摘要:

In 30 isolated, spontaneously beating right atrial preparations of the rabbit, the arrhyth- mogenic actions of ouabain were studied with microelectrodes. Ouabain (10−6M) uniformly produced the following events: (1) a gradual increase in sinus rate with periods of alternation of beat-to-beat atrial intervals, (2) a rapid rate and regular rhythm, (3) severe irregularity of rhythm, (4) total atrial arrest. Cycle length decreased from 394 msec ± 43 (mean ± SD) during control to 229 msec ± 26 during the period of rapid rate and regular rhythm (P< 0.001). Pretreatment with atropine or propranolol did not abolish this positive chronotropic action of ouabain. Maps of the spread of activation in the area of the sinus node in eight experiments revealed that the speeding up of rate is accompanied by a shift of dominant pacemaker site toward the sinoatrial border. In explanation, it is shown that sinoatrial border fibers develop strong diastolic depolarization, whereas dominant pacemaker fibers do so to a lesser extent or not at all. The atrial arrhythmias-best to be described as "digitalis-induced sinus tachycardia"-may represent the experimental counterpart of the so-called "paroxysmal atrial tachycardia with block" described as a common manifestation of digitalis intoxication in man. Circ Res 46: 406-414, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We evaluated the ability of a computer procedure to locate cardiac electrical activity from body surface potentials during normal and ectopic beats in six intact dogs. The location of the dipole that best reconstructed the signals recorded from 26 thoracic electrodes was computed by using a torso model. This model was designed from geometrical measurements made on the first dog. Chronically implanted subepicardial electrodes produced ectopic foci at three known locations: apex, and right and left ventricles. For the normal QRS complex, the dipole started in the middle of the septum, moved upward, then to the left, downward, and back to the right; it remained stationary at the level of the base during repolarization. After ectopic stimulation the dipole started its course at a distance of 1.9 ± 0.8 (SD) cm from the stimulus site and then traversed the heart, moving away from the ectopic site; during the T wave, it roughly followed the QRS path, but at a slower speed. The speed of the dipole ranged between 0 and 6 m/sec, and its orientation often did not coincide with the direction of its path. The location of the dipole appeared to be close to the corresponding wavefronts when these were unique and dipolar, especially during the early and terminal portions of the QRS. The results show that the initial location of the dipole can give the approximate position of an ectopic focus in vivo, and that the trajectory of the dipole during QRS can portray the passage of an ectopic beat across the heart. Circ Res 46: 415-425, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Norepinephrine (NE) activates isolated coronary conduit arteries by stimulating Ca2+uptake into the smooth muscle cells. Blockade of Ca2+influx by removal of Ca2+from the bathing medium or addition of 10 miu LaCl3prevents the NE-induced contraction in the dog coronary artery but still allows NE to induce a rapid transient contraction in the rabbit aorta. Under these conditions, NE stimulates45Ca2+efflux from rabbit aorta but fails to do so in the coronary artery. The difference in behaviour between the two arteries is attributed to the presence of an intracellular NE-sensitive Ca2+fraction in the rabbit aorta and its absence from the dog coronary artery. This difference also explains the much greater sensitivity of the NE-induced contractions in the dog coronary to the relaxant effects of the Ca2+antagonists, D600 and SKF525A, than that seen in the rabbit aorta. High K+-induced contractions of both the coronary artery and the aorta are equally sensitive to the Ca2+antagonists. Circ Res 46: 426-429, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Mechanisms involved in altering left ventricular (LV) diastolic properties during angina were studied in 10 chloralose-anesthetized dogs with chest and pericardium open. Proximal coronary artery stenoses of >90% were created in both left anterior descending and circumflex coronary arteries to abolish reactive hyperemia, and the heart was paced at nearly twice its resting rate (115 ± 4 to 200 ± 5 beats/min). After pacing, increases occurred in LV end-diastolic pressure (EDP, 10 ± 2 to 21 ± 2 mm Hg, P< 0.001), LV minimum diastolic pressure (5 ± 1 to 13 ± 2 mm Hg, P< 0.001), LV end-diastolic volume (55 ± 3 to 60 ± 2 ml,P< 0.001), LV end-systolic volume (28 ± 2 to 33 ± 2 ml,P< 0.001), right ventricular (RV) systolic pressure (RVP, 27 ± 2 to 32 ± 2 mm Hg,P< 0.01), RVEDP (5 ± 1 to 6 ± 1 mm Hg,P< 0.05), and time constant (T) of LV pressure fall in diastole (35 ± 4 to 53 ±4 msec,P< 0.001). Decreases occurred in LV peak systolic pressure (121 ± 5 to 102 ± 5 mm Hg, P< 0.001), LV maximum negative dp/dt (2300 ± 158 to 1319 ± 154 mm Hg/sec, P< 0.001), and LV ejection fraction (0.49 ± 0.02 to 0.44 ± 0.03, NS), whereas heart rate was not significantly different. LV diastolic pressure-volume curves were shifted upward for each dog; at any diastolic volume, pressure was higher than control. In four dogs, the pulmonary artery was abruptly constricted, and saline was infused to produce an acute increase in RV loading (RVP, 29 ± 1/6 ± 1 to 67 ± 5/11 ± 1 mm Hg,P< 0.001/P< 0.001), and the effect on the LV diastolic pressure-volume relation was examined. Only minor changes in this relation could be detected in contrast to the changes with pacing-induced ischemia. Since the upward shift in the LV diastolic pressure-volume curve in our ischemia model occurred in the absence of the pericardium and was associated with only small changes in RVEDP, we conclude that altered myocardial diastolic properties play an important role in this phenomenon. Circ Res 46: 430-439, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Recovery from unilateral postischemic acute renal failure produced by 1 hour of complete renal artery occlusion in the rat is incomplete and is associated with the eventual loss of renal mass. The loss in renal mass can be reversed by removal of the contralateral kidney. In the present study, clearance and micropuncture techniques were used to compare whole kidney and individual nephron function of normal and postischemic kidneys. In sham-operated control animals, the left kidney weight (LKW) averaged 0.41 g/100 g body weight (BW), the inulin clearance (Cin) averaged 541 μl/min per 100 g BW and single nephron glomerular filtration rate (SNGFR) averaged 15.4 nl/min per 100 g BW. The calculated number of nephrons, derived from the relationship Cin/SNGFR, was 37,780. Four weeks after the period of ischemia, the LKW of rats with the contralateral kidney in place averaged 0.30 g/100 g BW. Cinaveraged 158 μl/min per 100 g BW and SNGFR averaged 17.4 nl/min per 100 g BW. The calculated number of nephrons was 9460. In rats in which either the contralateral kidney had been removed or its ureter ligated 2 weeks following the period of ischemia (2 weeks prior to study) LKW averaged 0.66 g/100 g BW, Cinaveraged 415 μl/min per 100 g BW, and SNGFR averaged 19.4 nl/min per 100 g BW. The calculated number of nephrons was 24,152. The results indicate that the increases in size and Cinof the postischemic kidney which occurred in response to the contralateral nephrectomy or ureteral ligation were due to the functional recruitment of nephrons which otherwise would have become atrophic. These data also demonstrate that the extent of functional recovery from post- ischemic acute renal failure is not necessarily dependent on the nature of severity of the initial insult. Circ Res 46: 440-448, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Previous reports have shown that the intrarenal infusion of adenosine results in a relatively greater fall in superficial nephron glomerular filtration rate (GFR) than whole kidney GFR. This nonuniform decrease in GFR occurred despite a concomitant increase in total renal blood flow (RBF); thus, the present study was undertaken to assess the effect of intrarenally administered adenosine on the distribution of RBF. RBF distribution was measured with radiolabeled microspheres (15μn)in anesthetized dogs (n = 8) before and during the intrarenal artery infusion of adenosine (0.3 μmol/min). In dogs with elevated plasma renin activities (PRA), adenosine infusion produced no significant change in outer cortical blood flow (4.36 ± 0.50 vs. 4.41 ± 0.63 ml/min per g), whereas absolute inner cortical blood flow increased by 94% (1.54 ± 0.34 vs. 2.99 ± 0.52 ml/min per g). In dogs with low PRA, outer cortical blood flow was only minimally affected by adenosine infusion (6.39 ± 0.44 vs. 5.88 ± 0.33 ml/min per g), whereas inner cortical blood flow was increased from 4.91 ± 0.43 to 6.06 ± 0.38 ml/min per g. Although adenosine resulted in a deep cortical vasodilation in dogs with both high and low PRA (94% vs. 23%), the relative change was greater in the animals with high PRA. Additional experiments were performed in indomethacin- (or meclofenamate-) treated(n= 14) or phenoxybenz-amine-treated (n = 5) dogs to determine whether the deep cortical vasodilation is mediated by increased prostaglandin production or by inhibition of norepinephrine release. The increase in deep cortical flow during adenosine administration was not affected by either the blockade of prostaglandin synthesis or α-adrenergic receptors. We conclude that the effect of adenosine to preferentially dilate vessels of the inner cortex is independent of a prostaglandin-related or sympathetic adrenergic mechanism.

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