Nitric oxide synthase inhibition aggravates intestinal microvascular vasoconstriction and hypoperfusion of bacteremia
| Autor: | Richard N. Garrison, David A. Spain, Marcos F. Bar-Natan, Mark Wilson |
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| Rok vydání: | 1994 |
| Předmět: |
Male
medicine.medical_specialty Bacteremia Pharmacology In Vitro Techniques Critical Care and Intensive Care Medicine Arginine Nitric oxide Microcirculation Rats Sprague-Dawley chemistry.chemical_compound Ileum medicine Animals biology business.industry Hemodynamics Laser Doppler velocimetry Small intestine Surgery Rats Nitric oxide synthase medicine.anatomical_structure NG-Nitroarginine Methyl Ester chemistry Vasoconstriction biology.protein Amino Acid Oxidoreductases medicine.symptom Nitric Oxide Synthase business Perfusion Blood vessel |
| Zdroj: | The Journal of trauma. 36(5) |
| ISSN: | 0022-5282 |
| Popis: | Nitric oxide (NO) is an important hemodynamic mediator of sepsis; however, its visceral microcirculatory effects are largely unknown. To determine the role of systemic nitric oxide synthase (NO-S) inhibition on the microcirculation of the small intestine (SI), an intact loop of SI was exteriorized from decerebrate rats into a controlled tissue bath. Videomicroscopy was used to measure arteriolar diameters (A1, A3) and optical Doppler velocimetry was used to quantitate flow. In nonbacteremic controls inhibition of NO-S by N omega-nitro-L-arginine methyl ester (L-NAME; 1 mg/kg IV) caused vasoconstriction (A1 = -7%; A3 = -24% baseline values) and reduced A1 flow by 26%. Bacteremic controls received 10(9) Escherichia coli IV, which resulted in arteriolar constriction and hypoperfusion (A1 = -16%; A3 = -21%; A1 flow = -44%), despite increased cardiac output (+33%). Treatment of bacteremic rats with L-NAME corrected the increased cardiac output (-3%), but exacerbated vasoconstriction (A1 = -24%; A3 = -27%) and did not improve A1 flow (-49%). These data indicate that (1) NO mediates basal microvascular tone of the SI; (2) hyperdynamic bacteremia causes arteriolar constriction and hypoperfusion of the SI; and (3) although systemic NO-S inhibition normalizes cardiac output and increases blood pressure, it aggravates vasoconstriction in the SI and does not improve hypoperfusion. |
| Databáze: | OpenAIRE |
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