Abnormalities in arterial-ventricular coupling in older healthy persons are attenuated by sodium nitroprusside

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11
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article
Data de publicação
2011
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Editora
AMER PHYSIOLOGICAL SOC
Autores
CHANTLER, Paul D.
GERSTENBLITH, Gary
SCHULMAN, Steven P.
BECKER, Lewis C.
FERRUCCI, Luigi
FLEG, Jerome L.
LAKATTA, Edward G.
NAJJAR, Samer S.
Citação
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, v.300, n.5, p.H1914-H1922, 2011
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Unidades Organizacionais
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Resumo
Chantler PD, Nussbacher A, Gerstenblith G, Schulman SP, Becker LC, Ferrucci L, Fleg JL, Lakatta EG, Najjar SS. Abnormalities in arterial-ventricular coupling in older healthy persons are attenuated by sodium nitroprusside. Am J Physiol Heart Circ Physiol 300: H1914-H1922, 2011. First published March 4, 2011; doi:10.1152/ajpheart.01048.2010.-The coupling between arterial elastance (E(A); net afterload) and lea ventricular elastance (E(LV); pump performance), known as E(A)/E(LV), is a key determinant of cardiovascular performance and shifts during exercise due to a greater increase in E(LV) versus E(A). This normal exercise-induced reduction in E(A)/E(LV) decreases with advancing age. We hypothesized that sodium. nitroprusside (SNP) can acutely ameliorate the age-associated deficits in E(A)/E(LV). At rest and during graded exercise to exhaustion, EA was characterized as end-systolic pressure/stroke volume and E(LV) as end-systolic pressure/end-systolic volume. Resting E(A)/E(LV): did not differ between old (70 +/- 8 yr. n = 15) and young (30 +/- 5 yr. n = 17) subjects because of a tandem increase in E(A) and E(LV) in older subjects. During peak exercise, a blunted increase in E(LV) in old (7.8 +/- 3.1 mmHg/ml) versus young (11.4 +/- 6.5 mmHg/ml) subjects blunted the normal exercise-induced decline in E(A)/E(LV) in old (0.25 +/- 0.11) versus young (0.16 +/- 0.05) subjects. SNP administration to older subjects lowered resting E(A)/E(LV) by 31% via a reduction E(A) (10%) and an increase in E(LV) (47%) and lowered peak exercise E(A)/E(LV) (36%) via an increase in E(LV) (68%) without a change in E(A). Importantly, SNP attenuated the age-associated deficits in E(A)/E(LV) and E(LV) during exercise, and at peak exercise E(A)/E(LV) in older subjects on drug administration did not differ from young subjects without drug administration. In conclusion, some age-associated deficiencies in E(A)/E(LV), E(A), and E(LV), in older subjects can be acutely abolished by SNP infusion. This is relevant to common conditions in older subjects associated with a significant impairment of exercise performance such as frailty or heart failure with preserved ejection fraction.
Palavras-chave
aging, exercise
Referências
  1. SUNAGAWA K, 1983, AM J PHYSIOL, V245, pH773
  2. Lakatta EG, 2003, CIRCULATION, V107, P346, DOI 10.1161/01.CIR.0000048893.62841.F7
  3. VANDENHORN GJ, 1985, CIRC RES, V56, P252
  4. Chemla D, 2003, AM J PHYSIOL-HEART C, V285, pH614, DOI 10.1152/ajpheart.00823.2002
  5. Kass DA, 2005, HYPERTENSION, V46, P185, DOI 10.1161/01.HYP.0000168053.34306.d4
  6. PEPINE CJ, 1979, J CLIN INVEST, V64, P643, DOI 10.1172/JCI109505
  7. Laurent S, 2006, EUR HEART J, V27, P2588, DOI 10.1093/eurheartj/ehl254
  8. STARLING MR, 1993, AM HEART J, V125, P1659, DOI 10.1016/0002-8703(93)90756-Y
  9. SCHULMAN SP, 1992, AM J PHYSIOL, V263, pH1932
  10. COHENSOLAL A, 1994, J HYPERTENS, V12, P591
  11. Vila-Petroff MG, 1999, CIRC RES, V84, P1020
  12. FLEG JL, 1994, CIRCULATION, V90, P2333
  13. CARROLL JD, 1991, J CLIN INVEST, V87, P1002, DOI 10.1172/JCI115058
  14. SIMON AC, 1979, AM J CARDIOL, V44, P505, DOI 10.1016/0002-9149(79)90404-1
  15. Chantler PD, 2008, J APPL PHYSIOL, V105, P1342, DOI 10.1152/japplphysiol.90600.2008
  16. SUGA H, 1990, PHYSIOL REV, V70, P247
  17. Lakatta EG, 2003, CIRCULATION, V107, P139, DOI 10.1161/01.CIR.0000048892.83521.58
  18. MILLER RR, 1975, CIRCULATION, V51, P328
  19. WEINBERGER MH, 1991, HYPERTENSION, V18, P67
  20. Redfield MM, 2005, CIRCULATION, V112, P2254, DOI 10.1161/CIRCULATIONAHA.105.541078
  21. Shah AM, 2000, PHARMACOL THERAPEUT, V86, P49, DOI 10.1016/S0163-7258(99)00072-8
  22. Najjar SS, 2004, J AM COLL CARDIOL, V44, P611, DOI 10.1016/j.jacc.2004.04.041
  23. LASKEY WK, 1987, CIRCULATION, V75, P711
  24. Pauca AL, 2001, HYPERTENSION, V38, P932, DOI 10.1161/hy1001.096106
  25. KELLY RP, 1992, CIRCULATION, V86, P513
  26. YIN FCP, 1983, CIRCULATION, V67, P1330
  27. de Simone G, 1999, HYPERTENSION, V33, P800
  28. Chen CH, 1998, J AM COLL CARDIOL, V32, P1221, DOI 10.1016/S0735-1097(98)00374-X
  29. Chantler PD, 2005, AM J PHYSIOL-HEART C, V289, pH2059, DOI 10.1152/ajpheart.00022.2005
  30. Chemla D, 1998, AM J PHYSIOL-HEART C, V274, pH500
  31. FLEG JL, 1995, J APPL PHYSIOL, V78, P890
  32. FREIS ED, 1988, AM J CARDIOL, V61, P117, DOI 10.1016/0002-9149(88)91316-1
  33. LAKATTA EG, 1987, J AM COLL CARDIOL, V10, P1157
  34. LITTLE WC, 1991, AM J PHYSIOL, V261, pH70
  35. LIU ZR, 1986, AM J PHYSIOL, V251, pH588
  36. MILLER RR, 1982, PROG CARDIOVASC DIS, V24, P353, DOI 10.1016/0033-0620(82)90019-6
  37. Nussbacher A, 1999, AM J PHYSIOL-HEART C, V277, pH1863
  38. OGAWA H, 1984, JPN CIRC J, V48, P405
  39. POULEUR H, 1980, CIRCULATION, V61, P328
  40. RANDALL OS, 1986, J HYPERTENS, V4, pS293
  41. ROY LF, 1989, CIRCULATION, V79, P383
  42. SAGAWA K, 1977, AM J CARDIOL, V40, P748, DOI 10.1016/0002-9149(77)90192-8
  43. SEALS DR, 1994, MED SCI SPORT EXER, V26, P568
  44. Segers P, 2002, AM J PHYSIOL-HEART C, V282, pH1041
  45. SIMON AC, 1977, BRIT HEART J, V39, P799