface temperature was increased or decreased (by +1.56 ± 0.99°C and −1.10 ± 0.59°C, respectively), consistent changes were seen for the temperature distribution in the myocardium, but not for the local flow (endo/epi ratio: 1.06 ± 0.29 and 0.96 ± 0.21, respectively). These data suggest that myocardial blood flow is independent of tissue temperature.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The power output of the left ventricle as measured by the product of the Fourier components of aortic pressure and aortic flow is linked by definition to the arterial impedance facing the heart as measured by the quotient of these components. Consequently, the use of power measurements to assess ventricular performance can be ambiguous when accompanied by afterload changes. The heart is considered to function normally between two extremes, a constant flow pump, and a constant pressure pump, and two power limits are defined from these. The power limits describe the extent to which impedance changes can affect the power delivered by the left ventricle. Measured power changes that are found to lie outside the two limits can be unambiguously ascribed to changes in inotropic state. The results from preliminary dog experiments designed to test this method are reported. Cardiac sympathetic stimulation and isoprenaline infusion were used to provide a pure inotropic stimulus and a mixture of inotropic and afterload changes, respectively. The technique was able to detect inotropic changes in the heart even in the presence of simultaneous changes in afterload. Eight conventional indices of cardiac performance were monitored for comparison. The extent of their afterload dependence may not be as easily quantified.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

By using excised postmortem hearts obtained from 15 mongrel dogs with the pericardium intact, we investigated mechanical interactions between the four heart chambers from the standpoint of ventricular pressure-volume relationships. The interactions investigated were those between (1) the atrium and the ventricle, (2) the right ventricle and left ventricles, (3) the atrium and one ventricle vs. the other ventricle, and finally (4) the left and right atrium and the right ventricle vs. the left ventricle. For these purposes, we inserted compliant balloons into the four heart chambers without injuring the pericardium, i.e., we incised the base of the atria which was not covered with the pericardium. We obtained the right and/or left ventricular pressure-volume relationships under a constant pressure in three other heart chambers by changing the height of the reservoir connected to each balloon. As a result, both ventricular pressure-volume relationships were hardly affected by an increase in the atrial pressure ranging from 5 to 30 cm H2O with the pericardium removed, although the ventricle became less compliant due to an increase of the same magnitude of the opposite ventricular pressure. On the other hand, the effect of an increase in atrial pressure was distinct with the pericardium intact. Also, all mechanical interactions were enhanced dramatically with the intact pericardium. Thus, the pericardium plays an important role in these mechanical interactions, especially when the filling pressures of all heart chambers increase simultaneously. Clinically, these findings may be important to understanding ventricular functions as related to various heart disease--especially acute heart failure.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Proliferating nonmyocardial cells (NMCs) complicate primary heart cultures and may influence myocardial cell (MC) differentiation. In cultures from the day-old rat ventricle, we validated a method to arrest this proliferation; and we quantitated cross-striated cells and the chronotropic response to isoproterenol to assess MC differentiation. MCs were cultured at single cell density using an improved method. By 4 days, all cells could be identified as MCs or NMCs. In cultures treated for 3 days with bromodeoxyuridine (BrdU), 0.1 miw, serial cell counts were unchanged through 11 days. Among 50,000 cells from 110 cultures, 75–80% were MCs. In control cultures without BrdU, NMC density was 3- and 6-fold that in BrdU-treated cultures at days 5 and 8, respectively (P< 0.01), although the MCs were not overgrown. The MCs did not proliferate in either culture. The proportion of living MCs with cross-striations was similar in treated and control cultures at day 5 (72.6% vs. 69.9%, P > 0.05) but was lower in controls at day 8 (86.3% vs. 50.4%,P< 0.01). A sensitive (ED5010–100 pM), specific chronotropic response to L-isoproterenol was present in both treated and control cultures, but the maximum response was only 20–30% as great in controls on days 4 and 8 (P< 0.01). Baseline beating rates were the same. The MCs had well-differentiated ultrastructure, including a T system. By autoradiography, a maximum 18.4% of MCs had nuclear incorporation of3H-BrdU at day 8. Media conditioned by NMCs or by the control cultures did not change the cross-striations or isoproterenol response of BrdU-treated cultures. Thus, in a new culture preparation with few and stable NMCs, morphological and functional MC characteristics were different from those of MCs in cultures with proliferating NMCs. We suggest that an MC-NMC interaction can alter MC properties and that this effect should be considered in studies of primary rat heart cultures. The pure, stable, well-differentiated MCs in BrdU- treated cultures will be useful for studying MC growth, repair, and other time-dependent phenomena.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID