摘要:

We recorded 60 DC-extracellular electrograms simultaneously from epicardial and intra- mural sites of the left ventricle of isolated perfused porcine and canine hearts during the first 15 minutes after occlusion of the left anterior descending coronary artery. During coronary occlusion, maximal current flow across the ischemic border occurred when normal cells had repolarized and ischemic cells had not. At that moment, maximal current sources at the normal side of the ischemic border were in the order of 2 μA/mm3and maximal current sinks were -5 μA/mm3. During propagation of a broad wavefront in nonischemic myocardium, current sources in the wake of the wavefront were about twice as large. Ventricular premature beats usually followed deep negative T waves in ischemic myocardium, when “injury” currents were maximal. Earliest activity always occurred at the normal side of the ischemic border, and whenever Purkinje activity was recorded it preceded myocardial activity in both single premature beats and the initial beats of ventricular tachycardia (VT) or ventricular fibrillation (VF). For later beats of VT, circus movements with a diameter of 1-2 cm were responsible for continuation of the arrhythmia. Dimension and position of the reentrant circuit changed from beat to beat. In VF, fragmentation of wavefronts occurred, and multiple wavelets followed tortuous paths. Circus movements were seldom completed; when they were, their diameter was 0.5 cm. It is concluded that two mechanisms are responsible for the very early ischemic arrhythmias: one, a μfocalμ mechanism located at the normal side of the ischemic border, possibly induced by injury currents in normal Purkinje fibers and, two, macro- and micro-reentry in ischemic myocardium.Circ Res 47:151-165, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The catecholamines, dopamine, norepinephrine, and epinephrine, have been found in brain regions associated with cardiovascular regulation. We wished to determine whether central catecholaminergic neurons participate in the reflex alterations of cardiac autonomic nerve traffic associated with acute myocardial ischemia. Five groups of rats treated with a-methyltyrosine, an inhibitor of catecholamine biosynthesis, were examined. The experimental interventions included left coronary artery ligation, ligation with the left ventricle painted with lidocaine, ligation and bilateral cervical vagotomy, sham operation, and sham operation plus vagotomy. An untreated group of resting rats was also examined. Dopamine, norepinephrine, and epinephrine were measured 90 minutes later in thoracic cord, cerebellum, pons medulla, midbrain, posterior and anterior hypothalamus, thalamus and frontal cortex. Norepinephrine turnover was increased in thoracic cord, pons medulla and posterior hypothalamus, and dopamine turnover was increased in posterior hypothalamus in the ligated rats relative to those subjected to sham operation. These increases were abolished by topical lidocaine or vagotomy. The turnover of all three catecholamines was increased in anterior hypothalamus in both ligated and Udocaine-treated rats, but not in vagotomized animals. Thus, there is a reflex activation of noradrenergic nerves in the posterior hypothalamus, pons medulla, and thoracic cord (bulbospinal fibers), and of dopaminergic nerves in the pons medulla after left coronary artery ligation in the rat. This reflex arises from receptors in the ischemic ventricle and the afferent limb is in the vagus nerve. Coronary artery ligation also activates catecholaminergic nerves in the anterior hypothalamus; the afferent signals travel in the vagus but do not appear to originate in the ischemic ventricle.CircRes 47:166-172, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We developed a new ultrasonic triangulation technique to measure regional wall thickness and shear motion of the left ventricular wall under normal conditions and during complete and partial coronary occlusions. In 10 open-chest dogs, a left ventricular micromanometer was inserted, and a screw-driven arterial clamp and flowmeter were placed around the left circumflex coronary artery. A single miniature ultrasonic crystal was placed in the subendocardium of the left ventricular free wall in a region to be made ischemic, and three receiving crystals were sutured to the opposing epicardium at the corners of a 45-degree right triangle. By the trigonometric combination of three measured lengths from ultrasonic dimension gauges, the exact position of the endocardial crystal in X, Y, and Z coordinates could be displayed by computer. The endocardial surface moved in a longitudinal direction relative to the epicardial surface during normal systole [0.58 ± 0.26 (mean ± SEM) mm]. With coronary occlusion, this myocardial shear became less marked (0.11 ± 0.12 mm), and systolic wall thickening changed to thinning. When coronary occlusion was released, end-diastolic wall thickness and percnt wall thickening rapidly increased to 104.8% and 141.7% of control, respectively, concurrent with the reactive hyperemia. With partial coronary constriction, these postreperfusion changes were markedly reduced, suggesting a role for reactive hyperemia in postreperfusion wall thickness dynamics. These techniques allow measurement of shear and three-dimensional display of dimensions and thereby permit documentation of true wall thickness dynamics both during and after coronary occlusion.Circ Res 47:173-181, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Focal proliferation of smooth muscle cell (SMC) is an integral part of atherosclerotic plaque formation: characterization of regional variation in SMC growth kinetics is therefore important to the understanding of atherogenesis. SMC growth kinetics of rabbit abdominal and thoracic segments were compared. Rabbit aortas were denuded of endothelium and the animals killed after3H-thymidine and Evans blue injections at 0 to 48 days after denudation. Incorporation of3H-thymidine into both aortic segments peaked at 48 hours; no detectable incorporation occurred in the first 24 hours. Abdominal segment DNA specific activity (SA, dpm/μg DNA) and total kinetic activity (TKA, dpm/0.1 mm internal elastic lamina) at 48 hours were significantly greater than values for the thoracic aorta. Abdominal SA and TKA curves decreased exponentially after the 48-hour peak and paralleled thoracic levels after day 7. SA and TKA values for each segment reflected the subsequent SMC intimal growth rates as measured morphometrically. Therefore, both segments share similar growth kinetic charac-teristics; however, the abdominal response to intimal injury is greater than the thoracic and leads to greater myointimal proliferation. The difference in response to injury in the two segments suggests regional variation in SMC'swhich are phenotypically similar.Circ Res 47:182-189, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The extent to which the blood supply of normal and hypertrophied right ventricles originates from the right and left coronary arteries was investigated in conscious dogs. Right ventric-ular (RV) hypertrophy, induced by gradual, chronic (4-6 months) stenosis of the main pulmonary artery, was characterized by a 72% increase (P< 0.001) in RV weight to body weight ratio and a 106% increase (P< 0.001) in total RV transmural blood flow per gram (radioactive microsphere technique). In normal dogs, left main coronary artery occlusion (CAO) reduced blood flow only slightly to the central core of the RV free wall, but markedly (P< 0.001) to the peripheral zones. Right main CAO reduced blood flow in both RV central and peripheral zones to similar absolute levels in both normal animals and dogs with RV hypertrophy. Keeping in mind that pre-CAO control levels were greater in the presence of hypertrophy, the magnitude of the reduction in blood flow was significantly greater (P< 0.01) with right CAO in dogs with hypertrophy. Endocardial-epicardial perfusion ratios of both RV central and peripheral zones were significantly reduced (P< 0.02) both at rest and during right CAO in dogs with RV hypertrophy as compared to normal dogs with matched heart rates. These data indicate that the left coronary artery usually supplies a substantial fraction (∽37%) of total RV free wall perfusion in normal, conscious dogs. Moreover, it is seen that the marked, selective increases in transmural RV blood flow in RV hypertrophy are provided by the right but not the left coronary artery.Circ Res 47:190-200, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Decreases in regional endocardia] function (ultrasonic dimension technique) and blood flow (radioactive microsphere technique) were correlated in 14 conscious dogs with acute graded levels of coronary stenosis. Coronary stenosis affected overall ventricular function only slightly, but induced gradual reductions in regional blood flow (BF) and segment length (SL) shortening in the ischemic zone. The relationship was best fit by an exponential function relating % change in SL to % change in BF; i.e., SL(%Δ) = -161.6e−0.047BF(%Δ) (r= 0.92). In 14 segments, where no change in function was observed, blood flow fell by 6 ± 1%. However, 10-20% reductions of blood flow impaired function significantly. Severe reduction of blood flow was required to reduce function completely. In 12 segments exhibiting paradoxical motion, blood flow fell by 95 ± 2%, a value greater(P< 0.01) than in four akinetic segments, i.e., those with no shortening or lengthening (−82 ± 4%). These data, which show on one hand that only 10-20% reductions in blood flow impair function significantly and that, on the other hand, severe reductions in blood flow are required to abolish active shortening completely, indicate sensitive coupling between blood flow and function in the conscious dog with acute myocardial ischemia.Circ Res 47: 201-207, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Carotid baroreceptors of nine healthy young men and women were stretched or compressed with neck suction or pressure, before and after β-adrenergic and cholinergic blockade, to evaluate several nonlinearities of sinus node baroreflex responses. Sinus node inhibition was related linearly to the intensity of brief baroreceptor stimuli over a range extending from carotid-distending pressures of about 101 ± 5 (mean ± SE) to 160 ± 6 mm Hg (the subjects' average systolic pressure was 108 ± 2 mm Hg). Sinus node responses to sustained (5 seconds) neck suction or pressure were strikingly asymmetrical. Responses were abolished by atropine, or by atropine and propranolol. Propranolol alone augmented sinus node responses to both neck suction and pressure. These results suggest that, in normal human subjects, sinus node responses to abrupt alterations of afferent baroreceptor traffic are nonlinear and are mediated by fluctuations of efferent cholinergic activity. Most of the observed nonlinear behavior of the integrated reflex can be explained on the basis of known properties of afferent and central portions of the baroreflex arc.Circ Res 47: 208-216, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We determined the effect of changes in arterial Pco2on the relationship between O2delivery (DO2) and consumption (MVO2) by the myocardium of anesthetized dogs. Left anterior descending coronary blood flow (CVF), arterial and great cardiac vein O2content (GCVO2), and arterial pressure were measured. MVO2was raised by infusing various doses of isoproterenol (ISO) or norepi-nephrine (NE) into the right atrium. CBF, DO2, coronary conductance (CVC), and GCVO2were plotted as a function of MVO2using data obtained at high (⋍70 mm Hg) and low (⋍24 mm Hg) Pco2. When ISO was used to raise MVO2, we found that CBF, DO2, and CVC were slightly higher for a given MV02. In addition, GCVO2was ⋍7 vol % at high CO2, ⋍4 vol % at low CO2. When NE was used to raise MVO2, this difference was not observed at high MVO2's. Alpha-receptor blockade caused the results with NE to look more like the results with ISO. Indomethacin lowered GCVO2relative to MV02under resting conditions at both high and low Pco2, but not during infusion of ISO. These results indicate that (1) elevation of systemic arterial PCO2causes only a small increase in DO2relative to MVO2but that this results in a relatively large increase in tissue oxygenation, (2) NE causes a receptor-mediated vasocon-striction which competes with CO2vasodilation, and (3) prostaglandin release contributes a vasodilator influence at resting but not elevated MVO2.Circ Res 47: 217-225, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We transplanted neonatal hamster renal tissue into a hamster cheek pouch chamber and subjected the renal tissue to increases and decreases in extravascular pressure. A decrease in extra-vascular pressure decreased, and an increase in extravascular pressure increased, the diameter of preglomerular arterioles. Thus, the change in preglomerular arteriolar diameter was directly related to alterations in extravascular pressure. Neither saralasin nor indomethacin affected these changes, whereas papaverin prevented them. The efferent arterioles responded passively to changes in extra vascular pressure; i.e., the changes in their diameter were inversely related to changes in extravascular myogenic autoregulation of preglomerular vessels.CircRes 47: 226-230, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Isolated perfused kidneys removed from a rabbit 24-48 hours after renal vein constriction exhibited a markedly enhanced release of renal prostaglandins (PG's) induced by vasoactive peptides. Stimulation of the perfused renal vein-constricted kidney with 300 ng of bradykinin (BK) caused the release of 5980 ± 1409 ng of PGE2compared to a release of 290 ± 45 ng from the contralateral control kidney. Infusion of indomethacin abolished the PGE2formation (confirmed by radiochromatography) in both the renal vein-constricted and contralateral kidneys. Bradykinin and angiotensin II stimulation of the renal vein-constricted kidney (but not the contralateral kidney) also revealed the presence in the renal venous effluent of a rabbit aorta-contracting substance (RCS). Identification of the RCS as thromboxane A2(TxA2) was confirmed by determining the biological half life (38 ± 6 sec) in comparison with standard TxA2(30 ± 3 sec) and PG endoperoxide (135 ± 13 sec). Incubation with [l4C]arachidonate of the renal vein-constricted cortical or medullary microsomes resulted in the formation of [14C]-thromboxane B2. The renal thromboxane synthetase was inhibited by preincubation with imidazole. This study demonstrates exaggerated prostaglandin and thromboxane production by the kidney with renal vein constriction. These in vitro experiments suggest that relative changes in cortical synthesis of vasodilating PGE2and vasoconstricting TxA2xs may function to modulate renal vascular resistance in states of increased renal venous pressure.Circ Res 47: 231-237, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID