摘要:

Recovery cycles following premature atrial stimulation introduced during atrial pacing may fall into four categories: reset, incomplete interpolation, complete interpolation, and echo re-sponses. It has been postulated that the transition from reset to incomplete interpolation may represent the point at which premature beats can no longer enter the sinus node and reset it and thus reflect the refractory period of the sinus node. The purpose of this study was to explore the electrophysiological basis underlying the transition from reset to incomplete interpolation and. to assess the spatial orientation of refractoriness in the sinus node. In 15 rabbit sinus node preparations, premature atrial stimuli were introduced at varying degrees of prematurity while intracellular potentials were recorded with a microelectrode in the sinus node. In 12 of 15 experiments, transition from reset to incomplete interpolation immediately followed a sudden reduction in action potential amplitude, rendering the action potential incapable of resetting the node. This point was interpreted as the effective refractory period of the sinus node. During the zone of incomplete interpolation, low voltage depolarizations were seen in the node, interfering with diastolic depolarization and delaying the recovery beat. These small depolarizations were absent during the zone of complete interpolation. In six experiments, the micro-electrode was moved toward the crista terminalis in steps of 50 to 100 /im, and the stimulation sequence at each site was repeated. By examining relative action potential amplitude at various sites at the same premature interval, it was possible for us to construct curves showing the pattern of block of premature impulses. We found that progressively earlier premature beats are blocked at progressively greater distances from the node. Therefore, tissue between the crista terminalis and the sinus node provides a progressive gradation of refractoriness, rather than a discrete barrier.Circ Res 47: 742-756, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Prostacyclin (PGI2) and some of its major breakdown products (6-keto-PGFi,6-keto-PGEi, and 13,14-dihydro 6,15-diketo-PGFia) were studied in an isolated perfused cat heart preparation during myocardial ischemia. At an infusion rate of 10 ng/g heart weight per minute, PGI2and the related compounds caused no changes in perfusion pressure, contractile force (CF), the first derivative of the contractile force (dF/dt), and heart rate in control hearts perfused at coronary flows of 20-35 ml/min. Induction of global ischemia by perfusion at 0.6 to 0.7 ml/min for 120 minutes resulted in a significant release of creatine kinase (CK) activity and compounds having a free amino-nitrogen group into the perfusate. Ischemic hearts exhibited an increase in resting tension of 2.3 ± 0.2 g, mean ± SEM. Upon reperfusion, untreated ischemic hearts showed a partial restoration of mechanical performance, CF = 43 ± 5%, and dF/dt = 40 ± 5% of control. PGI2infusion inhibited the ischemic-induced CK release and the increase in perfusate amino-nitrogen concentration. Resting tension also remained low (i.e., 0.8 ± 0.1 g). Recovery of CF and dF/dt upon reperfusion was significantly higher (86 ± 8% and 88 ± 10%, respectively) than in the untreated ischemia group. Myocardial CK activity was significantly higher in PGI2-infused hearts (35.8 ± 2.6 IU/mg protein) compared to those infused with its vehicle (26.3 ± 2.8,P< 0.01).'Breakdown products of PGI2only slightly protected against ischemia. PGI2is beneficial in myocardial ischemia in vitro, even without its well known action preventing platelet aggregation and independent of its induction of coronary vasodilation.CircRes 47: 757-763, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Taurine (2-aminoethane sulfonic acid) is found in high concentrations in the heart, particularly in Purkinje fibers. We studied the transport of taurine in Purkinje fibers that were excised rapidly from the heart and placed in a vessel containing oxygenated Krebs-Henseleit solution (37 °C). After equilibration, 4.4X10−6M radiolabeled taurine[MC] was added to the bath. A computer compart-mental analysis of the uptake and efflux indicated the presence of two pools for uptake—a pool with a rapid kinetics Ki (ti/2= 0.80 min) and K2(t|/2= 176.30 min). These studies suggest that Purkinje fibers have the capacity to transport taurine rapidly. Michaelis-Menten procedures showed the presence of a high affinity and a low affinity transport process. Guanidinotaurine, at a 10:1 ratio, had no appreciable effect on taurine uptake, but 3-aminopropane phosphonic acid decreased taurine uptake by 42.7%. Ouabain and acetylstrophanthidin (10−5M) inhibited taurine uptake (Ki) by 34% and 73%, respectively. The inhibition of the rapid component of taurine uptake suggests that Ki is an energy-linked process possibly requiring Na+,K+-ATPase. Taurine uptake in a calcium-free medium was decreased by 58%. Verapamil (6 x 10"6M) decreased taurine uptake by 42%. Tetrodotoxin (3.4 x 10"5M) decreased taurine uptake by 51%. The requirement of calcium and sodium for taurine uptake suggests an important relationship between taurine, calcium, and sodium in the function of fibers in the cardiac conducting system.Circ Res 47: 763-769, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Rat portal veins were maintained in organ culture to study the development of charac-teristic denervation changes and a possible trophic effect of the neurotransmitter norepinephrine (NE). Vessels maintained in organ culture for 2 days showed supersensitivity to NE and Ba2+, a more rapid rate of relaxation from a Ba2+contracture, and partial depolarization of the myovascular cells. All of these changes except the quicker relaxation from Ba2+contracture could be prevented by incubating the preparations in a NE-containing medium. This evidence suggests that functional changes in vascular muscle cells are caused by the removal of a trophic influence of NE, but can be prevented by NE replacement. However, the failure of NE in the culture media to prevent the increased rate of relaxation from Ba2+contracture found after 2 days in organ culture suggests that NE is not the only trophic influence acting on the portal vein. In addition, incubation of veins in a NE-containing medium produced a marked subsensitivity to the contractile effects of NE, but not Ba2+, and thus possible desensitization of noradrenergic receptors. The data thus support a trophic role for NE in the rat portal vein.Circ Res 47: 770-775, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

In an attempt to understand the way automatic cells in the sinus node (SN) control the cardiac rhythm, we studied extracellular electrograms recorded from the SN region in conscious dogs. A SN electrode, containing 48 silver terminals arranged 1.5 mm apart, was implanted over the node, and an indifferent electrode was implanted on the superior vena cava. Through terminals of the SN electrode paired with the vena caval electrode, "unipolar" electrograms were recorded at 100 /iV/cm and with a time constant of 0.1 second. Low amplitude and low frequency deflections (dV/dt ⩽ 20 mV/ sec) which resulted from electrical activity of the node could be differentiated from the more rapid deflections due to atrial electrical activity. Electrical activity due to the inherent automaticity of what appeared to be groups of automatic cells was recognized as a slow negative-going diastolic slope followed by a slow negative-going, or negative and then positive-going, SN potential. Impulse propa-gation toward the SN electrode terminal in groups of automatic cells appeared as a slow positive-going deflection interrupting the diastolic slope. Adjacent groups of automatic cells located near the sites of earliest atrial activation discharged asynchronously before the earliest atrial activity; this suggests that multiple groups of automatic cells might initiate atrial activation. In addition to changes in rate and in location of the pacemaking groups of automatic cells, significant beat-to-beat variation in the sinoatrial interval contributed to the changes in atrial rate in "sinus arrhythmia." These studies provide a better understanding of SN function in conscious animals.Circ Res 47: 775-791, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Aortic valve leaflets undergo extraordinary flexion due to the complete reversal of their curvature during billions of cardiac cycles. The flexion stresses in the leaflet depend on its elastic modulus which we investigated in vivo and in vitro. In six dogs, we placed radiopaque markers on an aortic leaflet. Leaflet length was calculated from the marker positions recorded fluoroscopically. Aortic and ventricular pressures were recorded. Dogs were killed and leaflet stress-strain curves determined in vitro. Leaflet length in vivo decreased 10.4 ± 4.7% from diastole to systole in each cardiac cycle. Using the law of LaPlace, pressure gradients across the leaflets were converted into the stresses in the leaflets. The leaflets had an initial "elastic phase" of low modulus in systole followed by an "inelastic phase" of high modulus in diastole. The elastic modulus was 2.4 ± 0.7 x 106dynes/cm2in systole and 5.2 ± 1.7 x 107dynes/cm2in diastole. These results were similar to those obtained in vitro. Since flexion rigidity is proportional to (elastic modulus) x (thickness)3, the lower modulus in systole greatly reduces flexion stresses in the leaflet and increases leaflet longevity. The higher elastic modulus in diastole prevents excessive bulging or prolapse of the leaflet while it is subjected to the diastolic pressure gradient. We conclude that a natural or prosthetic leaflet which is thickened or has a high elastic modulus throughout the cardiac cycle will have a greater flexion stress that could cause early failure.Circ Res 47: 792-800, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID