scholarly journals Factors Affecting Morphological Changes of Neuronal Necrosis: Oxygen Free Radicals in the Ischemic Brain Damage

1987 ◽  
Vol 43 ◽  
pp. 97
Author(s):  
T. Koide ◽  
T.W. Wieloch ◽  
B.K. Siesjo
1986 ◽  
Vol 6 (5) ◽  
pp. 559-565 ◽  
Author(s):  
Tohru Koide ◽  
Tadeusz W. Wieloch ◽  
Bo K. Siesjö

In search of factors influencing the outcome of an ischemic insult, we induced 10 min of forebrain ischemia in rats and assessed neuronal necrosis by quantitative histopathology after 1 week of recovery. Procedures for inducing ischemia included bilateral carotid artery clamping and reduction of blood pressure to 40–50 mm Hg by bleeding. To facilitate rapid lowering of blood pressure, a ganglionic blocker, trimethaphan (TMP), was administered at the onset of ischemia. Omission of the ganglionic blocker proved to markedly ameliorate neuronal damage. Similarly favorable effects were obtained when a mixture of adrenaline and noradrenaline (1 μg kg−1 min−1 each) was infused during the early recirculation period in animals previously given TMP. Infusion of noradrenaline alone also ameliorated the damage, though the efficacy was somewhat less. The results suggest that catecholamines, released as a response to stress, ameliorate ischemic brain damage.


1995 ◽  
Vol 59 (5) ◽  
pp. 1316-1320 ◽  
Author(s):  
Bo K. Siesjö ◽  
Qi Zhao ◽  
Kerstin Pahlmark ◽  
Peter Siesjö ◽  
Ken-ichiro Katsura ◽  
...  

1990 ◽  
Vol 10 (3) ◽  
pp. 365-374 ◽  
Author(s):  
Hiroaki Minamisawa ◽  
Carl-Henrik Nordström ◽  
Maj-Lis Smith ◽  
Bo K. Siesjö

The influence of brain and body temperature on ischemic brain damage, notably on the density and distribution of selective neuronal vulnerability, was studied in SPF-Wistar rats subjected to 15 min of forebrain ischemia induced by bilateral occlusion of the common carotid arteries combined with arterial hypotension (50 mm Hg) in a room air environment. In one group of animals, the body temperature was maintained at 37°C but no attempt was made to prevent heat losses from the ischemic brain; i.e., the head was not heated during ischemia. Under those conditions the temperature of the caudoputamen and at a subcutaneous site over the skull bone spontaneously fell to ∼32°C. In four other groups, both the rectal and the subcutaneous skull temperatures were maintained at 38, 37, 35, and 33°C during the ischemia. Our results confirm those recently reported when brain temperature was varied during 20 min of ischemia, with body temperature kept constant. Thus, the histopathological outcome of the brain damage, as assessed after 7 days of recovery, was strongly temperature dependent. Whereas ischemia at 37–38°C consistently caused neuronal necrosis in the hippocampus, neocortex, and caudoputamen, spontaneous cooling of the brain during ischemia at a rectal temperature of 37°C significantly reduced the ischemic damage. Intentional lowering of temperature to 35°C markedly reduced and to 33°C virtually prevented neuronal necrosis in some but not all of the regions studied. While damage to the caudoputamen was extremely temperature sensitive, that affecting the CA1 sector of the hippocampus, and particularly the lateral reticular nucleus of the thalamus, was less so. Our results suggest that whatever biochemical events are responsible for selective neuronal vulnerability, they are temperature sensitive; however, since there are differences in sensitivity between different parts of the brain, more than one mechanism may be involved.


2003 ◽  
Vol 974 (1-2) ◽  
pp. 117-126 ◽  
Author(s):  
Ryu Otsuka ◽  
Naoto Adachi ◽  
Gen Hamami ◽  
Keyue Liu ◽  
Toshihiro Yorozuya ◽  
...  

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