Long-lasting neuroprotective effect of postischemic hypothermia and treatment with an anti-inflammatory/antipyretic drug : Evidence for chronic encephalopathic processes following ischemia
(1996) In Stroke 27(9). p.1578-1585- Abstract
Background and Purpose: It has been recognized that postischemic pharmacological interventions may delay the evolution of neuronal damage rather than provide long-lasting neuroprotection. Also, fever complicates recovery after stroke in humans. Here we report the effects of late postischemic treatment with hypothermia and an antipyretic/anti-inflammatory drug, dipyrone, on cell damage at 1 week and 2 months of survival. Methods: Rats were subjected to 10 minutes of forebrain ischemia hypothermia (33°C) was induced at 2 hours of recovery and maintained for 7 hours. Dipyrone (100 mg · kg-1 IP) was given every 3 hours from 14 to 72 hours of recovery. Temperature was measured every 6 hours for 60 days. Neuronal damage was... (More)
Background and Purpose: It has been recognized that postischemic pharmacological interventions may delay the evolution of neuronal damage rather than provide long-lasting neuroprotection. Also, fever complicates recovery after stroke in humans. Here we report the effects of late postischemic treatment with hypothermia and an antipyretic/anti-inflammatory drug, dipyrone, on cell damage at 1 week and 2 months of survival. Methods: Rats were subjected to 10 minutes of forebrain ischemia hypothermia (33°C) was induced at 2 hours of recovery and maintained for 7 hours. Dipyrone (100 mg · kg-1 IP) was given every 3 hours from 14 to 72 hours of recovery. Temperature was measured every 6 hours for 60 days. Neuronal damage was assessed at 7 days and 2 months of recovery. Results: From 17 to 72 hours of recovery, a period of hyperthermia was observed, which dipyrone abolished but postischemic hypothermia treatment did not. Dipyrone treatment diminished neuronal damage by 43% at 7 days, and at 2 months of survival, a minor (16%) protection was seen. Postischemic hypothermia treatment alone delayed neuronal damaged. In contrast, combined treatment of hypothermia followed by dipyrone markedly diminished neuronal damage by more than 50% at both 7 days and 2 months of recovery. Conclusions: Neuronal degeneration may be ongoing for months after a transient ischemic insult, and prolonged protective measures need to be instituted for long-lasting neuroprotective effects. Hyperthermia during recovery worsens ischemic damage, and processes associated with inflammatory may contribute to the development of neuronal damage. An early and extended period of postischemic hypothermia provides a powerful and long-lasting protection if followed by treatment with anti- inflammatory/antipyretic drugs.
(Less)
- author
- Coimbra, Cicero ; Drake, Mikael ; Boris-Möller, Fredrik LU and Wieloch, Tadeusz LU
- organization
- publishing date
- 1996-01-01
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- anti-inflammatory agents, hypothermia, neuronal damage, rats, temperature
- in
- Stroke
- volume
- 27
- issue
- 9
- pages
- 8 pages
- publisher
- American Heart Association
- external identifiers
-
- scopus:0029844856
- ISSN
- 0039-2499
- DOI
- 10.1161/01.STR.27.9.1578
- language
- English
- LU publication?
- yes
- id
- bb892124-06b2-47aa-9b78-231946ca7307
- date added to LUP
- 2019-06-13 16:04:47
- date last changed
- 2022-04-26 01:35:19
@article{bb892124-06b2-47aa-9b78-231946ca7307,
abstract = {{<p>Background and Purpose: It has been recognized that postischemic pharmacological interventions may delay the evolution of neuronal damage rather than provide long-lasting neuroprotection. Also, fever complicates recovery after stroke in humans. Here we report the effects of late postischemic treatment with hypothermia and an antipyretic/anti-inflammatory drug, dipyrone, on cell damage at 1 week and 2 months of survival. Methods: Rats were subjected to 10 minutes of forebrain ischemia hypothermia (33°C) was induced at 2 hours of recovery and maintained for 7 hours. Dipyrone (100 mg · kg<sup>-1</sup> IP) was given every 3 hours from 14 to 72 hours of recovery. Temperature was measured every 6 hours for 60 days. Neuronal damage was assessed at 7 days and 2 months of recovery. Results: From 17 to 72 hours of recovery, a period of hyperthermia was observed, which dipyrone abolished but postischemic hypothermia treatment did not. Dipyrone treatment diminished neuronal damage by 43% at 7 days, and at 2 months of survival, a minor (16%) protection was seen. Postischemic hypothermia treatment alone delayed neuronal damaged. In contrast, combined treatment of hypothermia followed by dipyrone markedly diminished neuronal damage by more than 50% at both 7 days and 2 months of recovery. Conclusions: Neuronal degeneration may be ongoing for months after a transient ischemic insult, and prolonged protective measures need to be instituted for long-lasting neuroprotective effects. Hyperthermia during recovery worsens ischemic damage, and processes associated with inflammatory may contribute to the development of neuronal damage. An early and extended period of postischemic hypothermia provides a powerful and long-lasting protection if followed by treatment with anti- inflammatory/antipyretic drugs.</p>}},
author = {{Coimbra, Cicero and Drake, Mikael and Boris-Möller, Fredrik and Wieloch, Tadeusz}},
issn = {{0039-2499}},
keywords = {{anti-inflammatory agents; hypothermia; neuronal damage; rats; temperature}},
language = {{eng}},
month = {{01}},
number = {{9}},
pages = {{1578--1585}},
publisher = {{American Heart Association}},
series = {{Stroke}},
title = {{Long-lasting neuroprotective effect of postischemic hypothermia and treatment with an anti-inflammatory/antipyretic drug : Evidence for chronic encephalopathic processes following ischemia}},
url = {{http://dx.doi.org/10.1161/01.STR.27.9.1578}},
doi = {{10.1161/01.STR.27.9.1578}},
volume = {{27}},
year = {{1996}},
}