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MeSH Review

Ventricular Pressure

 
 
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Disease relevance of Ventricular Pressure

 

High impact information on Ventricular Pressure

  • Despite the fact that glycolytic flux had been blocked both by iodoacetate and by absence of substrate, end-diastolic left ventricular pressure (EDP) remained unchanged (P > 0.15, n = 6) [6].
  • Dobutamine significantly increased the slope of the left ventricular end-systolic pressure-volume relation (Emax) and the slope of the dP/dtmax-end-diastolic volume relation (dE/dtmax), while significantly decreasing the time from end-diastole to end-systole (tmax) and the time constant (T) of the isovolumic fall in left ventricular pressure [7].
  • In 9 of 11 patients there was a substantial downward displacement of the diastolic pressure-volume curve during nitroprusside infusion, with left ventricular pressure being lower for any given volume with nitroprusside [8].
  • In patients with hypertrophic obstructive cardiomyopathy, synchronised and ventricular pacing at optimum AV interval for the individual reduces the intraventricular pressure gradient and improves functional tolerance [9].
  • However, in MCT-treated rats, LU 135252 therapy significantly reduced right ventricular pressure (39.7 +/- 2.1 mm Hg), potentiated acetylcholine-induced vasodilatation (delta Emax, from 1.6 +/- 0.2 to 3.7 +/- 0.4 mm Hg), and improved the responses to sodium nitroprusside (delta Emax, from 2.7 +/- 0.3 to 5.6 +/- 0.6 mm Hg) [10].
 

Chemical compound and disease context of Ventricular Pressure

 

Biological context of Ventricular Pressure

 

Anatomical context of Ventricular Pressure

 

Associations of Ventricular Pressure with chemical compounds

  • During isoproterenol compared with pacing, peak left ventricular pressure was higher (205 +/- 33 vs. 142 +/- 21 mm Hg, p less than 0.001), ejection fraction was higher (77 +/- 10% vs. 71 +/- 12%, p less than 0.02), and regional systolic nonuniformity was diminished [26].
  • The significant upward shift and attenuation by propranolol were also observed even when the left ventricular pressure was corrected by the subtraction of right atrial pressure [27].
  • Norepinephrine infusion increased systolic left ventricular pressure and SPG, while left ventricular end-diastolic pressure and left atrial pressure diminished [28].
  • We investigated the effects of nifedipine on left ventricular diastolic function in 17 asymptomatic or minimally symptomatic patients with hypertrophic cardiomyopathy by simultaneously measuring left ventricular pressure and volume with a catheter-tipped manometer and biplane cineangiography [29].
  • In 13 patients left ventricular pressure measurements were made with a micromanometer to permit assessment of peak negative dP/dt and the time constant of left ventricular isovolumic relaxation, T, before and after milrinone [30].
 

Gene context of Ventricular Pressure

  • The increase of isovolumic peak first derivative of left ventricular pressure (ET-1: -2%; molsidomine+ET-1: +16%; BQ 610+ET-1: +19%) after pretreatment with molsidomine or BQ 610 indicates that these drugs unmask the positive inotropy of ET-1 [31].
  • The first derivatives of intraventricular pressure (+/- dP/dt) were also significantly elevated, and this was associated with an increase in the affinity of the SR Ca(2+)-ATPase for Ca2+ in the phospholamban-deficient hearts [32].
  • 3.In the unstimulated perfused heart, the left ventricular pressure (LVP) and maximal rate of left ventricular force development (dP/dtmax) of eNOS-/- hearts were not significantly different from those of WT hearts (LVP: 97 +/- 11 mmHg WT vs. 111 +/- 11 mmHg eNOS-/-; dP/dtmax: 3700 +/- 712 mmHg s(-1) WT vs. 4493 +/- 320 mmHg s)-1) eNOS-/-) [33].
  • In HCM patients, the plasma BNP concentration may reflect the intraventricular pressure gradient and left ventricular diastolic dysfunction whereas the plasma ANP concentration reflects only the left ventricular diastolic dysfunction [34].
  • Balloon inflation to raise ventricular pressure in hearts perfused with cardioplegic solution also activated FAK and ERK1/2 [35].
 

Analytical, diagnostic and therapeutic context of Ventricular Pressure

References

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  16. Nifedipine protects the heart from the acute deleterious effects of cocaine if administered before but not after cocaine. Hale, S.L., Alker, K.J., Rezkalla, S.H., Eisenhauer, A.C., Kloner, R.A. Circulation (1991) [Pubmed]
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  22. Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man. Bourdillon, P.D., Lorell, B.H., Mirsky, I., Paulus, W.J., Wynne, J., Grossman, W. Circulation (1983) [Pubmed]
  23. Alpha-adrenergic-mediated reduction in coronary blood flow secondary to carotid chemoreceptor reflex activation in conscious dogs. Murray, P.A., Lavallee, M., Vatner, S.F. Circ. Res. (1984) [Pubmed]
  24. Doppler echocardiographic demonstration of the differential effects of right ventricular pressure and volume overload on left ventricular geometry and filling. Louie, E.K., Rich, S., Levitsky, S., Brundage, B.H. J. Am. Coll. Cardiol. (1992) [Pubmed]
  25. Effect of glucocorticoids on collagen accumulation in pulmonary vascular remodeling in the rat. Poiani, G.J., Tozzi, C.A., Thakker-Varia, S., Choe, J.K., Riley, D.J. Am. J. Respir. Crit. Care Med. (1994) [Pubmed]
  26. Beta-adrenergic stimulation with isoproterenol enhances left ventricular diastolic performance in hypertrophic cardiomyopathy despite potentiation of myocardial ischemia. Comparison to rapid atrial pacing. Udelson, J.E., Cannon, R.O., Bacharach, S.L., Rumble, T.F., Bonow, R.O. Circulation (1989) [Pubmed]
  27. Exercise-induced upward shift of diastolic left ventricular pressure-volume relation in patients with dilated cardiomyopathy. Effects of beta-adrenoceptor blockade. Sato, H., Hori, M., Ozaki, H., Yokoyama, H., Imai, K., Morikawa, M., Takeda, H., Inoue, M., Kamada, T. Circulation (1993) [Pubmed]
  28. Dynamic aspects of acute mitral regurgitation: effects of ventricular volume, pressure and contractility on the effective regurgitant orifice area. Yoran, C., Yellin, E.L., Becker, R.M., Gabbay, S., Frater, R.W., Sonnenblick, E.H. Circulation (1979) [Pubmed]
  29. Effects of nifedipine on left ventricular diastolic function in patients with asymptomatic or minimally symptomatic hypertrophic cardiomyopathy. Yamakado, T., Okano, H., Higashiyama, S., Hamada, M., Nakano, T., Takezawa, H. Circulation (1990) [Pubmed]
  30. Improvement in indexes of diastolic performance in patients with congestive heart failure treated with milrinone. Monrad, E.S., McKay, R.G., Baim, D.S., Colucci, W.S., Fifer, M.A., Heller, G.V., Royal, H.D., Grossman, W. Circulation (1984) [Pubmed]
  31. Inotropic effects of endothelin-1: interaction with molsidomine and with BQ 610. Beyer, M.E., Slesak, G., Hövelborn, T., Kazmaier, S., Nerz, S., Hoffmeister, H.M. Hypertension (1999) [Pubmed]
  32. Targeted ablation of the phospholamban gene is associated with markedly enhanced myocardial contractility and loss of beta-agonist stimulation. Luo, W., Grupp, I.L., Harrer, J., Ponniah, S., Grupp, G., Duffy, J.J., Doetschman, T., Kranias, E.G. Circ. Res. (1994) [Pubmed]
  33. Inotropic response to beta-adrenergic receptor stimulation and anti-adrenergic effect of ACh in endothelial NO synthase-deficient mouse hearts. Gödecke, A., Heinicke, T., Kamkin, A., Kiseleva, I., Strasser, R.H., Decking, U.K., Stumpe, T., Isenberg, G., Schrader, J. J. Physiol. (Lond.) (2001) [Pubmed]
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  38. Increased [18F]fluorodeoxyglucose accumulation in right ventricular free wall in patients with pulmonary hypertension and the effect of epoprostenol. Oikawa, M., Kagaya, Y., Otani, H., Sakuma, M., Demachi, J., Suzuki, J., Takahashi, T., Nawata, J., Ido, T., Watanabe, J., Shirato, K. J. Am. Coll. Cardiol. (2005) [Pubmed]
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