Endorphin mediation of mesenteric blood flow after endotoxemia in sheep

N. Navaratnam, David Herndon, L. C. Woodson, H. A. Linares, S. Morris, D. L. Traber

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background and Methods: The administration of endotoxin in small dosages to sheep results in an acute decrease followed by an increase in cardiac output. It has previously been determined that the initial decrease in output was the result of a reduction in blood flow to the mesenteric areas. These changes were associated with increased blood concentrations of β endorphin. The present study was accomplished to determine if the systemic cardiovascular response to endotoxin could be affected by the administration of an opiate receptor-blocking agent. Female range sheep (n = 12) were prepared for chronic study by implantation of cardiopulmonary catheters and a flow probe on the cephalic mesenteric artery. Endotoxin (Escherichia coli, 1 μg/kg) was administered to these animals. Half of the sheep were treated with naloxone (2 mg/kg + 2 mg/kg·hr), and the remainder with an equivalent volume of sodium chloride (0.9%). Results: In untreated sheep, cardiac indices decreased by 15% to 20% (5.1 ± 0.1 to 4.2 ± 0.4 L/min·m2) between 0 and 1 hr and 2 and 5 hrs after endotoxin (4.5 ± 0.2 L/min·m2), and then increased to a value 40% (7.2 ± 0.6 L/min·m2) above baseline by 12 hrs. Flow in the cephalic mesenteric artery decreased in a pattern similar to the reduction in cardiac index (962 ± 152 [time, T = 0] to 379 ± 111 [T = 0.8] and 384 ± 88 mL/min [T = 4.0], p < .05) but did not increase to the same extent (1008 ± 153 mL/min [T = 4.0],p > .05). There was a concomitant increase in the plasma β-endorphin concentrations as the blood flow decreased (5 ± 4 [T = 0] to 40 ± 15 pg/mL [T = 0.8; untreated group], p < .05; and 10 ± 4 to 50 ± 7 pg/mL [T = 0.8; naloxone-treated group], p < .05). In the naloxone-treated group, the same pattern of cardiac output change was noted with endotoxin; however, reduction of mesenteric artery flow was only 30% (1118 ± 129 to 908 ± 122 mL/min, p < .05) of the value seen in the untreated animals (962 ± 152 to 379 ± 111 mL/min, p < .05) These changes in mesenteric blood flow were statistically significant from one another. As the cardiac output increased in the sheep treated with the opiate antagonist, mesenteric blood flows increased 20% above the baseline value (1391 ± 199 mL/min, p < .05). Conclusions: The decrease in cardiac output noted with endotoxin can be accounted for by the decrease in the blood flow in the cephalic mesenteric artery. This phenomenon can be attributed, at least in part, to the release of endorphins. There is both a vasodilation and constriction during endotoxemia in the ovine model.

Original languageEnglish (US)
Pages (from-to)402-408
Number of pages7
JournalCritical Care Medicine
Volume20
Issue number3
StatePublished - 1992

Fingerprint

Endorphins
Endotoxemia
Sheep
Endotoxins
Mesenteric Arteries
Cardiac Output
Naloxone
Head
Opiate Alkaloids
Opioid Receptors
Constriction
Vasodilation
Sodium Chloride
Catheters

Keywords

  • bacterial translocation
  • cardiac output
  • cardiovascular
  • endorphins
  • endotoxins
  • Escherichia coli
  • lipopolysaccharide
  • naloxone
  • opiates
  • sepsis

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Navaratnam, N., Herndon, D., Woodson, L. C., Linares, H. A., Morris, S., & Traber, D. L. (1992). Endorphin mediation of mesenteric blood flow after endotoxemia in sheep. Critical Care Medicine, 20(3), 402-408.

Endorphin mediation of mesenteric blood flow after endotoxemia in sheep. / Navaratnam, N.; Herndon, David; Woodson, L. C.; Linares, H. A.; Morris, S.; Traber, D. L.

In: Critical Care Medicine, Vol. 20, No. 3, 1992, p. 402-408.

Research output: Contribution to journalArticle

Navaratnam, N, Herndon, D, Woodson, LC, Linares, HA, Morris, S & Traber, DL 1992, 'Endorphin mediation of mesenteric blood flow after endotoxemia in sheep', Critical Care Medicine, vol. 20, no. 3, pp. 402-408.
Navaratnam N, Herndon D, Woodson LC, Linares HA, Morris S, Traber DL. Endorphin mediation of mesenteric blood flow after endotoxemia in sheep. Critical Care Medicine. 1992;20(3):402-408.
Navaratnam, N. ; Herndon, David ; Woodson, L. C. ; Linares, H. A. ; Morris, S. ; Traber, D. L. / Endorphin mediation of mesenteric blood flow after endotoxemia in sheep. In: Critical Care Medicine. 1992 ; Vol. 20, No. 3. pp. 402-408.
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abstract = "Background and Methods: The administration of endotoxin in small dosages to sheep results in an acute decrease followed by an increase in cardiac output. It has previously been determined that the initial decrease in output was the result of a reduction in blood flow to the mesenteric areas. These changes were associated with increased blood concentrations of β endorphin. The present study was accomplished to determine if the systemic cardiovascular response to endotoxin could be affected by the administration of an opiate receptor-blocking agent. Female range sheep (n = 12) were prepared for chronic study by implantation of cardiopulmonary catheters and a flow probe on the cephalic mesenteric artery. Endotoxin (Escherichia coli, 1 μg/kg) was administered to these animals. Half of the sheep were treated with naloxone (2 mg/kg + 2 mg/kg·hr), and the remainder with an equivalent volume of sodium chloride (0.9{\%}). Results: In untreated sheep, cardiac indices decreased by 15{\%} to 20{\%} (5.1 ± 0.1 to 4.2 ± 0.4 L/min·m2) between 0 and 1 hr and 2 and 5 hrs after endotoxin (4.5 ± 0.2 L/min·m2), and then increased to a value 40{\%} (7.2 ± 0.6 L/min·m2) above baseline by 12 hrs. Flow in the cephalic mesenteric artery decreased in a pattern similar to the reduction in cardiac index (962 ± 152 [time, T = 0] to 379 ± 111 [T = 0.8] and 384 ± 88 mL/min [T = 4.0], p < .05) but did not increase to the same extent (1008 ± 153 mL/min [T = 4.0],p > .05). There was a concomitant increase in the plasma β-endorphin concentrations as the blood flow decreased (5 ± 4 [T = 0] to 40 ± 15 pg/mL [T = 0.8; untreated group], p < .05; and 10 ± 4 to 50 ± 7 pg/mL [T = 0.8; naloxone-treated group], p < .05). In the naloxone-treated group, the same pattern of cardiac output change was noted with endotoxin; however, reduction of mesenteric artery flow was only 30{\%} (1118 ± 129 to 908 ± 122 mL/min, p < .05) of the value seen in the untreated animals (962 ± 152 to 379 ± 111 mL/min, p < .05) These changes in mesenteric blood flow were statistically significant from one another. As the cardiac output increased in the sheep treated with the opiate antagonist, mesenteric blood flows increased 20{\%} above the baseline value (1391 ± 199 mL/min, p < .05). Conclusions: The decrease in cardiac output noted with endotoxin can be accounted for by the decrease in the blood flow in the cephalic mesenteric artery. This phenomenon can be attributed, at least in part, to the release of endorphins. There is both a vasodilation and constriction during endotoxemia in the ovine model.",
keywords = "bacterial translocation, cardiac output, cardiovascular, endorphins, endotoxins, Escherichia coli, lipopolysaccharide, naloxone, opiates, sepsis",
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TY - JOUR

T1 - Endorphin mediation of mesenteric blood flow after endotoxemia in sheep

AU - Navaratnam, N.

AU - Herndon, David

AU - Woodson, L. C.

AU - Linares, H. A.

AU - Morris, S.

AU - Traber, D. L.

PY - 1992

Y1 - 1992

N2 - Background and Methods: The administration of endotoxin in small dosages to sheep results in an acute decrease followed by an increase in cardiac output. It has previously been determined that the initial decrease in output was the result of a reduction in blood flow to the mesenteric areas. These changes were associated with increased blood concentrations of β endorphin. The present study was accomplished to determine if the systemic cardiovascular response to endotoxin could be affected by the administration of an opiate receptor-blocking agent. Female range sheep (n = 12) were prepared for chronic study by implantation of cardiopulmonary catheters and a flow probe on the cephalic mesenteric artery. Endotoxin (Escherichia coli, 1 μg/kg) was administered to these animals. Half of the sheep were treated with naloxone (2 mg/kg + 2 mg/kg·hr), and the remainder with an equivalent volume of sodium chloride (0.9%). Results: In untreated sheep, cardiac indices decreased by 15% to 20% (5.1 ± 0.1 to 4.2 ± 0.4 L/min·m2) between 0 and 1 hr and 2 and 5 hrs after endotoxin (4.5 ± 0.2 L/min·m2), and then increased to a value 40% (7.2 ± 0.6 L/min·m2) above baseline by 12 hrs. Flow in the cephalic mesenteric artery decreased in a pattern similar to the reduction in cardiac index (962 ± 152 [time, T = 0] to 379 ± 111 [T = 0.8] and 384 ± 88 mL/min [T = 4.0], p < .05) but did not increase to the same extent (1008 ± 153 mL/min [T = 4.0],p > .05). There was a concomitant increase in the plasma β-endorphin concentrations as the blood flow decreased (5 ± 4 [T = 0] to 40 ± 15 pg/mL [T = 0.8; untreated group], p < .05; and 10 ± 4 to 50 ± 7 pg/mL [T = 0.8; naloxone-treated group], p < .05). In the naloxone-treated group, the same pattern of cardiac output change was noted with endotoxin; however, reduction of mesenteric artery flow was only 30% (1118 ± 129 to 908 ± 122 mL/min, p < .05) of the value seen in the untreated animals (962 ± 152 to 379 ± 111 mL/min, p < .05) These changes in mesenteric blood flow were statistically significant from one another. As the cardiac output increased in the sheep treated with the opiate antagonist, mesenteric blood flows increased 20% above the baseline value (1391 ± 199 mL/min, p < .05). Conclusions: The decrease in cardiac output noted with endotoxin can be accounted for by the decrease in the blood flow in the cephalic mesenteric artery. This phenomenon can be attributed, at least in part, to the release of endorphins. There is both a vasodilation and constriction during endotoxemia in the ovine model.

AB - Background and Methods: The administration of endotoxin in small dosages to sheep results in an acute decrease followed by an increase in cardiac output. It has previously been determined that the initial decrease in output was the result of a reduction in blood flow to the mesenteric areas. These changes were associated with increased blood concentrations of β endorphin. The present study was accomplished to determine if the systemic cardiovascular response to endotoxin could be affected by the administration of an opiate receptor-blocking agent. Female range sheep (n = 12) were prepared for chronic study by implantation of cardiopulmonary catheters and a flow probe on the cephalic mesenteric artery. Endotoxin (Escherichia coli, 1 μg/kg) was administered to these animals. Half of the sheep were treated with naloxone (2 mg/kg + 2 mg/kg·hr), and the remainder with an equivalent volume of sodium chloride (0.9%). Results: In untreated sheep, cardiac indices decreased by 15% to 20% (5.1 ± 0.1 to 4.2 ± 0.4 L/min·m2) between 0 and 1 hr and 2 and 5 hrs after endotoxin (4.5 ± 0.2 L/min·m2), and then increased to a value 40% (7.2 ± 0.6 L/min·m2) above baseline by 12 hrs. Flow in the cephalic mesenteric artery decreased in a pattern similar to the reduction in cardiac index (962 ± 152 [time, T = 0] to 379 ± 111 [T = 0.8] and 384 ± 88 mL/min [T = 4.0], p < .05) but did not increase to the same extent (1008 ± 153 mL/min [T = 4.0],p > .05). There was a concomitant increase in the plasma β-endorphin concentrations as the blood flow decreased (5 ± 4 [T = 0] to 40 ± 15 pg/mL [T = 0.8; untreated group], p < .05; and 10 ± 4 to 50 ± 7 pg/mL [T = 0.8; naloxone-treated group], p < .05). In the naloxone-treated group, the same pattern of cardiac output change was noted with endotoxin; however, reduction of mesenteric artery flow was only 30% (1118 ± 129 to 908 ± 122 mL/min, p < .05) of the value seen in the untreated animals (962 ± 152 to 379 ± 111 mL/min, p < .05) These changes in mesenteric blood flow were statistically significant from one another. As the cardiac output increased in the sheep treated with the opiate antagonist, mesenteric blood flows increased 20% above the baseline value (1391 ± 199 mL/min, p < .05). Conclusions: The decrease in cardiac output noted with endotoxin can be accounted for by the decrease in the blood flow in the cephalic mesenteric artery. This phenomenon can be attributed, at least in part, to the release of endorphins. There is both a vasodilation and constriction during endotoxemia in the ovine model.

KW - bacterial translocation

KW - cardiac output

KW - cardiovascular

KW - endorphins

KW - endotoxins

KW - Escherichia coli

KW - lipopolysaccharide

KW - naloxone

KW - opiates

KW - sepsis

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