Abstract
We determined if the cardiopulmonary response to endotoxin (LPS) is mediated by bradykinin (BK). Sheep (n = 30) were prepared for chronic study with cardiopulmonary catheters, and chronic lung lymph fistulae. They were divided into the following study groups: A) BK infusion; B) LPS; C) LPS with angiotensin converting enzyme inhibitor (ACEI); D) ACEI alone; E) LPS with BK antagonist. Cardiac index and mean arterial pressure fell (6.9 ± 0.4 to 5.3 ± 0.3 L/min/m2 and 93 ± 4 to 72 ± 3 mmHg, respectively), and pulmonary lymph flow increased (10.5 ± 3.0 to 17.8 ± 4.3 ml/hr) during BK infusion. Addition of ACEI during BK infusion reduced the amount of BK necessary to induce a comparable response (125 to 2 μg/kg/hr). Administration of ACEI to LPS animals did not significantly alter their cardiopulmonary responses. BK antagonist did not change the response to LPS. Although the kallikrein-kinin pathway is believed to be activated during the septic response, our data do not lend support for the hypothesis that bradykinin is an important mediator of the cardiopulmonary changes.
Original language | English (US) |
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Pages (from-to) | 224-230 |
Number of pages | 7 |
Journal | Circulatory Shock |
Volume | 34 |
Issue number | 2 |
State | Published - 1991 |
Keywords
- angiotensin converting enzyme inhibitor
- cardiovascular
- endotoxin
- lung lymph
- microvascular permeability
- pulmonary
- sepsis
- sheep
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine