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Natriuretic peptides in sheep with pressure overload left ventricular hypertrophy
Tekijät: Charles CJ, Kaaja RJ, Espiner EA, Nicholls MG, Pemberton CJ, Richards AM, Yandle TG
Julkaisuvuosi: 1996
Journal: Clinical and Experimental Hypertension
Tietokannassa oleva lehden nimi: Clinical and experimental hypertension (New York, N.Y. : 1993)
Lehden akronyymi: Clin Exp Hypertens
Vuosikerta: 18
Numero: 8
Aloitussivu: 1051
Lopetussivu: 71
Sivujen määrä: 21
ISSN: 1064-1963
DOI: https://doi.org/10.3109/10641969609081034
Tiivistelmä
To examine tissue and plasma atrial (ANP) and brain natriuretic peptide (BNP) responses to left ventricular hypertrophy (LVH) 7 sheep underwent suprarenal aortic banding (20 mmHg initial pressure differential). Median survival time was 15 days. Proximal mean aortic pressure (MAP) increased from 65.1 +/- 5.0 mmHg (baseline) to 111.6 +/- 7.5 mmHg (day 7, p < 0.0001). Distal systolic aortic pressure fell from 85.5 +/- 8.7 mmHg (baseline) to 55.6 +/- 6.4 mmHg (day 7, p = 0.0002). Maximal plasma ANP (26.9 +/- 3.6 vs 10.1 +/- 1.2 pmol/L, p = 0.005) and BNP (15.3 +/- 3.6 vs. 3.5 +/- 1.0 pmol/L, p = 0.006) were recorded at 15 +/- 4.0 days. Coarctation induced rapid increases in PRA and plasma aldosterone and a fall in urinary sodium. Post-mortem examination of hearts confirmed LVH. Compared with controls, tissue ANP concentration was reduced in left atrium (p = 0.04) and LV (p = 0.04). BNP concentration was reduced in left atrium (p = 0.02) but tended to be higher in LV. In conclusion, suprarenal aortic coarctation leads to progressive hypertension resulting in LVH, progressive increases in plasma ANP and BNP and, in most cases, death from heart failure.
To examine tissue and plasma atrial (ANP) and brain natriuretic peptide (BNP) responses to left ventricular hypertrophy (LVH) 7 sheep underwent suprarenal aortic banding (20 mmHg initial pressure differential). Median survival time was 15 days. Proximal mean aortic pressure (MAP) increased from 65.1 +/- 5.0 mmHg (baseline) to 111.6 +/- 7.5 mmHg (day 7, p < 0.0001). Distal systolic aortic pressure fell from 85.5 +/- 8.7 mmHg (baseline) to 55.6 +/- 6.4 mmHg (day 7, p = 0.0002). Maximal plasma ANP (26.9 +/- 3.6 vs 10.1 +/- 1.2 pmol/L, p = 0.005) and BNP (15.3 +/- 3.6 vs. 3.5 +/- 1.0 pmol/L, p = 0.006) were recorded at 15 +/- 4.0 days. Coarctation induced rapid increases in PRA and plasma aldosterone and a fall in urinary sodium. Post-mortem examination of hearts confirmed LVH. Compared with controls, tissue ANP concentration was reduced in left atrium (p = 0.04) and LV (p = 0.04). BNP concentration was reduced in left atrium (p = 0.02) but tended to be higher in LV. In conclusion, suprarenal aortic coarctation leads to progressive hypertension resulting in LVH, progressive increases in plasma ANP and BNP and, in most cases, death from heart failure.
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