Metabolism and function of dog's brain recovering from longtime ischemia

Hinzen, D. H.; Müller, U; Sobotka, P; Gebert, E.; Lang, R.; Hirsch, Hans Joachim

doi:10.1152/ajplegacy.1972.223.5.1158

Cited by 80 publications

(17 citation statements)

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“…DURING partial constriction of the canine common carotid artery, there are frequent recurring decreases of a transient nature in the blood flow in the constricted artery and in the cerebrum. 1 Participation of vasospasm, platelet aggregation, thrombus formation and embolism in this recurring CBF reduction has been demonstrated angiographically and histologically. 1 This experimental phenomenon resembles transient focal cerebral ischemic attacks in that cerebral artery flow reduction occurs spontaneously and recurrently in both.…”

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confidence: 93%

“…1 Participation of vasospasm, platelet aggregation, thrombus formation and embolism in this recurring CBF reduction has been demonstrated angiographically and histologically. 1 This experimental phenomenon resembles transient focal cerebral ischemic attacks in that cerebral artery flow reduction occurs spontaneously and recurrently in both. It is not known whether thromboxane A,, which causes platelet aggregation and contraction of vascular smooth muscles,*-* and prostaglandin I,, which inhibits platelet aggregation and relaxes vascular smooth muscles,*" 7 participate in this experimental phenomenon.…”

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confidence: 93%

“…1 "* In contrast, clinical experience as well as a number of experimental studies have shown that following, for example, cardiac arrest, signs of irreversible brain damage may develop even if the primary ischemia only lasts a few minutes. 9 The ultimate recovery of the brain following transient ischemia is not only dependent on the duration and intensity of the ischemia, but also on pathophysiological events during post-ischemia.…”

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confidence: 99%

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Platelet embolism in rabbit brain.

Passero¹,

Battistini²,

Fieschi³

1981

Stroke

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SUMMARY Transient cerebral ischemia was induced in rabbits by sdectire infusion of arachldonlc add (0J5 mg/kg in 15 sec) into the internal carotid artery. Platelet emboll caused transient ischemia of the brain, reaching a maximum within a few seconds after injection. After embolism the EEG flattened, blood flow stopped in almost tbe entire injected hemisphere, cortical pH gradually fell from 731 ± 0.09 to 7.05 ± 0.10 and cortical K + actirity rose from 4.7 ± 1.8 to 12.7 ± 6.4 mmol/kg H,O. Complete ischemia lasted 3-5 min; then cerebral circulation was gradually restored without reactire hyperemia. Forty-fire mm after embolization, circulation had been resumed in almost the entire Injected hemisphere, whereas metabolic changes were still disturbed. Eighty percent of the animals recorered complete neurological function and 20% showed permanent damage confirmed by hlstologlcal examination after 1 week of recorery.Stroke,Voll2,No6,1981SEVERAL INVESTIGATIONS have given evidence that the brain has a capacity to recover both metabolic and neurophysiological functions following an extremely long period of ischemia.

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confidence: 93%

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confidence: 93%

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Platelet embolism in rabbit brain.

Passero¹,

Battistini²,

Fieschi³

1981

Stroke

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“…2 ' 3 It has been recognized that suppression of energy metabolism is rapidly reversible after complete ischemia of at least one hour, although physiological functions and complex metabolic processes, such as spontaneous EEG activity or protein biosynthesis, are inhibited for considerably longer. 4 ' 5 The activity of energy metabolism is frequently expressed in terms of the adenylate energy charge, i.e., the relative amount of phosphorylated compounds in the adenylate pool. 6 Following complete ischemia of 15 minutes, the energy charge may return to 99%,' and after one hour of ischemia to 93%, 8 even when severe functional suppression is still apparent.…”

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Cerebral Uptake of Glucose and Oxygen in the Cat Brain After Prolonged Ischemia

Hossmann

Sakaki

Kimoto

1976

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102

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SUMMARY In cats, total cerebral ischemia of one hour's duration was produced by arterial clamping and lowering of the blood pressure. Following ischemia the brains were recirculated with blood for various periods between 30 minutes and six hours. CBF and uptake of O 2 and glucose were determined and correlated with the electrophysiological recovery of the brain.In four of 20 cats recovery was absent because of respiratory or circulatory insufficiency. In 16 cats signs of progressive electrophysiological function returned. These animals exhibited postischemic hyperemia; electrical excitability of the brains recovered within IS minutes, and the adenylate energy charge returned to more than 95% of the preischemic value within 30 minutes. O z uptake was significantly reduced for about one hour, but returned to or above normal as soon as spontaneous ECoC activity began to reappear. Glucose uptake was initially in the normal range until the cerebral glucose stores were replenished, but then followed a time course similar to that of O 2 .It is concluded that aerobic glycolysis may return after one hour's ischemia if the brain is adequately resupplied with glucose and O 2 .

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“…In these exposures to 100% nitrogen. This model has lost much of preparations blood flow can be varied over a wide range its interest because of poor reproducibility and the comsimply by adjusting the pump speed of the extracorporeal plexity of the pathophysiology which includes major circulation system [72]. cardiocirculatory abnormalities.…”

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confidence: 99%