Abstract
In order to help clarify the role of the renin-angiotensin system in the evolution of the post-hemorrhagic circulatory shock syndrome, captopril, a potent inhibitor of the conversion of angiotensin I to angiotensin II, was infused into a hemorrhagic shock model in the cat. The hemorrhage protocol had arterial blood withdrawn until a mean arterial blood pressure (MABP) of 40 mm Hg developed. Oligemia was maintained for a period of 2.5 hr, after which time all remaining shed blood was reinfused and the cats observed for an additional 2 hr. Coincident with the large reduction in MABP, superior mesenteric artery flow (SMAF) was similarly reduced as recorded by a noncannulating electromagnetic flow probe fitted around the artery. Post-oligemic plasma activities of cathepsin D (CD) and alkaline phosphatase (AP) were elevated 11-fold and 3-fold respectively; intestinal morphological damage was graded at 2.8 ± 0.6 on a 0-4 scale of increasing severity (control: 0.03 ± 0.02). Captopril was administered at an initial priming dose of 0.5 mg/kg followed by a continuous infusion of 0.5 mg/kg/hr. Improved post-reinfusion maintenance of MABP and SMAF was noted. Plasma elevations in enzyme activity were more moderate: 8-fold for CD, 1.5-fold for AP. Intestinal morphologic damage was graded at 2.5 ± 0.3. Blockade of angiotensin II formation by captopril thus demonstrated beneficial effects on post-oligemic hemodynamic status and on the degree of cellular enzyme release without significant improvement in intestinal morphology.
Original language | English |
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Pages (from-to) | 144-152 |
Number of pages | 9 |
Journal | Archives Internationales de Pharmacodynamie et de Therapie |
Volume | 259 |
Issue number | 1 |
State | Published - 1982 |
Keywords
- Alkaline Phosphatase/metabolism
- Animals
- Blood Pressure/drug effects
- Captopril/pharmacology
- Cathepsin D
- Cathepsins/pharmacology
- Cats
- Hemodynamics/drug effects
- Intestines/blood supply
- Male
- Proline/analogs & derivatives
- Regional Blood Flow/drug effects
- Shock, Hemorrhagic/physiopathology
- Splanchnic Circulation/drug effects