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

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Levine, T.B. et al.

Hemodynamic and regional blood flow response to captopril in congestive heart failure.

In 19 patients with moderate to severe congestive heart failure the over-all hemodynamic response to captopril was compared with its effect on regional blood flow. Ninety minutes after administering a single dose of captopril (25 to 150 mg), right atrial pressure decreased from 6.1 +/- 6.1 to 3.2 +/- 5.1 mm Hg (p less than 0.001), pulmonary artery pressure from 33.1 +/- 8.3 to 26.5 +/- 9.1 mm Hg (p less than 0.001), pulmonary capillary wedge pressure from 22.4 +/- 6.2 to 15.2 +/- 7.4 mm Hg to (p less than 0.001), mean arterial pressure from 77.2 +/- 8.0 to 66.5 +/- 13.7 mm Hg (p less than 0.001), and systemic vascular resistance from 1,630 +/- 503 to 1,233 +/- 443 dyne-s-cm-5 (p less than 0.001), and cardiac index increased from 2.0 +/- 0.6 to 2.4 +/- 0.7 l/minute/m2 (p less than 0.001). Despite the significant increase in cardiac index there was no increase in either hepatic blood flow (203 +/- 212 to 142 +/- 101 units, N.S.) or forearm blood flow (2.2 +/- 0.9 to 2.2 +/- 1.0 ml/100 g per minute, N.S.) after captopril. Similarly, the global reduction in systemic vascular resistance was not accompanied by a reduction in either hepatic vascular resistance (0.93 +/- 0.90 to 0.83 +/- 0.69 units, N.S.) or forearm vascular resistance (41.3 +/- 18.4 to 34.9 +/- 12.4 mm Hg/ml/100 g per minute, N.S.). The over-all improvement in hemodynamics that is seen when captopril is given to patients with severe heart failure does not apply uniformally to all vascular beds. The heterogeneous response reflects the variable vasoconstrictor part played by the renin-angiotensin system in regulating flow to individual regional circulations.[1]

References

Hemodynamic and regional blood flow response to captopril in congestive heart failure. Levine, T.B., Olivari, M.T., Cohn, J.N. Am. J. Med. (1984) [Pubmed]

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