Effects of hypothermia for a short period on histologic outcome and extracellular glutamate concentration during and after cardiac arrest in rats

Ken Takata, Yoshimasa Takeda, Tetsufumi Sato, Hideki Nakatsuka, Masataka Yokoyama, Kiyoshi Morita

Research output: Contribution to journalArticle

61 Citations (Scopus)

Abstract

Objective: To evaluate the therapeutic effects of hypothermia for a short period (20 mins, 31°C) using a cardiac arrest model (5 mins) in rats. Design: Prospective animal study. Setting: Experimental laboratory in a university hospital. Subjects: Male Wistar rats (n = 42). Intervention: Direct current (DC) potential and extracellular glutamate concentrations (microdialysis) were monitored in the hippocampal region. Histologic observation was performed 7 days later. Measurements and Main Results: No animal died or showed severe complications as a result of hypothermia for a short period. In nontreated animals (group F), extracellular glutamate concentration simultaneously increased with the onset of membrane depolarization and continued to increase during the reperfusion period (maximum, 212% ± 40% of the pre-ischemia level) until the onset of DC recovery. In animals in which hypothermia was initiated before the onset of ischemia (group A), extracellular glutamate concentration did not increase during the ischemia period. When hypothermia was initiated at the onset of resuscitation (group B), the glutamate concentration immediately decreased. In animals in which hypothermia was initiated at 4.9 ± 1.3 mins (immediately after DC recovery, group C), 10 mins (group D), and 20 mins (group E) after the onset of resuscitation, changes in extracellular glutamate concentration were the same as those in nontreated animals. The percentage of injured neurons was significantly attenuated (compared with group F, 82% ± 10%) when hypothermia was initiated before DC recovery (group A, 5% ± 3%; group B, 29% ± 22%) or immediately after DC recovery (group C, 58% ± 18%, 9.9 ± 1.3 mins after the onset of ischemia). Conclusions: Hypothermia for a short period decreased glutamate concentration when it was initiated before DC recovery and attenuated neuronal damage when it was initiated before or immediately after DC recovery. The therapeutic time window for hypothermia for a short period is about 10 mins after the onset of ischemia.

Original languageEnglish
Pages (from-to)1340-1345
Number of pages6
JournalCritical Care Medicine
Volume33
Issue number6
DOIs
Publication statusPublished - Jun 2005

Fingerprint

Heart Arrest
Hypothermia
Glutamic Acid
Ischemia
Resuscitation
Induced Hypothermia
Microdialysis
Therapeutic Uses
Reperfusion
Wistar Rats
Observation
Prospective Studies
Neurons
Membranes

Keywords

  • Brain hypothermia
  • Brain ischemia
  • Cardiac arrest
  • Depolarization
  • Glutamate
  • Hippocampus

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Effects of hypothermia for a short period on histologic outcome and extracellular glutamate concentration during and after cardiac arrest in rats. / Takata, Ken; Takeda, Yoshimasa; Sato, Tetsufumi; Nakatsuka, Hideki; Yokoyama, Masataka; Morita, Kiyoshi.

In: Critical Care Medicine, Vol. 33, No. 6, 06.2005, p. 1340-1345.

Research output: Contribution to journalArticle

Takata, Ken ; Takeda, Yoshimasa ; Sato, Tetsufumi ; Nakatsuka, Hideki ; Yokoyama, Masataka ; Morita, Kiyoshi. / Effects of hypothermia for a short period on histologic outcome and extracellular glutamate concentration during and after cardiac arrest in rats. In: Critical Care Medicine. 2005 ; Vol. 33, No. 6. pp. 1340-1345.
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T1 - Effects of hypothermia for a short period on histologic outcome and extracellular glutamate concentration during and after cardiac arrest in rats

AU - Takata, Ken

AU - Takeda, Yoshimasa

AU - Sato, Tetsufumi

AU - Nakatsuka, Hideki

AU - Yokoyama, Masataka

AU - Morita, Kiyoshi

PY - 2005/6

Y1 - 2005/6

N2 - Objective: To evaluate the therapeutic effects of hypothermia for a short period (20 mins, 31°C) using a cardiac arrest model (5 mins) in rats. Design: Prospective animal study. Setting: Experimental laboratory in a university hospital. Subjects: Male Wistar rats (n = 42). Intervention: Direct current (DC) potential and extracellular glutamate concentrations (microdialysis) were monitored in the hippocampal region. Histologic observation was performed 7 days later. Measurements and Main Results: No animal died or showed severe complications as a result of hypothermia for a short period. In nontreated animals (group F), extracellular glutamate concentration simultaneously increased with the onset of membrane depolarization and continued to increase during the reperfusion period (maximum, 212% ± 40% of the pre-ischemia level) until the onset of DC recovery. In animals in which hypothermia was initiated before the onset of ischemia (group A), extracellular glutamate concentration did not increase during the ischemia period. When hypothermia was initiated at the onset of resuscitation (group B), the glutamate concentration immediately decreased. In animals in which hypothermia was initiated at 4.9 ± 1.3 mins (immediately after DC recovery, group C), 10 mins (group D), and 20 mins (group E) after the onset of resuscitation, changes in extracellular glutamate concentration were the same as those in nontreated animals. The percentage of injured neurons was significantly attenuated (compared with group F, 82% ± 10%) when hypothermia was initiated before DC recovery (group A, 5% ± 3%; group B, 29% ± 22%) or immediately after DC recovery (group C, 58% ± 18%, 9.9 ± 1.3 mins after the onset of ischemia). Conclusions: Hypothermia for a short period decreased glutamate concentration when it was initiated before DC recovery and attenuated neuronal damage when it was initiated before or immediately after DC recovery. The therapeutic time window for hypothermia for a short period is about 10 mins after the onset of ischemia.

AB - Objective: To evaluate the therapeutic effects of hypothermia for a short period (20 mins, 31°C) using a cardiac arrest model (5 mins) in rats. Design: Prospective animal study. Setting: Experimental laboratory in a university hospital. Subjects: Male Wistar rats (n = 42). Intervention: Direct current (DC) potential and extracellular glutamate concentrations (microdialysis) were monitored in the hippocampal region. Histologic observation was performed 7 days later. Measurements and Main Results: No animal died or showed severe complications as a result of hypothermia for a short period. In nontreated animals (group F), extracellular glutamate concentration simultaneously increased with the onset of membrane depolarization and continued to increase during the reperfusion period (maximum, 212% ± 40% of the pre-ischemia level) until the onset of DC recovery. In animals in which hypothermia was initiated before the onset of ischemia (group A), extracellular glutamate concentration did not increase during the ischemia period. When hypothermia was initiated at the onset of resuscitation (group B), the glutamate concentration immediately decreased. In animals in which hypothermia was initiated at 4.9 ± 1.3 mins (immediately after DC recovery, group C), 10 mins (group D), and 20 mins (group E) after the onset of resuscitation, changes in extracellular glutamate concentration were the same as those in nontreated animals. The percentage of injured neurons was significantly attenuated (compared with group F, 82% ± 10%) when hypothermia was initiated before DC recovery (group A, 5% ± 3%; group B, 29% ± 22%) or immediately after DC recovery (group C, 58% ± 18%, 9.9 ± 1.3 mins after the onset of ischemia). Conclusions: Hypothermia for a short period decreased glutamate concentration when it was initiated before DC recovery and attenuated neuronal damage when it was initiated before or immediately after DC recovery. The therapeutic time window for hypothermia for a short period is about 10 mins after the onset of ischemia.

KW - Brain hypothermia

KW - Brain ischemia

KW - Cardiac arrest

KW - Depolarization

KW - Glutamate

KW - Hippocampus

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