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慢性普萘洛尔治疗可降低清醒犬的肺动脉压。

Chronic propranolol treatment decreases pulmonary artery pressure in conscious dogs.

作者信息

Voelkel N F, Walker B R, Reeves J T

出版信息

Clin Physiol Biochem. 1984;2(4):176-83.

PMID:6488695
Abstract

Daily administration of propranolol to 9 chronically instrumented, trained dogs for 2 weeks caused significant (p less than 0.05) decreases in heart rate (70 +/- 8 to 57 +/- 6 beats/min), cardiac output (3.6 +/- 0.3 to 2.9 +/- 0.2 liters/min), pulmonary arterial pressure (15.7 +/- 0.5 to 10.0 +/- 0.5 mm Hg) and total pulmonary vascular resistance (4.6 +/- 0.6 to 3.3 +/- 0.4 units). Nadolol, a structurally dissimilar beta-adrenergic receptor antagonist, caused a similar decrease in total pulmonary resistance. Acute meclofenamate administration did not return to normal pulmonary arterial pressure and resistance in the dogs chronically treated with beta-adrenergic receptor blockers. We therefore conclude that chronic beta-adrenergic receptor blockade lowered pulmonary arterial pressure and resistance by a mechanism independent of cyclooxygenase. In addition, chronic beta-adrenergic receptor blockade did not affect the potential for hypoxic vasoconstriction.

摘要

对9只长期植入仪器并经过训练的犬每日给予普萘洛尔,持续2周,可使心率(从70±8次/分钟降至57±6次/分钟)、心输出量(从3.6±0.3升/分钟降至2.9±0.2升/分钟)、肺动脉压(从15.7±0.5毫米汞柱降至10.0±0.5毫米汞柱)和总肺血管阻力(从4.6±0.6单位降至3.3±0.4单位)显著降低(p<0.05)。纳多洛尔,一种结构不同的β-肾上腺素能受体拮抗剂,可使总肺阻力产生类似降低。急性给予甲氯芬那酸未能使长期接受β-肾上腺素能受体阻滞剂治疗的犬的肺动脉压和阻力恢复正常。因此,我们得出结论,慢性β-肾上腺素能受体阻滞通过一种独立于环氧化酶的机制降低了肺动脉压和阻力。此外,慢性β-肾上腺素能受体阻滞不影响低氧性血管收缩的可能性。

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