Abstract
The present study was undertaken to determine the conditions under which acute periods of hemorrhagic shock induce bacterial translocation. Rats (at least six per group) were anesthetized intraperitoneally with the barbiturate, pentobarbital (50 or 65 mg/kg), or the inhalation anesthetic methoxyflurane. Following anesthesia, the femoral artery was catheterized, from which blood was withdrawn to maintain a mean arterial blood pressure of 30 mmHg for 30, 60, or 90 min, followed by reinfusion of shed blood. Instrumented, but nonshocked animals served as controls. Rats were sacrificed at 0, 2, or 24 hr postshock, and quantitative bacterial cultures of the mesenteric lymph node complex (MLN), liver, and spleen were made. Within groups, the effects of heparinization were also determined. In pentobarbital- treated animals, regardless of the extent of heparinization, consistent translocation to both MLN and distant organs occurred when shock was prolonged for 90 min, and assessment of translocation was made 24 hr after reinfusion of shed blood. Furthermore, a mortality rate of ~30% was found in rats subjected to this protocol. The magnitude of translocation was less consistent, and did not differ from that in sham shock controls, under other conditions of shock and evaluation. In rats anesthetized with methoxyflurane, no mortality occurred, and no statistical significance between the incidence or degree of translocation in shocked animals vs. sham shock controls could be demonstrated, regardless of the shock protocol. In additional studies, effects of these anesthetics on intestinal morphology and superior mesenteric arterial (SMA) flow in the context of hemorrhagic shock were assessed. Compared to methoxyflurane counterparts, histologic aberrations were found in the ileum of pentobarbital-treated animals following shock and resuscitation, and SMA flow was profoundly inhibited during shock and resuscitation. Thus, we conclude that acute periods of hemorrhagic shock in rats of 90 min duration or less do not enhance bacterial translocation, regardless of the time of sacrifice after resuscitation. The finding of translocation in pentobarbital-treated animals is most likely due to the adverse effects of this anesthetic on the splanchnic circulation and the resultant vascular compromise to the intestinal mucosa.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 212-220 |
| Number of pages | 9 |
| Journal | Circulatory Shock |
| Volume | 40 |
| Issue number | 3 |
| State | Published - 1993 |
| Externally published | Yes |
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Keywords
- heparinization
- methoxyflurane
- mucosal morphology
- pentobarbital
- splanchnic blood flow
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Reevaluation of the linkage between acute hemorrhagic shock and bacterial translocation in the rat. / LaRocco, M. T.; Rodriguez, L. F.; Chen, C. Y.; Smith, G. S.; Russell, D. H.; Myers, S. I.; Cocanour, Christine S; Reed, R. L.; Miller, T. A.
In: Circulatory Shock, Vol. 40, No. 3, 1993, p. 212-220.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Reevaluation of the linkage between acute hemorrhagic shock and bacterial translocation in the rat
AU - LaRocco, M. T.
AU - Rodriguez, L. F.
AU - Chen, C. Y.
AU - Smith, G. S.
AU - Russell, D. H.
AU - Myers, S. I.
AU - Cocanour, Christine S
AU - Reed, R. L.
AU - Miller, T. A.
PY - 1993
Y1 - 1993
N2 - The present study was undertaken to determine the conditions under which acute periods of hemorrhagic shock induce bacterial translocation. Rats (at least six per group) were anesthetized intraperitoneally with the barbiturate, pentobarbital (50 or 65 mg/kg), or the inhalation anesthetic methoxyflurane. Following anesthesia, the femoral artery was catheterized, from which blood was withdrawn to maintain a mean arterial blood pressure of 30 mmHg for 30, 60, or 90 min, followed by reinfusion of shed blood. Instrumented, but nonshocked animals served as controls. Rats were sacrificed at 0, 2, or 24 hr postshock, and quantitative bacterial cultures of the mesenteric lymph node complex (MLN), liver, and spleen were made. Within groups, the effects of heparinization were also determined. In pentobarbital- treated animals, regardless of the extent of heparinization, consistent translocation to both MLN and distant organs occurred when shock was prolonged for 90 min, and assessment of translocation was made 24 hr after reinfusion of shed blood. Furthermore, a mortality rate of ~30% was found in rats subjected to this protocol. The magnitude of translocation was less consistent, and did not differ from that in sham shock controls, under other conditions of shock and evaluation. In rats anesthetized with methoxyflurane, no mortality occurred, and no statistical significance between the incidence or degree of translocation in shocked animals vs. sham shock controls could be demonstrated, regardless of the shock protocol. In additional studies, effects of these anesthetics on intestinal morphology and superior mesenteric arterial (SMA) flow in the context of hemorrhagic shock were assessed. Compared to methoxyflurane counterparts, histologic aberrations were found in the ileum of pentobarbital-treated animals following shock and resuscitation, and SMA flow was profoundly inhibited during shock and resuscitation. Thus, we conclude that acute periods of hemorrhagic shock in rats of 90 min duration or less do not enhance bacterial translocation, regardless of the time of sacrifice after resuscitation. The finding of translocation in pentobarbital-treated animals is most likely due to the adverse effects of this anesthetic on the splanchnic circulation and the resultant vascular compromise to the intestinal mucosa.
AB - The present study was undertaken to determine the conditions under which acute periods of hemorrhagic shock induce bacterial translocation. Rats (at least six per group) were anesthetized intraperitoneally with the barbiturate, pentobarbital (50 or 65 mg/kg), or the inhalation anesthetic methoxyflurane. Following anesthesia, the femoral artery was catheterized, from which blood was withdrawn to maintain a mean arterial blood pressure of 30 mmHg for 30, 60, or 90 min, followed by reinfusion of shed blood. Instrumented, but nonshocked animals served as controls. Rats were sacrificed at 0, 2, or 24 hr postshock, and quantitative bacterial cultures of the mesenteric lymph node complex (MLN), liver, and spleen were made. Within groups, the effects of heparinization were also determined. In pentobarbital- treated animals, regardless of the extent of heparinization, consistent translocation to both MLN and distant organs occurred when shock was prolonged for 90 min, and assessment of translocation was made 24 hr after reinfusion of shed blood. Furthermore, a mortality rate of ~30% was found in rats subjected to this protocol. The magnitude of translocation was less consistent, and did not differ from that in sham shock controls, under other conditions of shock and evaluation. In rats anesthetized with methoxyflurane, no mortality occurred, and no statistical significance between the incidence or degree of translocation in shocked animals vs. sham shock controls could be demonstrated, regardless of the shock protocol. In additional studies, effects of these anesthetics on intestinal morphology and superior mesenteric arterial (SMA) flow in the context of hemorrhagic shock were assessed. Compared to methoxyflurane counterparts, histologic aberrations were found in the ileum of pentobarbital-treated animals following shock and resuscitation, and SMA flow was profoundly inhibited during shock and resuscitation. Thus, we conclude that acute periods of hemorrhagic shock in rats of 90 min duration or less do not enhance bacterial translocation, regardless of the time of sacrifice after resuscitation. The finding of translocation in pentobarbital-treated animals is most likely due to the adverse effects of this anesthetic on the splanchnic circulation and the resultant vascular compromise to the intestinal mucosa.
KW - heparinization
KW - methoxyflurane
KW - mucosal morphology
KW - pentobarbital
KW - splanchnic blood flow
UR - http://www.scopus.com/inward/record.url?scp=0027322723&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027322723&partnerID=8YFLogxK
M3 - Article
C2 - 8348683
AN - SCOPUS:0027322723
VL - 40
SP - 212
EP - 220
JO - Journal of inflammation
JF - Journal of inflammation
SN - 1078-7852
IS - 3
ER -