Hemostatic effects of stress hormone infusion

B. A. Rosenfeld, N. Faraday, D. Campbell, K. Dise, W. Bell, Pascal Goldschmidt-Clermont

Research output: Contribution to journalArticle

65 Citations (Scopus)

Abstract

Background: Surgery causes changes in hemostasis, leading to a hypercoagulable state. This postoperative increase in hemostatic function is attenuated in patients receiving regional anesthesia compared with those receiving general anesthesia. Regional anesthesia also decreases the neuroendocrine response to surgery compared with general anesthesia, and this effect is hypothesized to be responsible for the differences in hemostasis. To test the hypothesis that neuroendocrine hormones cause changes in hemostasis, we infused stress hormones into normal volunteers and measured hemostatic function. Methods: After drug screening, 12 normal volunteers were studied. On two admissions, volunteers randomly received either stress hormone (epinephrine, cortisol, or glucagon) or placebo infusion for 24 h. During infusion, patients remained at bed rest and received controlled meals. Blood was obtained from indwelling venous catheters before infusion and 2, 8, and 24 h after the start of infusion. Blood was analyzed for neuroendocrine hormone concentrations, glucose, complete blood count, coagulation proteins, platelet reactivity, and activity of the fibrinolytic system. Results: In the stress hormone group, concentrations of epinephrine, norepinephrine, cortisol, glucagon, and insulin were increased during the infusion period compared with those in the placebo group. Glucose concentrations and white blood cell counts were increased in the stress hormone group compared with those in the placebo group. Circulating fibrinogen concentrations increased 30% and ex vivo collagen-induced platelet reactivity increased 123% (aggregation) and 103% (dense granule release) in the stress hormone infusion group, whereas there was no change in the placebo group. Fibrinolytic proteins were similar in both groups, demonstrating a decrease in plasminogen activator inhibitor-1 activity at 8 and 24 h (196% in the hormone group vs. 199% in the placebo group). Conclusions: Infusion of stress hormones to concentrations found during surgery is safely tolerated and causes metabolic changes observed with surgery. Stress hormone infusion increases ex vivo platelet reactivity and fibrinogen concentrations that resemble changes seen postoperatively but does not recreate the postoperative decrease in fibrinolytic activity. Differences in neuroendocrine response between types of anesthesia may explain some postoperative changes in platelet function and acute phase reactivity, but additional uncharacterized factors are responsible for the differences in fibrinolysis.

Original languageEnglish
Pages (from-to)1116-1126
Number of pages11
JournalAnesthesiology
Volume81
Issue number5
StatePublished - Jan 1 1994
Externally publishedYes

Fingerprint

Hemostatics
Hormones
Placebos
Blood Platelets
Hemostasis
Conduction Anesthesia
Glucagon
Fibrinogen
General Anesthesia
Epinephrine
Hydrocortisone
Healthy Volunteers
Glucose
Bed Rest
Preclinical Drug Evaluations
Indwelling Catheters
Blood Cell Count
Plasminogen Activator Inhibitor 1
Blood Coagulation
Fibrinolysis

Keywords

  • Blood, coagulation: fibrinolysis; platelet reactivity
  • Hormones, stress: cortisol; glucagon
  • Sympathetic nervous system, catecholamines: epinephrine

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Rosenfeld, B. A., Faraday, N., Campbell, D., Dise, K., Bell, W., & Goldschmidt-Clermont, P. (1994). Hemostatic effects of stress hormone infusion. Anesthesiology, 81(5), 1116-1126.

Hemostatic effects of stress hormone infusion. / Rosenfeld, B. A.; Faraday, N.; Campbell, D.; Dise, K.; Bell, W.; Goldschmidt-Clermont, Pascal.

In: Anesthesiology, Vol. 81, No. 5, 01.01.1994, p. 1116-1126.

Research output: Contribution to journalArticle

Rosenfeld, BA, Faraday, N, Campbell, D, Dise, K, Bell, W & Goldschmidt-Clermont, P 1994, 'Hemostatic effects of stress hormone infusion', Anesthesiology, vol. 81, no. 5, pp. 1116-1126.
Rosenfeld BA, Faraday N, Campbell D, Dise K, Bell W, Goldschmidt-Clermont P. Hemostatic effects of stress hormone infusion. Anesthesiology. 1994 Jan 1;81(5):1116-1126.
Rosenfeld, B. A. ; Faraday, N. ; Campbell, D. ; Dise, K. ; Bell, W. ; Goldschmidt-Clermont, Pascal. / Hemostatic effects of stress hormone infusion. In: Anesthesiology. 1994 ; Vol. 81, No. 5. pp. 1116-1126.
@article{d7c0a2a184614d9fb9ab9d6b41aebf51,
title = "Hemostatic effects of stress hormone infusion",
abstract = "Background: Surgery causes changes in hemostasis, leading to a hypercoagulable state. This postoperative increase in hemostatic function is attenuated in patients receiving regional anesthesia compared with those receiving general anesthesia. Regional anesthesia also decreases the neuroendocrine response to surgery compared with general anesthesia, and this effect is hypothesized to be responsible for the differences in hemostasis. To test the hypothesis that neuroendocrine hormones cause changes in hemostasis, we infused stress hormones into normal volunteers and measured hemostatic function. Methods: After drug screening, 12 normal volunteers were studied. On two admissions, volunteers randomly received either stress hormone (epinephrine, cortisol, or glucagon) or placebo infusion for 24 h. During infusion, patients remained at bed rest and received controlled meals. Blood was obtained from indwelling venous catheters before infusion and 2, 8, and 24 h after the start of infusion. Blood was analyzed for neuroendocrine hormone concentrations, glucose, complete blood count, coagulation proteins, platelet reactivity, and activity of the fibrinolytic system. Results: In the stress hormone group, concentrations of epinephrine, norepinephrine, cortisol, glucagon, and insulin were increased during the infusion period compared with those in the placebo group. Glucose concentrations and white blood cell counts were increased in the stress hormone group compared with those in the placebo group. Circulating fibrinogen concentrations increased 30{\%} and ex vivo collagen-induced platelet reactivity increased 123{\%} (aggregation) and 103{\%} (dense granule release) in the stress hormone infusion group, whereas there was no change in the placebo group. Fibrinolytic proteins were similar in both groups, demonstrating a decrease in plasminogen activator inhibitor-1 activity at 8 and 24 h (196{\%} in the hormone group vs. 199{\%} in the placebo group). Conclusions: Infusion of stress hormones to concentrations found during surgery is safely tolerated and causes metabolic changes observed with surgery. Stress hormone infusion increases ex vivo platelet reactivity and fibrinogen concentrations that resemble changes seen postoperatively but does not recreate the postoperative decrease in fibrinolytic activity. Differences in neuroendocrine response between types of anesthesia may explain some postoperative changes in platelet function and acute phase reactivity, but additional uncharacterized factors are responsible for the differences in fibrinolysis.",
keywords = "Blood, coagulation: fibrinolysis; platelet reactivity, Hormones, stress: cortisol; glucagon, Sympathetic nervous system, catecholamines: epinephrine",
author = "Rosenfeld, {B. A.} and N. Faraday and D. Campbell and K. Dise and W. Bell and Pascal Goldschmidt-Clermont",
year = "1994",
month = "1",
day = "1",
language = "English",
volume = "81",
pages = "1116--1126",
journal = "Anesthesiology",
issn = "0003-3022",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Hemostatic effects of stress hormone infusion

AU - Rosenfeld, B. A.

AU - Faraday, N.

AU - Campbell, D.

AU - Dise, K.

AU - Bell, W.

AU - Goldschmidt-Clermont, Pascal

PY - 1994/1/1

Y1 - 1994/1/1

N2 - Background: Surgery causes changes in hemostasis, leading to a hypercoagulable state. This postoperative increase in hemostatic function is attenuated in patients receiving regional anesthesia compared with those receiving general anesthesia. Regional anesthesia also decreases the neuroendocrine response to surgery compared with general anesthesia, and this effect is hypothesized to be responsible for the differences in hemostasis. To test the hypothesis that neuroendocrine hormones cause changes in hemostasis, we infused stress hormones into normal volunteers and measured hemostatic function. Methods: After drug screening, 12 normal volunteers were studied. On two admissions, volunteers randomly received either stress hormone (epinephrine, cortisol, or glucagon) or placebo infusion for 24 h. During infusion, patients remained at bed rest and received controlled meals. Blood was obtained from indwelling venous catheters before infusion and 2, 8, and 24 h after the start of infusion. Blood was analyzed for neuroendocrine hormone concentrations, glucose, complete blood count, coagulation proteins, platelet reactivity, and activity of the fibrinolytic system. Results: In the stress hormone group, concentrations of epinephrine, norepinephrine, cortisol, glucagon, and insulin were increased during the infusion period compared with those in the placebo group. Glucose concentrations and white blood cell counts were increased in the stress hormone group compared with those in the placebo group. Circulating fibrinogen concentrations increased 30% and ex vivo collagen-induced platelet reactivity increased 123% (aggregation) and 103% (dense granule release) in the stress hormone infusion group, whereas there was no change in the placebo group. Fibrinolytic proteins were similar in both groups, demonstrating a decrease in plasminogen activator inhibitor-1 activity at 8 and 24 h (196% in the hormone group vs. 199% in the placebo group). Conclusions: Infusion of stress hormones to concentrations found during surgery is safely tolerated and causes metabolic changes observed with surgery. Stress hormone infusion increases ex vivo platelet reactivity and fibrinogen concentrations that resemble changes seen postoperatively but does not recreate the postoperative decrease in fibrinolytic activity. Differences in neuroendocrine response between types of anesthesia may explain some postoperative changes in platelet function and acute phase reactivity, but additional uncharacterized factors are responsible for the differences in fibrinolysis.

AB - Background: Surgery causes changes in hemostasis, leading to a hypercoagulable state. This postoperative increase in hemostatic function is attenuated in patients receiving regional anesthesia compared with those receiving general anesthesia. Regional anesthesia also decreases the neuroendocrine response to surgery compared with general anesthesia, and this effect is hypothesized to be responsible for the differences in hemostasis. To test the hypothesis that neuroendocrine hormones cause changes in hemostasis, we infused stress hormones into normal volunteers and measured hemostatic function. Methods: After drug screening, 12 normal volunteers were studied. On two admissions, volunteers randomly received either stress hormone (epinephrine, cortisol, or glucagon) or placebo infusion for 24 h. During infusion, patients remained at bed rest and received controlled meals. Blood was obtained from indwelling venous catheters before infusion and 2, 8, and 24 h after the start of infusion. Blood was analyzed for neuroendocrine hormone concentrations, glucose, complete blood count, coagulation proteins, platelet reactivity, and activity of the fibrinolytic system. Results: In the stress hormone group, concentrations of epinephrine, norepinephrine, cortisol, glucagon, and insulin were increased during the infusion period compared with those in the placebo group. Glucose concentrations and white blood cell counts were increased in the stress hormone group compared with those in the placebo group. Circulating fibrinogen concentrations increased 30% and ex vivo collagen-induced platelet reactivity increased 123% (aggregation) and 103% (dense granule release) in the stress hormone infusion group, whereas there was no change in the placebo group. Fibrinolytic proteins were similar in both groups, demonstrating a decrease in plasminogen activator inhibitor-1 activity at 8 and 24 h (196% in the hormone group vs. 199% in the placebo group). Conclusions: Infusion of stress hormones to concentrations found during surgery is safely tolerated and causes metabolic changes observed with surgery. Stress hormone infusion increases ex vivo platelet reactivity and fibrinogen concentrations that resemble changes seen postoperatively but does not recreate the postoperative decrease in fibrinolytic activity. Differences in neuroendocrine response between types of anesthesia may explain some postoperative changes in platelet function and acute phase reactivity, but additional uncharacterized factors are responsible for the differences in fibrinolysis.

KW - Blood, coagulation: fibrinolysis; platelet reactivity

KW - Hormones, stress: cortisol; glucagon

KW - Sympathetic nervous system, catecholamines: epinephrine

UR - http://www.scopus.com/inward/record.url?scp=0027947406&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027947406&partnerID=8YFLogxK

M3 - Article

C2 - 7978470

AN - SCOPUS:0027947406

VL - 81

SP - 1116

EP - 1126

JO - Anesthesiology

JF - Anesthesiology

SN - 0003-3022

IS - 5

ER -