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1. |
Controversies in Cardiovascular Research |
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Circulation Research,
Volume 39,
Issue 1,
1976,
Page 1-1
Michael Rosen,
Brian Hoffman,
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ISSN:0009-7330
出版商:OVID
年代:1976
数据来源: OVID
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2. |
Is the Cell Membrane Na+,K+‐TPase Enzyme System the Pharmacological Receptor for Digitalis? |
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Circulation Research,
Volume 39,
Issue 1,
1976,
Page 2-7
Arnold Schwartz,
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ISSN:0009-7330
出版商:OVID
年代:1976
数据来源: OVID
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3. |
Modulation of Ca2+Control of Dog and Rabbit Cardiac Myofibrils by Mg2+Comparison with Rabbit Skeletal Myofibrils |
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Circulation Research,
Volume 39,
Issue 1,
1976,
Page 8-14
R. Solaro,
John Shiner,
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摘要:
Increases in free Mg1+from 0.04 to 10.0 mM with constant pH 7.0, 0.10 M ionic strength, and 2 mM MgATP2-caused a rightward shift of the free Ca-relative ATPase relation for both cardiac and skeletal myofibrils. The specific activity of cardiac myofibrillar ATPase over a wide range of free Ca2+was, however, depressed in 0.04 vs. 1.0 mM Mg2+, whereas a similar decrease in free Mglrslightly enhanced skeletal myofibrillar ATPase. Lowering free Mg2+from 1.0 to 0.04 m,M caused similar increases in cardiac and skeletal myofibrillar bound calcium, which were largely attributable to increased calcium binding to myofibrillar myosin. Raising free Mg2+from 1.0 to 10.0 mM caused only a slight decrease of skeletal myofibrillar bound calcium, and this change was attributable to myo fibrillar myosin. The same increase in free Mg2+caused cardiac myofibrils to bind increased amounts of calcium and this change was not attributable to myofibrillar myosin. By subtracting calcium bound to myofibrillar myosin, we were able to estimate calcium binding by myofibrillar (roponin. The transition between basal and maximal ATPase in 1.0 and 10 mM Mg2+was found to be asso ciated with binding of an additional 2 mol/mol of either skeletal or cardiac myofibrillar troponin.
ISSN:0009-7330
出版商:OVID
年代:1976
数据来源: OVID
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4. |
Continuous Determination of Beat‐to‐Beat Stroke Volume from Aortic Pressure Pulses in the Dog |
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Circulation Research,
Volume 39,
Issue 1,
1976,
Page 15-23
Maurice Bourgeois,
Barry Gilbert,
GOetz von Bernuth,
Earl Wood,
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摘要:
Present methods for measurement of stroke volume from die aortic pressure pulse are not suitable for beat-to-beat determinations during non-steady state conditions because these methods assume that each systolic ejection is equal to the peripheral runoff during the same beat We bare tested a new method which allows determination of an aortic pressure-volume conversion factor over a wide range of pressures during transient changes in stroke volume and infusions of vasoactive drugs in 6 dogs with chronically implanted aortic electromagnetic flowmeters. Each aortic diastolic pressure decay is approximated by an exponential the time constant of which is used to calculate the pressure loss during systole due to blood flow into the periphery. The total increment in aortic pressure due to systolic ejection, if there were no flow from the aorta during systole, then is calculated. The total systolic increment (Delta;Psv) is assumed to describe the pressure-volume characteristics during systole and is related to stroke volume by a constant multiplier that is derived from the indicator-dilution measurements of cardiac out put. The values for beat-to-beat variations that were determined by use of the aortic electromagnetic flowmeter and by this aortic pres sure pulse method were found to be within the range of measurement errors of stroke volume determined from individual aortic electro magnetic flow pulses.
ISSN:0009-7330
出版商:OVID
年代:1976
数据来源: OVID
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5. |
External Detection and Visualization of Myocardial Ischemia with11C‐Substrates in Vitro and in Vivo |
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Circulation Research,
Volume 39,
Issue 1,
1976,
Page 24-32
Edward Weiss,
Edward Hoffman,
Michael Phelps,
Michael Welch,
Philip Henry,
Michel Ter-Pogossian,
Burton Sobel,
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摘要:
To characterize externally detectable changes in myocardial metabolism of free fatty acids (FFA) and glucose associated with ischemia, isovolumically beating rabbit hearts were perfused under conditions of selected flows with cyclotron-produced, short-lived (t1/2= 20.4 minutes),11C-labeled isotopes of glucose and FFA. Tension-time index decreased 83% and lactate production increased from 0.5 ± 1.9 (se) to 5.3 ± 2.1 μmol/min per g of dry weight reflecting myocardial ischemia after flow was reduced from 20 to 5 ml/min. After 30 minutes of low flow the myocardial accumula tion of11C-octanoate, expressed as the extraction fraction, declined from 56 ± 15% to 30 ± 3%, reflecting metabolic suppression of FFA extraction during low flow. Effects attributable exclusively to prolonged residence time were excluded. Similar results were obtained with11C-palmitate. The myocardial aridity for11C-palmitate was demonstrable by rectilinear whole body scanning in dogs given 5 mCi of the agent intravenously. Diminished11C-palmitate uptake in zones of myocardium rendered iscbemic for 20 minutes prior to reflow in intact dogs was delineated by elettrocardiographically gated positron-emission traasaxial computer reconstruction tomography. Thus, diminished "C-FFA extraction, externally de tectable, accompanies decreased perfusion in isolated perfused hearts, and decreased "C-FFA uptake reflecting myocardial is chemia in vivo can be evaluated noninvasively by positron-emission traasaxial tomography.
ISSN:0009-7330
出版商:OVID
年代:1976
数据来源: OVID
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6. |
Effects of Acutely Induced Hypertension in Cats on Pial Arteriolar Caliber, Local Cerebral Blood Flow, and the Blood‐Brain Barrier |
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Circulation Research,
Volume 39,
Issue 1,
1976,
Page 33-41
Eric Mackenzie,
Svend Strandgaard,
David Graham,
John Jones,
A. Harper,
J. Farrar,
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摘要:
Acute hypertension was induced in 19 anesthetized cats by the intravenous administration of angiotensin. The caliber of pial arteries was measured by a television image-splitting tech nique and local cerebral Mood flow by the hydrogen clearance technique. As the blood pressure was increased, pial arterioles constricted and cerebral blood flow remained relatively constant, showing that autoregulation of cerebral blood flow was intact. At mean arterial pressures of more than 170 mm Hg arteriolar dilation appeared. In smaller arterioles (initial diameter less than 100 μm) a segmental dilation (the "sausage-string" phenomenon) frequently preceded uniform dilation. This arteriolar dilation was associated with a marked increase in local cerebral blood flow indicating that the upper level of autoregulation had been breached. In no cat was vasospasm or a decrease in Mood flow observed during induced hypertension. Hypertension also caused dysfunction of the blood-brain barrier since, in 17 out of 19 of the cats examined, there was extravasation of protein-bound Evans blue into brain tissue. In only one of the 19 cats subjected to neuropatbological analysis was ischemic brain damage identified and this was restricted to minimal ischemic cell change. The results indicate that severe, induced hyperten sion in cats produces cerebral arteriolar dilation, an increase of cere bral blood flow, and dysfunction of the blood-brain barrier. These observations may be of importance in understanding the pathogenesis of hypertensive encephalopathy.
ISSN:0009-7330
出版商:OVID
年代:1976
数据来源: OVID
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7. |
Physiological Loading of Isolated Mammalian Cardiac Muscle |
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Circulation Research,
Volume 39,
Issue 1,
1976,
Page 42-53
Walter Paulus,
Victor Claes,
Dirk Brutsaert,
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摘要:
Cal papillary muscles were subjected to a complex loading function resulting from an analysis of the heart as a pump. The papillary muscle was assumed to be a hypothetical bundle of circumferential muscle fibers in the wall of a simplified cylindrical ventricle. The loading included inertia, resistive, and capacitire components of the cardiovascular system. Changes of ventricular dimensions were taken into account by application of a Laplace relationship. When this complex dynamic loading function was imposed on a shortening muscle by means of an electromagnetic feedback system, the developed force continuously changed with time. The time coarse of this changing force corresponded to the time course of calculated stress in the intact ejecting heart. Directly displayed force-velocity loops also were similar to loops obtained for the intact heart. Loads proportional to velocity of shortening (damping), acceleration of shortening (inertia), and to the square of shortening velocity (Bernoulli) were investigated separately. Car diac muscle appeared rather insensitive to inertia! loads, and the contribution of inertia) loads in the early phase of a contraction under physiological pump loading was minimal. Moreover, during all these dynamic loadings, as long as loading was dynamically increasing or decreasing, velocity of shortening was respectively lower or higher at any muscle length and total load, when compared to velocity at the same length and load under static (constant preload and afterload only) loading.
ISSN:0009-7330
出版商:OVID
年代:1976
数据来源: OVID
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8. |
Compression of the Coronary Arteries by the Fibrillating Canine Heart |
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Circulation Research,
Volume 39,
Issue 1,
1976,
Page 53-57
James Downey,
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摘要:
We performed experiments to test whether the subendocardial ischemia which reportedly accompanies electite ren-tricnlar fibrillation (VF) during cardiopulmonary bypass might be tbe result of mechanical compression of the coronary ressels. The left coronary artery of the open-cbest, anesthetized dog was cannulated and perfused with arterial Mood through an extracorporeal circuit. Coronary inflow rate was held constant with a pump and tbe coronary ressels were dilated maximally by infusing adenosine. Any change in perfusion pressure or the transmaral distribution of flow in these hearts would hare been due to changes in compression. When the hearts were stopped in diastole by vagal stimulation, infusion of microspheres ISfitain diameter rerealed a subendocardial to subepicardial (inner to outer) flow ratio (I/O) of 1.2. When the same hearts were caused to fibrillate spontaneously (not electrically maintained) the I/O fell to 0.9. Little change in coronary perfuskw pressure occurred between arrest and VF. When tbe contractile actirity during VF was attenuated by intracoronary sodium pento-barbital (120 rug) tbe I/O rose toward that seen during arrest However, augmentation of muscle actirity by infusion of iso-proterenol during VF failed to change the I/O. Finally the I/O fell ia proportion to the degree of distention ui the fibrillating rentride. The results that we observed indicate that muscular contraction dur ing VF preferentially inhibits subendocardial flow through vascular compression.
ISSN:0009-7330
出版商:OVID
年代:1976
数据来源: OVID
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9. |
Turbulent Blood Flow in the Ascending Aorta of Humans with Normal and Diseased Aortic Valves |
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Circulation Research,
Volume 39,
Issue 1,
1976,
Page 58-65
Paul Stein,
Hani Sabbah,
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摘要:
Turbulent Mood flow may contribute to a variety of pathophysiological effects. Because of its postulated importance, this study was undertaken to determine whether turbulent flow does in fact occur in the human body. In 15 persons (seven normal, seven aortic valvular disease, one prosthetic aortic valve), point velocity was measured in the ascending aorta with a hot-film anemometer probe. In one normal individual with a high cardiac output, turbulent flow occurred above the aortic valve during peak flow which corresponded to a peak Reynolds number of 10,000. In toe other six normal subjects (peak Reynolds numben of 5,700-8,900), flow was highly disturbed during peak ejection. Each of the subjects with aortic valvular disease and the subject with a prosthetic aortic valve showed turbulent flow during nearly the entire period of ejection, with Fourier components of velocity of significant magnitude up to 320 Hz (the maximum frequency we could evaluate with the equipment available). The turbulence energy density was higher in subjects with abnormal valves (3.2-14.6 ergs/cm'), than in normal subjects (0.6-2.9 ergs/cm1). In subjects with aortic stenosis, turbulence was observedthroughout theascending aorta and in the innominate artery. In others, the turbulence dissipated more proximally. The results of this study indicate that turbulent flow can occur in the as cending aorta of subjects with normal cardiac function; and it occurs consistently in the ascending aorta of individuals with abnormal aor tic valves.
ISSN:0009-7330
出版商:OVID
年代:1976
数据来源: OVID
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10. |
Studies on the Nature of a Prostaglandin Receptor in Canine and Rabbit Vascular Smooth Muscle |
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Circulation Research,
Volume 39,
Issue 1,
1976,
Page 66-75
Stanley Greenberg,
Philip Kadowitz,
John Long,
William Wilson,
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摘要:
The contractile response of rabbit renal arteries and canuK tibia] arteries to prostaglandins A,, B,, Fto, E,, E,, D,, and B, was associated with a reduction in total sulfhydryl group content of smooth musde. The total sulfhydryl content of rabbit renal and canine tibial arteries and was not affected by norepinephrine or potassium chloride. Reduction of disulfide groaps with dithlothreitol (DTT) selectively inhibited contractile responses to angiotensin and prostaglandins; 5.5'-Ditfalobisnitrobeazoic acid (DTNB), a sulfhy-dryl group-oxidizing agent, reversed the inhibitory effect of DTT on toe contractile responses to prostaglandins. Alkylation of free sulfhydryl groups with ethacrynic acid did not affect the contractile response of isolated canine tibial or rabbit renal arteries to any agonist studied. Etfaacrynic add added to muscle strips exposed to DTT resulted in alkylation of sulfhydryl groups produced by reduction of disulfide bonds and irrerersibly prevented DTNB-ioduced reversal of DTT inhibition of contractile responses to prostaglandins. However, addition of ethacrynic add to muscle strips contracted by prostaglandins did not inhibit subsequent responses to these acidic lipids. These findings support the hypothesis that con tractile responses of rabbit renal and canine tibial arteries to prosta glandins are dependent on interactions between prostaglandins and disulfide groups located in or on the vascular smooth muscle cell, and the concept that membrane disulfide groups may be integral com ponents of vascular smooth muscle receptors for prostaglandins.
ISSN:0009-7330
出版商:OVID
年代:1976
数据来源: OVID
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