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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Diastole

 
 
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Disease relevance of Diastole

  • Furthermore, time from the beginning of diastole to diastolic peak velocity corrected by square root(RR) indicating acceleration of diastolic flow velocity in constrictive pericarditis was significantly less than that in restrictive cardiomyopathy and control subjects (2.8+/-1.2 versus 4.8+/-0.8 and 4.4+/-0.6, respectively; P<.001) [1].
  • The characteristic hemodynamic features of restrictive cardiomyopathy (normal or reduced cardiac index, normal ventricular systolic function, and "dip and plateau" early in diastole) are traditionally associated with pathologic evidence of inflammation, infiltration and fibrosis [2].
  • These observations are consistent with a mechanism of cytosolic calcium overload induced by ouabain, resulting in persistent active myofilament tension development throughout diastole, to cause the observed decrease in diastolic chamber distensibility during ischemia in the ouabain group.(ABSTRACT TRUNCATED AT 400 WORDS)[3]
  • In 5 additional dog hearts fixed in diastole by rapid glutaraldehyde infusion after coronary occlusion, myocardial creep measured by the segment length transducers paralleled sarcomere elongation measured by electron microscopy [4].
  • Nitroglycerin infusion reduced left ventricular size and filling pressure, redistributed diastolic filling to later in diastole as characterized by reduced filling fraction at one-third diastole (left ventricular dysfunction 48.8 +/- 9.7%, nitroglycerin 17.9 +/- 7.9%, p less than 0.001) and shifted downward left ventricular pressure-area plots [5].
 

High impact information on Diastole

  • The atrial septal defect area ranged from 0.2 to 2.4 cm2 (diastole) to 0.5 to 5.6 cm2 (systole) [6].
  • Studies were performed in canine hearts (16) arrested in systole (8) with calcium chloride or arrested in diastole (8) with potassium chloride [7].
  • 7. A highly characteristic pattern showing a prominent peak in coronary velocity in early diastole was observed in 86% of patients, and this pattern was enhanced after injection of intracoronary papaverine [8].
  • Episodes characterized as PVT (n = 20) were associated with amiodarone therapy and had occasional MAP diastole and a significantly longer mean cycle length of 257 +/- 22 msec (p < 0.001) [9].
  • Percent volume increase during the first half of diastole (%V1) was smaller in the AS1 than in the AS2 group [10].
 

Chemical compound and disease context of Diastole

 

Biological context of Diastole

  • Administration of isoproterenol in doses that increased heart rate from 69 +/- 9 to 99 +/- 12 beats/min produced a decrease in diastolic time from 485 +/- 98 to 312 +/- 47 msec and only a slight decrease in percent diastole, from 54.2 +/- 4.3% to 50.6 +/- 3.9% [12].
  • Nitroprusside reduced left ventricular size and filling pressure, increased cardiac output, improved relaxation and redistributed diastolic filling to later in diastole as characterized by a reduced 1/3 filling fraction (19.4 +/- 7.4% versus 51.4 +/- 10%, p less than 0.001) [13].
  • Cardiovascular phase, especially diastole, influences attention and the event-related potential (ERP) of the right hemisphere of the brain [14].
  • Mechanism for bupivacaine depression of cardiac conduction: fast block of sodium channels during the action potential with slow recovery from block during diastole [15].
  • CONCLUSIONS: It is possible that the end-stage ventricles of these patients respond to the reduction in pulmonary and systemic resistances secondary to prostaglandin E1 infusion by increasing stroke volume, with a redistribution of diastolic filling to later in diastole [16].
 

Anatomical context of Diastole

  • The results indicated that (1) the flow profiles, although less blunt than those in the descending aorta, are still nonparabolic, (2) the wall shear in the coronary arteries maintains a high value through diastole, and (3) during intravenous infusions of dipyridamole both coronary flow and wall shear increase [17].
  • Left atrial appendage emptying and filling velocities corresponding to early and late ventricular diastole, respectively, were measured using volume expansion and phenylephrine infusion [18].
  • The purpose of this study was to investigate the role of titin in the length-dependent deactivation that occurs during early diastole, when the myocyte is shortened below slack length [19].
  • METHODS: Selective, beat-to-beat elevations of afterload were induced in anaesthetised open-chest rabbits (n = 9) by abrupt narrowing of the ascending aorta during the diastole of the preceding heartbeat [20].
  • Cardiac troponin I (cTnI) is a phosphoprotein subunit of the troponin-tropomyosin complex that is thought to inhibit cardiac muscle contraction during diastole [21].
 

Associations of Diastole with chemical compounds

  • Atropine, in doses commonly used clinically, may significantly reduce diastolic time and the percent diastole [12].
  • The vasodilator effect of intracoronary norepinephrine injections was determined during prolonged diastoles to avoid the chronotropic and intropic effects of norepinephrine [22].
  • In the microscopic study, shocks were also given during diastole, with delta F recordings at the three recording regions [23].
  • With glucose as the sole substrate, the high energy phosphates, ATP and phosphocreatine, reached maximum values during diastole and minimum values during systole.(ABSTRACT TRUNCATED AT 250 WORDS)[24]
  • Synergistic interaction between angiotensin II (Ang II) and evolving cardiodepression may play an important role in worsening chamber function, particularly in diastole [25].
 

Gene context of Diastole

  • This causes an abnormal Ca2+ leak through the Ca2+ channel located in the RyR, leading to an increase in the cytosolic Ca2+ during diastole, prolongation of the Ca2+ transient, and delayed/slowed diastolic Ca2+ re-uptake [26].
  • CLIC-2 is one of only a few cytosolic inhibitors of cardiac RyR2 channels, and may suppress their activity during diastole and during stress [27].
  • Thus, block of hIRK may persist during diastole and might thereby affect cardiac excitability [28].
  • In this way, phospholamban is an important regulator of SERCA2-mediated myocardial relaxation during diastole [29].
  • Taken together these observations suggest that VIC may have contractile properties, which can account for a controlled tonus, actively correlated with the cyclically changing forces acting on valves during diastole and systole [30].
 

Analytical, diagnostic and therapeutic context of Diastole

References

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  2. Clinical profile of restrictive cardiomyopathy. Benotti, J.R., Grossman, W., Cohn, P.F. Circulation (1980) [Pubmed]
  3. Effects of ouabain and isoproterenol on left ventricular diastolic function during low-flow ischemia in isolated, blood-perfused rabbit hearts. Lorell, B.H., Isoyama, S., Grice, W.N., Weinberg, E.O., Apstein, C.S. Circ. Res. (1988) [Pubmed]
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  11. Dobutamine effects on systole and diastole in rats with myocardial infarction. Cove, C.J., Widman, S.C., Liang, C.S., Schenk, E.A., Hood, W.B. Am. J. Med. Sci. (1995) [Pubmed]
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  14. Cardiovascular phase relationships to the cortical event-related potential of schizophrenic, depressed, and normal subjects. Sandman, C.A., Vigor-Zierk, C.S., Isenhart, R., Wu, J., Zetin, M. Biol. Psychiatry (1992) [Pubmed]
  15. Mechanism for bupivacaine depression of cardiac conduction: fast block of sodium channels during the action potential with slow recovery from block during diastole. Clarkson, C.W., Hondeghem, L.M. Anesthesiology (1985) [Pubmed]
  16. Combined hemodynamic echocardiographic Doppler evaluation of prostaglandin E1 effects in patients with severe dilated cardiomyopathy undergoing evaluation for heart transplantation. Barbieri, E., Perini, P., Marino, P., Zardini, P. J. Heart Lung Transplant. (1995) [Pubmed]
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  19. Titin determines the Frank-Starling relation in early diastole. Helmes, M., Lim, C.C., Liao, R., Bharti, A., Cui, L., Sawyer, D.B. J. Gen. Physiol. (2003) [Pubmed]
  20. Afterload induced changes in myocardial relaxation: a mechanism for diastolic dysfunction. Leite-Moreira, A.F., Correia-Pinto, J., Gillebert, T.C. Cardiovasc. Res. (1999) [Pubmed]
  21. Protein kinase C and A sites on troponin I regulate myofilament Ca2+ sensitivity and ATPase activity in the mouse myocardium. Pi, Y., Zhang, D., Kemnitz, K.R., Wang, H., Walker, J.W. J. Physiol. (Lond.) (2003) [Pubmed]
  22. Feedforward control of coronary blood flow via coronary beta-receptor stimulation. Miyashiro, J.K., Feigl, E.O. Circ. Res. (1993) [Pubmed]
  23. Optical transmembrane potential measurements during defibrillation-strength shocks in perfused rabbit hearts. Zhou, X., Ideker, R.E., Blitchington, T.F., Smith, W.M., Knisley, S.B. Circ. Res. (1995) [Pubmed]
  24. Energy levels at systole vs. diastole in normal hamster hearts vs. myopathic hamster hearts. Sievers, R., Parmley, W.W., James, T., Wikman-Coffelt, J. Circ. Res. (1983) [Pubmed]
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