ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Pressure-induced cardiac enlargement was created in neonatal (21 days of age) and adult (250-275 g) rats by abdominal aortic constriction. Sham-operated and aorta-constricted neonates were studied 2, 3, 4, and 5 weeks after surgery. Left ventricular weight was elevated by approximately 50% at all times studied. Radioautography demonstrated a marked elevation in3H-thymidine-labeled nuclei in cardiac muscle and nonmusde cells in aortaconstricted neonates. Other experiments examined the functional characteristics of hearts subjected to pressure overload while in either the neonatal or the adult state. Five weeks after surgery, left ventricular pressure and left ventricular weight were elevated to nearly identical degrees in both groups of experimental rat*. Under control conditions, heart rate and the maximum rate of left ventricular pressure development were not altered significantly in either neonatal or adult rats with aortic constriction. Aortic peak flow velocity, cardiac index, and stroke index also were within normal limits in neonates with aortic constriction; however, these measurements were reduced significantly in adults with aortic constriction. Stroke volume augmentation in response to saline infusion and inotropic responsiveness to isoproterenol were unaltered in aorta-constricted neonates but were markedly attenuated in aorta-constricted adults. The maintenance of normal heart functional characteristics represents a major point of distinction between pressure-induced cardiac enlargement in neonatal and aduh rats which correlates with the presence or absence of cardiac muscle ceD proliferation during adaptive heart growth.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Experimental hyperthyroidism induced in rats by daily injections of 20μg of 3+-,3+-,5-triiodothyronlne (T,) resulted in a prompt increase in cardiac weight and RNA content. The mechanism of the RNA synthesis stimulation was studied by comparing template activity of myocardial chromatin from rats treated with T3for 7 days with chromatin from euthyroid controls. Hyperthyroidism resulted in significant enhancement of chromatin template activity (184 ± 7.1 pmol1H-UMP/mg per minute va. 106 ± 4.8 pmol3H-UMP/mg per minute;P< 0.001) and a significantly higher (102% more) number of transcription initiation sites. Dissociation of chromatin and subsequent reconstitution with nudeoproteins from both hyper- and euthyroid rats demonstrated that the non-hlstone nuclear fraction (NHPs) accounted for the differences in RNA synthesis between the two groups. Sodium dodecyl sulfate (SDS) poryacrylamide gel electrophoretic patterns of NHPs were similar for the two groups, but NHPs from hyperthyroid rats exhibited significantly higher degrees of phospborylation because of higher nuclear protein kinase activity (71 ± 2.6 (JL mol PJmg per minute vs. 37 ± 1.9 μmol P|/mg per minute in controls,P< 0.01). In vitro stimulation of RNA synthesis by NHPs was enhanced by the addition of protein kinase and cyclic adenosine 3+-,5+-monophosphate findings suggest that stimulation of RNA synthesis in the myocardium of hyperthyroid rats is mediated by the nuclear NHPs and is dependent on phosphorylation of these proteins by nuclear protein kinases.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Infusion of small amounts of plasma (1-2%) into isolated hearts perfused with Tyrode+-s solution causes vasoconstriction and augments regulation of coronary flow in response to changes in perfusion pressure (autoregulation). When plasma infusion is stopped, the vasoconstrictor effect dissipates within 5 minutes, whereas the autoregnlatory response remains for about 15 minutes. Thus the plasma-augmented autoregubtory response is not dependent on plasma-Induced vasoconstriction. Indomethadn (10 μml), an inhibitor of prostaglandin synthetase, causes coronary vasodflation and also abolishes the lingering autoregulatory response. These effects of indomethacin are counteracted by the addition of 1.5% plasma to the perfusate. Purification procedures led to the extraction of an active material from plasma which migrates as a single substance in thin layer chromatograms. This substance causes coronary vasoconstriction, augments autoregulation, and counteracts the effects of indometbacin in isolated rabbit hearts as effectively as plasma. The purified vasoactive substance stimulates a 2-fold increase in cardiac microsomal prostaglandin synthesis and a 5-fold increase using renal microsomal preparations. This substance counteracts indomethadn-induced inhibition of prostaglandin synthesis in microsomal preparations. These results provide convincing evidence that the effects of this pbtma constituent on the coronary vasculature are mediated by stimulation of prostaglandin synthesis. Thus it appears that prostaglandin synthesis plays an integral role In both the maintenance of coronary vascular tone and the autoregulatory response in isolated rabbit hearts.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

We analyzed mechanical properties of kitten papillary muscles both at rest and in BiI+contractore by the frequency response method. Hie mosde length was perturbed sinusoidal)}, with an amplitude less than 0.3% of Lou, over a frequency range from 0.1 to 60 Hz to determine the dynamic stiffness, F(ω;)/L(ω;), in which F(ω) = amplitude of the force response wave, L(ω) = amplitude of sinusoidal length wave, and ω = frequency, and the phase shift of F(ω) relative to L(ω). In resting muscles, the dynamic stiffness increased minutely with increasing frequency and the phase relation showed a small lead over the entire frequency range. In muscles in contracture at low temperature (22-24°C), the stiffness first decreased with increasing frequency from about 0.2 to 1 Hz, then increased with a slope of 10-fold/decade, and finally plateaued over the range above 8 Hz. The phase relation snowed a small lag between 0.3 and 0.5 Hz, but a clear lead of up to 60° between 0.8 and 16 Hz. With an increase in temperature to 36°C, the peculiar decrease in stiffness and the phase lag in the low frequency region decreased in size and shifted to a higher frequency region (about 4 Hz). These findings led us to two alternative, approximate analogues, which are similar to but simpler than that previoudy proposed for a twitching papillary muscle.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Open-tip microelectrodes containing a potassium-sensitive liquid ion exchanger (Coming 477317) were used to study the effects of ouabain on the intraceUular potassium activity and the transmembrane potentials of beating canine cardiac Purkinje fibers. The preparations were superfused with Tyrode+-s solution containing ouabain, 2 × 10−7M, and potassium, 4 mM, for 30 minutes. At the end of this period, intracellular potassium activity had decreased from the control value of 130.0 mM to 112.2 mM. The resting membrane potential determined through conventional 3 M KG-filed microelectrodes decreased from−83. 6 to−78.8 mV. Comparison of the decrease in the potassium equilibrium potential with the decrease in the resting membrane potential suggests that there was an accumulation of potassium at the exterior surface of the cell membrane. The effect of ouabain on the resting membrane potential, therefore, was due to a change in the transmembrane potassium ion gradient. This, In turn, resulted from a decrease in intracellular potassium activity and, apparently, from an increased potassium activity at the cell surface.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

We studied tension changes in vertebrate cardiac muscles resulting from quick stretches and releases and sinusoidal length changes during sustained contractures at various amplitudes of length change and at various temperatures. Muscles in contracture respond to lengthening with activation and to release with deactivation in tension, both of which are delayed. The amplitude of the delayed tension reached as much as 100 g/cm11 % AL but was dependent on the musde length and level of activation. Delayed tension amplitude averaged about 15 to 25 g/ cm11% AL. The delayed tension rise is an active process, a reaction of the rayofibrillar system to the length change. Muscle stiffness increases during the delayed tension rise while muscle length is kept constant. With sinusoidal length changes, characteristic frequency responses appear in tension and in stiffness. At room temperature, in papillary muscle, tension change is delayed in respect to the length changed in the frequency range 0.05-1.2 cycles/sec, giving rise to work output. The power output increases with the square of the amplitude and can exceed 0.6 mNm/cyde− g. At the frequency of mrimal work output, the phase shift may be more than 50°, leading to the paradox that muscle force decreases for a period of time while the muscle U undergoing stretch. At higher frequencies (>1.2 cycles/sec), the tension change precedes the length change, Indicating that the muscle now absorbs work. In the latter same frequency range, the dynamic stiffness may drop by as much as a factor of 6. The time constant of delayed tension onset, the frequency range of power output, and stiffness changes suggest that the kinetics and turnover frequency of the crossbridges are specific for each animal and that an optimal timing exists between the biochemical and mechanical cycle such that the optimal frequency of mechanical performance correlates with the frequency of the natural heart beat.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Recognition of states in which the heart is vulnerable to arrhythmia would be a helpful guide to prophylaxis. The possibility of recognizing such states from the ECG is suggested by the already established relations between abnormally disparate recovery to both vulnerability to arrhythmia and ECG waveform. In this study, canine QRS, T, and QRST isoarea maps were determined from ECGs recorded at 192 body sites during control states and conditions of enhanced susceptibility to arrhythmia. Vulnerable states were produced by ouabain intoxication, hypothermia, premature beats, and epinephrine infusion. A hypothetical series of QRST isoarea maps that would be expected to occur without increased local inequalities of recovery was derived by adding the control QRS isoarea map to a fraction (α) of the control T isoarea map and allowing the fraction to vary from α = 1 to α =−1. One QRST isoarea map selected from the derived series was subtracted from a QRST isoarea map during each state of enhanced arrhythmia vulnerability. Derived maps were selected to minimize the average amplitude of the residual maps. RMS values of the residual maps systematically increased with increasing prematurity of depolarization, with time after a toxic injection of a dose of ouabain, with increasing hypothermia, and during the first 3 minutes of epinephrine infusion. Also, the RMS values of the residual maps decreased in hypothermic dogs during rewarming. Our findings suggest that states of vulnerability to arrhythmia due to increased disparity of recovery can be identified by analysis of ECG waveforms recorded from lead systems sensitive to electrical activity in local cardiac regions.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

In pentobrabital-anesthetized open-chest dogs, myocardial adenosine content is elevated by 5 or 15 seconds of left coronary artery occlusion and falls exponentially to control levels during reactive hyperemia. The rate constants for adenosine dissipation are (mean ± SEM):−0.08 ± 0.01 and−0.034 ± 0.007 sec"1after 5- and 15-second ocdusion, respectively. Kinetic analysis of the reactive hyperemia flow curves (Circ Res 14/15 (suppl I): 81-85, 1963) predicts rates of−0.069 ± 0.009 sec"+- and−0.04 ± 0.009 sec"1, indicating that changes in adenosine levels can account for the way coronary flow changes during this response. The log (dose-) response curve relating reactive hyperemia flow to tissue adenosine concentration has a steeper slope and is half-maximal at a lower adenosine concentration than the dose-response curve obtained by intracoronary infusions of adenosine in oxygenated hearts, indicating that the coronary vasoactivity of adenosine is enhanced during reactive hyperemia. This could explain why theophyfline antagonizes the coronary vasodlatory effect of adenosine in oxygenated hearts but has relatively little effect on reactive hyperemia.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Human postmortem digital arteries obtained between 6 and 60 hours after death were used for in vitro studies of vascular smooth muscle physiology and pharmacology. Isometric tension was recorded from spiral strips in tissue baths at 37°C. The responses were durable and reproducible and were similar to those of 10 operative specimens of visceral arteries. The contractile force of the preparations was unrelated to the time elapsed since death. Norepinephrine, 5-hydroxytryptamine, and barium chloride gave the strongest responses; histamlne and potassium chloride were weaker agonists. Hie order of sensitivities to the agonists tested was angiotensin > 5- hydroxytryptamine > norepinephrine > histamlne > barium chloride > potassium chloride. Both competitive (phentolamlne) and noncompetitive (phenoxybenzamlne) antagonism of DorepiDephrine was demonstrated. Pbentolamine was also a weak inhibitor of 5-hydroxytryptamine. Cyprobeptadine was a potent antagonist of 5-hydroxytryptamine, but had less effect against norepinephrine. This suggests the presence of separate receptors for 5- hydroxytryptamine and norepinephrine in these vessels. The response to barium chloride was inhibited by the calcium-antagonist, verapamil. The α-adrenoceptor antagonist, phentolamlne, was not effective against barium chloride. We conclude that human postmortem digital arteries can be studied effectively in vitro. The preparation should be useful for the evaluation of drugs that are thought to act at a peripberal vascular site.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID