摘要:

Thirteen dogs in whom at least one morphologically distinct sustained ventricular tachycardia (VT) could be reproducibly initiated by programmed cardiac stimulation 18 ± 3 days following experimental myocardial infarction were placed on total cardiopulmonary by pass for detailed study of the endocardial and epicardial activation during VT under hemodynamically stable conditions. Thirteen morphologically distinct monomorphic VTs were investigated by simultaneous epicardial, endocardial, and intramural bipolar recordings. Local electrograms were used to generate computer-assisted isochronous-activation sequence maps. A complete reentry circuit could be mapped on the epicardial surface in 4 animals and on the endocardial surface in one other animal. In the remaining 8 animals, there was a gap period lasting 43–62 msec in the cardiac cycle during which no endocardial or epicardial activity was observed. In 6 of the 8 animals, bipolar intramural recordings from sites closely associated with regions of endocardial and epicardial conduction block showed intramural activity progressing slowly during the gap period. In these 6 animals, a reentry circuit could be completed by incorporating the local electrograms recorded from the intramural sites. VT could be reproducibly terminated by selectively rendering only these intramural sites refractory by critically timed extrastimuli that failed to result in global ventricular capture. VT could be terminated by epicardial cooling in 2 of the 4 animals with epicardial reentry. By contrast, epicardial cryoablation did not effect intramural reentry and failed to interrupt VT. In this study, intramural pathways constituted an integral part of the reentry circuit in a large proportion of the VTs.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

We have examined the kinetics of closure of sodium channels using single-channel recordings in cell - attached and excised membrane patches of rabbit ventricular myocytes. Sodium-channel closure was dependent on membrane potential. The closing rate initially decreased with depolarization. The rate then passed through a minimum and increased at strongly depolarized potentials. We attempted to determine the separate voltage dependence of the deactivation and inactivation rate constants using the method of Aldrich, Corey, and Stevens. In a majority of experiments, the method did not give internally consistent results. As an alternative approach, batrachotoxin was used to remove inactivation and determine the voltage dependence of deactivation rate. The deactivation rate decreased with depolarization. To account for the increase in the closing rate at strongly depolarized test potentials, one must postulate voltage dependence of inactivation. The ensemble average current relaxed with a time course that was usually best described by the sum of two exponentials. The larger of the two rate constants that described the relaxation was strongly voltage-dependent, increasing with depolarization. The larger rate constant may reflect voltage-dependent inactivation. We found evidence of two possible mechanisms for the slow component of relaxation: 1) cardiac sodium channels may open repetitively during a given depolarizing epoch, and 2) channels may return from the inactivated state with low probability and burst for as much as 200 msec with open times that are longer than those during usual gating. The slow component appears to be more prominent in cardiac muscle than in nerve and may play an important role in the control of the action potential duration and the inotropic state of the heart.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Arginine-vasopressin (AVP), angiotensin II (AII), and norepinephrine (NE) are known to stimulate prostaglandin (PG) synthesis in the intact rat kidney perfused with Tyrode's solution by a mechanism that requires intracellular Ca2+, while PG synthesis elicited by bradykinin (BK) is independent of Ca2+. To elucidate further the differences in the mechanism of action of BK and other vasoactive agents, in this preparation we have investigated the effect of 1) caffeine, an agent known to interfere with the uptake and storage of Ca2+in intracellular sites, on renal output of PGE2and 6-keto-PGF1αelicited by AVP, AI, NE, and BK; 2) various combinations of the maximal doses of BK, All, AVP, and NE on renal PG synthesis; and 3) RHC 80267, an inhibitor of diglyceride and monoglyceride lipase, on the output of PGs produced by these vasoactive agents. Infusion of 1 mM caffeine inhibited PG output elicited by AVP, AII, and NE but not that caused by BK in the absence of extracellular Ca2+. Combined administration of maximal doses of BK (2.8 nmol) with that of AII (0.28 nmol), AVP (0.27 nmol), or NE (3.2 nmol) but not AVP and AII, NE and AVP, or NE and AII produced an additive effect on renal PG output in the presence or absence of Ca2+. The renal vasoconstrictor effect of AVP, AII, and NE produced in the presence of Ca2+was not additive and remained unaltered when given together with BK. Administration of 12 μM RHC 80267 attenuated BK-induced renal PG output in concentrations that did not alter the effect of either AVP, AII, or NE to increase PG output or renal vasoconstriction in the presence of Ca2+. These data suggest that BK stimulates renal PG synthesis by a mechanism that is different from that of other vasoactive agents and probably involves activation of a distinct lipase that releases arachidonic acid from diglycerides or monoglycerides derived from phospholipids or triglycerides.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Extravascular lung water and vascular permeability-surface area products were measured with a multiple indicator dilution method in 6 premature lambs with hyaline membrane disease 1–5 hours following delivery by cesarean section. The indicators used were51Cr-labelled erythrocytes,I25I-albumin,3H-water, and14C-urea. Results were compared with previously obtained data in newborn lambs without hyaline membrane disease also delivered by cesarean section. Extravascular lung water was significantly higher in lambs with hyaline membrane disease [23.2 ± 1.0 (SEM) vs. 10.7 ± 1.4 ml/kg body wt]. Vascular permeability-surface area products for14C-urea were significantly lower in lambs with hyaline membrane disease (0.30 ± 0.10 vs 0.78 ± 0.11 ml/s per kg). It is concluded that extravascular lung water is high in lambs with hyaline membrane disease. Permeability-surface area products forl4C-urea is low in lambs with hyaline membrane disease, which probably indicates a decrease in detectable surface area for exchange due to derecruitment or hypoperfusion of pulmonary exchange vessels in edematous and hypoxic areas of the lungs.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

To determine the relative importance of protein degradation in the development of starvation-induced cardiac atrophy, in vivo fractional synthetic rates of total cardiac protein, myosin heavy chain, actin, light chain 1, and light chain 2 were measured in fed and fasted rabbits by continuous infusion of [3H] leucine. In addition, the rate of left ventricular protein accumulation and loss were assessed in weight-matched control and fasted rabbits. Rates of total cardiac protein degradation were then estimated as the difference between rates of synthesis and growth. Fasting produced left ventricular atrophy by decreasing the rate of left ventricular protein synthesis (34.8 ± 1.4,27.3 ± 3.0, and 19.3 ± 1.2 mg/day of left ventricular protein synthesized for 0-, 3-, and 7-day fasted rabbits, respectively). Inhibition of contractile protein synthesis was evident by significant reductions in the fractional synthetic rates of all myofibrillar protein subunits. Although fractional rates of protein degradation increased significantly within 7 days of fasting, actual amounts of left ventricular protein degraded per day were unaffected. Thus, prolonged fasting profoundly inhibits the synthesis of new cardiac protein, including the major protein constituents of the myofibril. Both this inhibition in new protein synthesis as well as a smaller but significant reduction in the average half-lives of cardiac proteins are responsible for atrophy of the heart in response to fasting.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The vagal nerves modulate adrenergic effects on sinus cycle length, atrioventricular (AV) nodal conduction, and refractoriness of atria and ventricles. We tested whether varying levels of vagalsympathetic input could yield the same spontaneous sinus cycle length but also alter effective refractory periods of the right atrium, right ventricle, and left ventricle and AV nodal conduction times. Dogs anesthetized by α-chloralose were studied in the open-chest, neurally decentralized state. In 10 dogs, sinus cycle length was maintained constant during 3 levels of bilateral ansae subclaviae stimulation (4 msec, 3 mA at 1, 2, and 4 Hz) by titrating simultaneous bilateral vagal stimulation (varying pulse width and frequency). Each combination of ansae subclaviae-vagal stimulation yielded the same sinus cycle length as the control value, but refractory periods of right atrium and right and left ventricles shortened progressively as the frequency of ansae subclaviae stimulation increased. Atrioventricular nodal conduction time (AH interval) shortened in 2 dogs and lengthened in 3 dogs. His-Purkinje conduction time (HV interval) was unchanged. In 9 dogs, the effects of simultaneous unilateral ansae subclaviae stimulation at 2 Hz and ipsilateral vagal stimulation that yielded the same sinus cycle length were determined. Right-sided ansae subclaviae–vagal stimulation shortened refractoriness of right atrium and anterior left ventricle significantly. The AH interval lengthened in 1 dog. Left ansae subclaviae–vagal stimulation shortened the refractory periods of anterior and posterior left ventricle significantly and reduced the AH interval in 3 dogs. In 8 dogs, the effects of bilateral ansae subclaviae stimulation alone at 2 Hz, vagal stimulation alone at an intensity required to keep the sinus cycle length constant during ansae subclaviae stimulation, and simultaneous bilateral ansae subclaviae and vagal stimulation were tested. The right atrial refractory period was shortened significantly by ansae subclaviae stimulation alone and by vagal stimulation alone and was shortened further by simultaneous stimulation of both autonomic limbs. The right and left ventricular refractory periods were shortened by ansae subclaviae stimulation alone and by simultaneous stimulation of both limbs but tended to be prolonged by vagal stimulation alone and when added to ansae subclaviae stimulation. In 7 dogs, the effects of simultaneous stimulation of bilateral ansae subclaviae at 2 Hz and vagi at intensities that maintained the AH interval constant at an atrial pacing cycle length of 300 msec were determined. During these stimulation parameters, the sinus cycle length was prolonged by 90 msec or more in 3 dogs and varied within 15 msec in the remaining 4 dogs, while refractoriness of atrium and ventricle shortened significantly. We conclude that multiple combinations of ansae subclaviae–vagal stimulation that do not alter the spontaneous sinus cycle length can lengthen or shorten AV nodal conduction time and can shorten atrial and ventricular refractory periods. Under these conditions, sinus cycle length is not an indicator of autonomic input to the AV node, atrium, and ventricle of the canine heart. Similarly, under autonomic conditions that yielded a constant AH interval, atrial and ventricular refractory periods shortened and spontaneous sinus cycle length lengthened or shortened.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Thromboxane A2(TXA2)/prostagtandin H2(PGH2) are potent vasoconstrictors whose contractile effects are mediated by increases in cellular calcium. Stable analogues of these compounds have shown calcium ionophore activity at high concentrations. To determine if effects of TXA2/PGH2analogues on45Ca2+fluxes are receptor mediated, the effects of the stable TXA2/PGH2mimetic U46619 and the TXA2/PGH2receptor antagonist I-PTA-OH on45Ca2*fluxes in cultured human vascular smooth muscle cells were studied. The smooth muscle cells were cultured from human saphenous vein explants, and they retained the morphologic and immunologic characteristics of vascular smooth muscle cells. U46619 stimulated45Ca2*efflux in a dose-dependent manner with an EC50of 398 ± 26 nM (n= 4). The maximal45Ca2*efflux in response to U46619 (5 μM) was significantly greater (p = 0.006) than the45Ca2*efflux induced by KC1 (40 mM). I-PTA-OH inhibited the U46619-induced45Ca2*efflux but had no effect on KCl-induced45Ca2*efflux. These results suggest that the effects of U46619 in increasing vascular smooth muscle cell calcium efflux are receptor mediated. Furthermore, vascular smooth muscle cells with functional TXA2/PGH2receptors were cultured from human saphenous veins and provide a potentially useful in vitro system for the further study of TXA2/PGH2receptor-mediated phenomena in human vascular tissue.

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID