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21. |
Functional and Structural Changes in the Rabbit Ear Artery after Sympathetic Denervation |
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Circulation Research,
Volume 49,
Issue 2,
1981,
Page 478-485
ROSEMARY BEVAN,
HIROMICHI TSURU,
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摘要:
We studied the tissue weight, dimensions, contractility, elasticity, and sensitivity to exogenous norepinephrine (NE) of denervated «nd innervated segments of the central ear arteries of white New Zealand rabbits. Three different age groups received unilateral superior cervical ganglionectomies, “growing” at 3–4 weeks, “young adult” at 9–11 weeks, and “mature” at 16–20 weeks. In the growing group, 8 weeks after ganglionectomy, the denervated arteries showed mean decreases in tissue weight (11%), total wall thickness (12%), cross-sectional area of media (17%), contractility (16%), and increases in the tangential modulus of elasticity and sensitivity to NE (2.3-fold) compared to the contralateral control vessels. The change in medial cross-sectional area was significant in the growing and young adult but not the mature animals. The other changes, however, although consistently seen, differed quantitatively among the groups. These results indicate that an intact innervation is necessary for normal development and maintenance of the artery wall. However, the precise consequences of this influence vary at different ages. Whether this influence involves a special trophic factor is not known.
ISSN:0009-7330
出版商:OVID
年代:1981
数据来源: OVID
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22. |
Relative Location of α‐ and β‐Adrenoceptors to Sites of Release of Sympathetic Transmitter in the Rabbit Facial Vein |
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Circulation Research,
Volume 49,
Issue 2,
1981,
Page 486-491
RAYMOND WINQUIST,
JOHN BEVAN,
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摘要:
We studied α- and β-adrenoceptor-mediated responses of rabbit facial vein rings to adrcnergic stimulation to determine the location of the two types of receptors in relation to the sympathetic nerve terminals. Transmural electrical nerve stimulation (TNS) at low frequency elicited large β-receptor-mediated relaxation responses in rings pretreated with phentolamine (6 × 10−7M). These responses were significantly greater than the corresponding a-receptor-mediated contractions in rings pretreated with propranolol (10−6M). Blockade of neuronal uptake with desmethylimipramine (DMI, 10−7M) increased significantly the neurogenic relaxation but had little effect on neurogenic contractility. DMI pretreatment caused a shift to the left (x 8.6) in the relaxant dose-response curve to exogenous l-norepinephrine (NE). The NE contractile dose-response curve was also shifted to the left after DMI pretreatment but by a significantly smaller amount (X 3.1). Neurogenic activation of β- receptors evoked almost maximal relaxations in facial vein rings (85% at 2 Hz), whereas the maximum neurogenic contraction was approximately half the maxiinum contraction with exogenous NE (40% at 6 Hz). These results imply that the β-adrenoceptors in the rabbit facial vein are located in close proximity to sites of adrenergic transmitter release and neuronal reuptake, whereas the a-receptors are more distant.
ISSN:0009-7330
出版商:OVID
年代:1981
数据来源: OVID
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23. |
Effects of lndomethacin, Renal Denervation, and Propranolol on Plasma Renin Activity in Conscious Dogs with Chronic Thoracic Caval Constriction |
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Circulation Research,
Volume 49,
Issue 2,
1981,
Page 492-500
STEPHEN ECHTENKAMP,
JAMES DAVIS,
JACK DEFORREST,
BRIAN ROWE,
RONALD FREEMAN,
ANDREA SEYMOUR,
JOHN DIETZ,
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摘要:
The role of renal prostaglandins and the adrenergie nervous system in the control of rcnin release was studied in conscious dogs with thoracic caval constriction. lndomethacin reduced plasma renin activity (PRA) in intact animals with thoracic caval constriction by 43% but failed to change PRA after surgical renal denervation and during chronic propranolol administration; adrenergie blockade reduced the initial control level of PRA before indomethacin from 15 to 4 ng angiotensin I/ml per hr. Renal hemodynamic function was markedly reduced by indomethacin both before and after adrenergie blockade. These observations indicate that prostaglandins are involved ha the control of renin release, but they appear to have a more important role in the control of renal arterior resistance. The adrenergic nervous system also plays a role in the hyperreninemia of caval constriction and, possibly, a greater role than the renal prostaglandins. In the first experimental design, surgical renal denervation and daily oral propransolol administration in dogs with caval constriction reduced PRA to normal in two of seven dogs and a natriuresis occurred. In four of the five remaining animals, PRA fell, but not to normal, and renal sodium excretion failed to increase. In a second experimental design, the kidneys were denervated and propranolol was given before the dogs were subjected to caval constriction and propranolol was continued for 5 days; PRA increased markedly, sodium retention occurred, and ascites formed. Under these circumstances, compensatory mechanisms secondary to caval constriction led to increased PRA in spite of adrenergie blockade.
ISSN:0009-7330
出版商:OVID
年代:1981
数据来源: OVID
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24. |
In Vivo Characterization of the Adrenergic Receptors in the Working Canine Heart |
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Circulation Research,
Volume 49,
Issue 2,
1981,
Page 501-510
DANIEL COUSINEAU,
COLIN ROSE,
CARL GORESKY,
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摘要:
The analysis of multiple indicator dilution data shows that the ratio of the interstitial space size available for tracer norepinephrine to that for sucrose is greater than one. The space increment appears to be consequent to binding of tracer to sites in the interstitial space, so we examined the hypothesis that these could be adrenergic receptors. Following the injection of desmethylimipraraine or tyramine to increase norepinephrine values, increases in heart rate and rate-pressure product were found to correlate closely with decreases in the tracer norepinephrine:sucrose space ratio. Although capillary and interstitial norepinephrine values are ordinarily disparate, in the subset of experiments in which measured circulating plasma levels are close to equal in aorta and coronary sinus, the interstitial values will virtually equal plasma levels. In this group of experiments, the space ratio values can be related to interstitial norepinephrine values. The ratios were found to diminish with increase in the levels of interstitial norepinephrine, apparently due to a progressively greater occupancy of adrenergic receptors by the endogeneoua norepinephrine and, at high levels of circulating norepinephrine, when there was intense cardiac sympathetic stimulation, the space ratio approached unity. Quantitative analysis of this behavior enabled us to obtain in vivo estimates of the equilibrium dissociation constant (0.64 nue) and the density or concentration of receptor sites (271 fmol/g). The dissociation constant lies in the physiological midrange of interstitial norepinephrine concentrations.
ISSN:0009-7330
出版商:OVID
年代:1981
数据来源: OVID
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25. |
Effect of Autonomic Blockade on Ventricular Refractoriness and Atrioventricular Nodal Conduction in HumansEvidence Supporting a Direct Cholinergic Action on Ventricular Muscle Refractoriness |
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Circulation Research,
Volume 49,
Issue 2,
1981,
Page 511-517
ERIC PRYSTOWSKY,
WARREN JACKMAN,
ROBERT RINKENBERGER,
JAMES HEGER,
DOUGLAS ZIPES,
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摘要:
In humane, the parasympathetic nervous system predominates over the sympathetic nervous system in control of heart rate, but little is known about the relative influences of cholinergic and adrenergic tone on the electrophysiological properties of the ventricle and atrioventricular (AV) node. Thirteen subjects were studied using standard electrophysiological testing techniques in the control state and after propranolol (0.15 mg/kg, iv) plus atropine (0.03 mg/kg, iv) to assess the effect of autonomic blockade on ventricular and AV nodal refractoriness and AV nodal conduction. Eight subjects received propranolol first (group A) and five were given atropine first (group B). For groups A and B, the spontaneous sinus cycle length significantly decreased from control after administration of propranolol and atropine [813 ± 107 (SD) to 613 ± 57 msec and 842 ± 188 to 637 ± 115 msec, respectively]. Ventricular effective (ERP) and functional (FRP) refractory periods insignificantly increased from control after propranolol was given (group A); however, both ventricular ERP and FRP significantly shortened to less than control values after atropine was added (238 ± 23 to 218 ± 19 msec and 261 ± 22 to 243 ± 17 msec, respectively). Similar results for ventricular refractoriness occurred after administration of atropine and propranolol in group B subjects. The shortest atrial pacing cycle length sustaining 1:1 AV nodal conduction after administration of propranolol and atropine did not significantly change from control values (386 ± 109 to 372 ± 74 msec). These data suggest that (1) resting vagal tone exerts a significant effect on human ventricular refractoriness and the effect can occur in the presence of β-adrenergic blockade, and (2) in contrast to the markedly predominant effect of the parasympathetic nervous system on sinus nodal automaticity, vagal and adrenergic tone exert a balanced effect on resting AV nodal conduction.
ISSN:0009-7330
出版商:OVID
年代:1981
数据来源: OVID
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26. |
Blood Pressure Response to Central and /or Peripheral Inhibition of Phenylethanolamine N‐Methyltransferase in Normotensive and Hypertensive Rats |
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Circulation Research,
Volume 49,
Issue 2,
1981,
Page 518-524
JESSIE BLACK,
BERNARD WAEBER,
MARGARET BRESNAHAN,
IRENE GAVRAS,
HARALAMBOS GAVRAS,
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摘要:
We studied the effects on blood pressure and heart rate of two different phenylethanolamine JV-methyltransferase (PNMT) inhibitors in normotensive, in two-kidney renal hypertensive, and in deoxycorticosterone-salt (DOC-salt) hypertensive rats. One compound (SK&F 64139) blocks the conversion of norepinephrine to epinephrine in both the central and the peripheral nervous system, whereas the other (SK&F 26861) does not cross the blood-brain barrier and therefore is active mostly in the adrenal glands. In the rats given SK&F 29661, practically no acute blood pressure changes were observed. Central PNMT inhibition with SK&F 64139 induced only a minor blood pressure and heart rate response in normotensive and two-kidney renal hypertensive rats. However, in DOC-salt hypertensive rats, it reduced arterial pressure to approximately normal levels and concomitantly glowed pulse rate. There was a close correlation between the magnitude of the blood pressure response observed in all SK&F 64139-treated animals and the control plasma norepinephrine (r = −0.795, P < 0.001) and epinephrine (r = −0.789, P < 0.001) levels. These results suggest an important role for central epinephrine in regulating the peripheral sympathoadrenomedullary and the baroreceptor reflex activity, particularly when the maintenance of the high blood pressure is not renin-dependent.
ISSN:0009-7330
出版商:OVID
年代:1981
数据来源: OVID
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27. |
Myosin Isoenzymic Changes in Several Models of Rat Cardiac Hypertrophy |
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Circulation Research,
Volume 49,
Issue 2,
1981,
Page 525-532
JEAN-JACQUES MERCADIER,
ANNE-MARIE LOMPRE,
CLAUDINE WISNEWSKY,
JEANNE-LYSE SAMUEL,
JOSIANE BERCOVICI,
BERNARD SWYNGHEDAUW,
KETTY SCHWARTZ,
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摘要:
We studied the effect of chronic mechanical overloading on the isoenzymic composition of rat cardiac myosin in several experimental models: aortic stenosis (AS), aortic incompetence (AI), aortocaval fistula (ACF), overload of the non-infarcted area after left coronary ligation (INF), and overload of the spontaneously hypertensive rats (SHR). Samples of the left and right ventricles were isolated from these hearts, and myosins were analyzed by electrophoresis in non-dissociating conditions. The myosin isoenzymes were called VI, V2, and V3 in order of decreasing mobility, according to the nomenclature of Hoh et al. Controls of the Wistar and Wistar Kyoto (WKY) strains were almost exclusively VI. A slow age-dependent shift toward V3 was observed in the left ventricles of adult Wistar rats, which at 30 weeks of age (body weight 600 g) contained approximately 15% of this form. In all models of cardiac hypertrophy, an isoenzymic redistribution was observed with a significant increase in V3. The level of V3 was statistically correlated with the degree of hypertrophy in the AS, (ns 11, r - 0.6, P < 0.05), the AI (n = 14, r - 0.88, P< 0.001), and the AS + AI (n a 14, r= 0.69, P < 0.01) but not in the ACF (TJ = 16, r = 0.46). The isoenzymic changes could account for the decreases in both myosin ATPase activity and cardiac contractility described previously in our laboratory and by others. They also demonstrate that changes in myosin isoenzymes represent a general response of the rat heart, to chronic mechanical overloading.
ISSN:0009-7330
出版商:OVID
年代:1981
数据来源: OVID
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28. |
Tissue Mechanics of Canine Pericardium in Different Test EnvironmentsEvidence for Time‐Dependent Accommodation, Absence of Plasticity, and New Roles for Collagen and Elastin |
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Circulation Research,
Volume 49,
Issue 2,
1981,
Page 533-544
J. LEE,
DEREK BOUGHNER,
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摘要:
We have tested the mechanical properties of isolated canine pericardium at 37°C in Hanks' solution, and compared those results with similar tests on tissue at room temperature, both in Hanks' solution and merely kept moist with saline. Pericardium, which is nearly isotropic due to the layers of collagen aligned in different directions, is a composite material made up of collagen and elastin fibers in a viscous ground substance matrix. Rapidly applied loads result in a stress-strain response similar to the previous in vivo pressure-volume curves. Slowly applied loads produce an accommodatioii effect as fiber geometry rearranges through the viscous ground substance. Plasticity of the pericardium, long accepted as fact, is not present An accommodation effect is produced instead by shifts in the stress-strain curve due to cyclic loading, stress relaxation, and creep. The slow time course of the accommodation effect is responsible for the differences in hemodynamic effect between an acute and a chronic pericardial effusion. The mechanical properties of the pericardium are due primarily to collagen, which establishes the high ultimate tensile strength and high final slope of the stress-strain curves. The initial extensible portion of the stress-strain curve probably is due to initial rearrangement of collagen fiber weave under stress. Temperature dependence and previous digestion studies indicate a major role for elastin in determining the stress-strain response and limits to stress relaxation and creep.
ISSN:0009-7330
出版商:OVID
年代:1981
数据来源: OVID
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29. |
The Arrhythmogenic Actions of Histamine on Human Atrial Fibers |
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Circulation Research,
Volume 49,
Issue 2,
1981,
Page 545-550
ROBERTO LEVI,
JAMES MALM,
FREDERICK BOWMAN,
MICHAEL ROSEN,
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摘要:
We used standard microelectrode techniques to study the effects of hintamine on right atrial tissues from patients undergoing corrective cardiac surgery. In the 10−6to 10−4M range, higtamine increased maximum diastolic potential, action potential amplitude, and automaticity. In some preparations, histamine also induced delayed afterdepolarizations and triggered activity. The potency of histamine in increasing automuticity was about 10 times less than that of epinephrine, Propranolol (2 × 10−7M), which abolished the chronotropic effect of epinephrine, did not alter the effect of histamine. Conversely, the effect of histamine but not that of epinephrine was antagonized by cimetidine (3 × 10−5to 1 ×−2M). This suggests that Hi receptors mediate the chronotropic effects of histamine on the human heart. The slow channel blocker verapamil (2 × 10−5to 2 × 10−6M) counteracted the effects of histamine on automaticity, delayed afterdepolarizations, and triggered activity, suggesting that in human atrium histamine may act by increasing slow inward (presumably Ca1+) current. If one considers these arrhythmogenic effects of histamine and the fact that human cardiac tissue contains large amounts of histamine, our experiments lend further support to the concept that histamine release can induce arrhythmias.
ISSN:0009-7330
出版商:OVID
年代:1981
数据来源: OVID
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30. |
News from the American Heart Association |
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Circulation Research,
Volume 49,
Issue 2,
1981,
Page 551-556
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ISSN:0009-7330
出版商:OVID
年代:1981
数据来源: OVID
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