| Autor: |
Atkins JL; Division of Military Casualty Research, Walter Reed Army Institute of Research, 503 Robert Grant Ave., Silver Spring, MD 20910, USA. james.atkins@na.amedd.army.mil, Johnson KB, Pearce FJ |
| Jazyk: |
angličtina |
| Zdroj: |
American journal of physiology. Heart and circulatory physiology [Am J Physiol Heart Circ Physiol] 2007 Feb; Vol. 292 (2), pp. H776-85. Date of Electronic Publication: 2006 Oct 20. |
| DOI: |
10.1152/ajpheart.00381.2006 |
| Abstrakt: |
Oxygen inhalation is recommended for the initial care of trauma victims. The improved survival seen in early hemorrhage is normally associated with an increase in blood pressure. Although clinical use of oxygen can occur late after hemorrhage, the effects of late administration have not been specifically examined. Anesthetized rats were studied using an isobaric hemorrhage model with target pressures of either 70 or 40 mmHg. At various times after hemorrhage, the feedback control of the blood pressure was stopped and the inspired gas was changed from room air to 100% oxygen. The results show that shortly after hemorrhage to 70 mmHg, oxygen inhalation results in an increase in mean arterial blood pressure of 60 +/- 3 mmHg, which is associated with a large increase in total peripheral resistance from 0.89 +/- 0.05 to 1.25 +/- 0.1 peripheral resistance units. The blood pressure response is essentially unchanged with time, and it is not altered by a 10-min exposure to N(G)-nitro-l-arginine methyl ester. At a target pressure of 40 mmHg, the initial blood pressure response to oxygen is the same, but it gradually decreases as the animal develops a lactic acidosis. We conclude that the therapeutic value of oxygen needs to be separately evaluated for late hemorrhage. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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