Hemorrhage and intracranial hypertension in combination increase cerebral production of thromboxane A2

D. L. Kong, Donald Prough, J. M. Whitley, C. Taylor, S. Vines, D. D. Deal, Douglas Dewitt

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Background and Methods: To determine the effects of reduced cerebral perfusion pressures produced by hemorrhage alone or in combination with intracranial hypertension on thromboxane A2 (TxA2) production, we undertook a randomized study in 38 anesthetized, mongrel dogs. Animals were subjected to 30 mins of hemorrhagic shock with normal (group 1) or increased (group 2) intracranial pressure (ICP). Group 1 animals (n = 22) were hemorrhaged to reduce cerebral perfusion pressure to 40 mm Hg for 30 mins. In group 2 (n = 16), cerebral perfusion pressure was reduced by the combination of less severe hypotension and intracranial hypertension (20 mm Hg). Cerebral and systemic hemodynamic measurements were recorded, including cerebral blood flow (sagittal sinus outflow method); ICP; cerebral perfusion pressure; and arterial and cerebral venous concentrations of TxB2 (double-antibody radioimmunoassay technique), the major metabolite of TxA2. Data were obtained at baseline and at the beginning and end of the 30-min shock period. Results: Hemorrhagic shock significantly (p < .05) decreased cerebral blood flow in both groups. At the beginning of the shock period, cerebral blood flow was higher in group 1 than in group 2 (p < .05) and venous-arterial differences in TxB2 increased significantly (p < .05) in group 2, but not in group 1. At the end of the 30-min shock period, venous-arterial levels of TxB2 remained significantly (p < .05) higher in group 2. Conclusions: Increased cerebral production of TxA2 during hypotension accompanied by intracranial hypertension may contribute to the severity of neural damage produced by the combination of head trauma and shock.

Original languageEnglish (US)
Pages (from-to)532-538
Number of pages7
JournalCritical Care Medicine
Volume19
Issue number4
StatePublished - 1991
Externally publishedYes

Fingerprint

Cerebrovascular Circulation
Thromboxane A2
Intracranial Hypertension
Hemorrhage
Shock
Hemorrhagic Shock
Intracranial Pressure
Hypotension
Craniocerebral Trauma
Radioimmunoassay
Hemodynamics
Dogs

Keywords

  • Brain
  • Brain injury
  • Cerebral ischemia
  • Hemorrhagic
  • Hypoperfusion
  • Hypovolemia
  • Intracranial hypertension
  • Intracranial pressure
  • Shock
  • Thromboxane

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Hemorrhage and intracranial hypertension in combination increase cerebral production of thromboxane A2 . / Kong, D. L.; Prough, Donald; Whitley, J. M.; Taylor, C.; Vines, S.; Deal, D. D.; Dewitt, Douglas.

In: Critical Care Medicine, Vol. 19, No. 4, 1991, p. 532-538.

Research output: Contribution to journalArticle

Kong, D. L. ; Prough, Donald ; Whitley, J. M. ; Taylor, C. ; Vines, S. ; Deal, D. D. ; Dewitt, Douglas. / Hemorrhage and intracranial hypertension in combination increase cerebral production of thromboxane A2 In: Critical Care Medicine. 1991 ; Vol. 19, No. 4. pp. 532-538.
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abstract = "Background and Methods: To determine the effects of reduced cerebral perfusion pressures produced by hemorrhage alone or in combination with intracranial hypertension on thromboxane A2 (TxA2) production, we undertook a randomized study in 38 anesthetized, mongrel dogs. Animals were subjected to 30 mins of hemorrhagic shock with normal (group 1) or increased (group 2) intracranial pressure (ICP). Group 1 animals (n = 22) were hemorrhaged to reduce cerebral perfusion pressure to 40 mm Hg for 30 mins. In group 2 (n = 16), cerebral perfusion pressure was reduced by the combination of less severe hypotension and intracranial hypertension (20 mm Hg). Cerebral and systemic hemodynamic measurements were recorded, including cerebral blood flow (sagittal sinus outflow method); ICP; cerebral perfusion pressure; and arterial and cerebral venous concentrations of TxB2 (double-antibody radioimmunoassay technique), the major metabolite of TxA2. Data were obtained at baseline and at the beginning and end of the 30-min shock period. Results: Hemorrhagic shock significantly (p < .05) decreased cerebral blood flow in both groups. At the beginning of the shock period, cerebral blood flow was higher in group 1 than in group 2 (p < .05) and venous-arterial differences in TxB2 increased significantly (p < .05) in group 2, but not in group 1. At the end of the 30-min shock period, venous-arterial levels of TxB2 remained significantly (p < .05) higher in group 2. Conclusions: Increased cerebral production of TxA2 during hypotension accompanied by intracranial hypertension may contribute to the severity of neural damage produced by the combination of head trauma and shock.",
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AU - Kong, D. L.

AU - Prough, Donald

AU - Whitley, J. M.

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AU - Vines, S.

AU - Deal, D. D.

AU - Dewitt, Douglas

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N2 - Background and Methods: To determine the effects of reduced cerebral perfusion pressures produced by hemorrhage alone or in combination with intracranial hypertension on thromboxane A2 (TxA2) production, we undertook a randomized study in 38 anesthetized, mongrel dogs. Animals were subjected to 30 mins of hemorrhagic shock with normal (group 1) or increased (group 2) intracranial pressure (ICP). Group 1 animals (n = 22) were hemorrhaged to reduce cerebral perfusion pressure to 40 mm Hg for 30 mins. In group 2 (n = 16), cerebral perfusion pressure was reduced by the combination of less severe hypotension and intracranial hypertension (20 mm Hg). Cerebral and systemic hemodynamic measurements were recorded, including cerebral blood flow (sagittal sinus outflow method); ICP; cerebral perfusion pressure; and arterial and cerebral venous concentrations of TxB2 (double-antibody radioimmunoassay technique), the major metabolite of TxA2. Data were obtained at baseline and at the beginning and end of the 30-min shock period. Results: Hemorrhagic shock significantly (p < .05) decreased cerebral blood flow in both groups. At the beginning of the shock period, cerebral blood flow was higher in group 1 than in group 2 (p < .05) and venous-arterial differences in TxB2 increased significantly (p < .05) in group 2, but not in group 1. At the end of the 30-min shock period, venous-arterial levels of TxB2 remained significantly (p < .05) higher in group 2. Conclusions: Increased cerebral production of TxA2 during hypotension accompanied by intracranial hypertension may contribute to the severity of neural damage produced by the combination of head trauma and shock.

AB - Background and Methods: To determine the effects of reduced cerebral perfusion pressures produced by hemorrhage alone or in combination with intracranial hypertension on thromboxane A2 (TxA2) production, we undertook a randomized study in 38 anesthetized, mongrel dogs. Animals were subjected to 30 mins of hemorrhagic shock with normal (group 1) or increased (group 2) intracranial pressure (ICP). Group 1 animals (n = 22) were hemorrhaged to reduce cerebral perfusion pressure to 40 mm Hg for 30 mins. In group 2 (n = 16), cerebral perfusion pressure was reduced by the combination of less severe hypotension and intracranial hypertension (20 mm Hg). Cerebral and systemic hemodynamic measurements were recorded, including cerebral blood flow (sagittal sinus outflow method); ICP; cerebral perfusion pressure; and arterial and cerebral venous concentrations of TxB2 (double-antibody radioimmunoassay technique), the major metabolite of TxA2. Data were obtained at baseline and at the beginning and end of the 30-min shock period. Results: Hemorrhagic shock significantly (p < .05) decreased cerebral blood flow in both groups. At the beginning of the shock period, cerebral blood flow was higher in group 1 than in group 2 (p < .05) and venous-arterial differences in TxB2 increased significantly (p < .05) in group 2, but not in group 1. At the end of the 30-min shock period, venous-arterial levels of TxB2 remained significantly (p < .05) higher in group 2. Conclusions: Increased cerebral production of TxA2 during hypotension accompanied by intracranial hypertension may contribute to the severity of neural damage produced by the combination of head trauma and shock.

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KW - Hypoperfusion

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KW - Thromboxane

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