Anoxia of Canine Brain Without Damage

Neely, William A.; Youmans, Julian R.

doi:10.1001/jama.1963.63700130004011a

Cited by 83 publications

(17 citation statements)

References 5 publications

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“…Reversible complete brain ischemia was induced with a method similar to that described by Neely and Youmans (1963) as modified by Ljunggren et ai. (l974b) and Nordstrom et ai.…”

Section: Complete "Compression" Ischemiamentioning

confidence: 99%

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Brain Lactic Acidosis and Ischemic Cell Damage: 1. Biochemistry and Neurophysiology

Rehncrona

Rosén

Siesjö

1981

J Cereb Blood Flow Metab

562

158

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Summary: This study explores the influence of severe lactic acidosis in the ischemic rat brain on postischemic recovery of the tissue energy state and neurophysiological parameters. Severe incomplete brain ischemia (cerebral blood flow below 5% of normal) was induced by bilateral carotid artery clamp ing combined with hypovolemic hypotension. We varied the production of lactate in the tissue by manipulating the blood glucose concentrations. A 30-min period of incomplete ischemia induced in food-deprived animals caused lactate to accumulate to 15-16 f,tmol g�l in cortical tissue. Upon recirculation these animals showed: (1) a considerable recovery of the cortical energy state as evaluated from the tissue concentrations of phosphocreatine, ATP, ADP, and AMP; and (2) return of spontaneous electrocortical activity as well as of somatosensory evoked response (SER). In contrast, administration of glucose to food-deprived animals prior to ischemia caused an increase in tissue lactate concentration to about 35 f,tmol g�l. These animals did not recover energy balance in the tissue and neurophysiological functions did not return. In other experiments the production of lactate during 30 min of complete compression ischemia was increased from about 12 f,tmol g�l (normoglycemic animals) to 20-30 f,tmol g�l by preischemic hyperglycemia and. in separate animals, com bined hypercapnia. The recovery of the cortical energy state upon recirculation was significantly poorer in hyperglycemic animals. It is concluded that a high degree of tissue lactic acidosis during brain ischemia impairs postischemic recovery and that different degrees of tissue lactic acidosis may explain why severe incomplete ischemia, in certain experimental models, is more deleteri ous than complete brain ischemia.

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“…Reversible complete brain ischemia was induced with a method similar to that described by Neely and Youmans (1963) as modified by Ljunggren et ai. (l974b) and Nordstrom et ai.…”

Section: Complete "Compression" Ischemiamentioning

confidence: 99%

“…, 1977;Rehncrona et aI. , 1979b), and neuro physiological parameters (Hossmann and Sato, 1970;Hossmann and Kleihues, 1973), as well as of neurological function (Neely and Youmans, 1963;Miller and Myers, 1970). These results contrast with those showing that similar or shorter periods of hypoxia combined with unilateral carotid artery oc clusion (Salford et aI.…”

mentioning

confidence: 94%

Brain Lactic Acidosis and Ischemic Cell Damage: 1. Biochemistry and Neurophysiology

Rehncrona

Rosén

Siesjö

1981

J Cereb Blood Flow Metab

562

158

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show abstract

“…Anderson and Kubicek, 6 using electromagnetic blood flow transducers, found a mean increase of 54% in the basilar arterial blood flow in dogs after intravenous administration of betahistine. Suga and Snow 7 reported a marked increase in cochlear blood flow in guinea pigs using electrical impedance plethysmography, and Martinez 8 showed that in guinea pigs and chinchillas there was dilatation of the capillary network between the stria vascularis of the cochlea with increased blood flow.…”

Section: Comparative Responses Of the Carotid And Vertebral Arterial mentioning

confidence: 99%

Influence of several plasma fractions on post-ischemic microvascular reperfusion in the central nervous system.

Hallenbeck¹,

Furlow²

1978

Stroke

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SUMMARY In order to test the hypothesis that plasma contains native constituents capable of interacting in zones of acute tissue damage to impair microcirculatory flow, "C-antipyrine autoradiographic blood flow studies were performed in 30 splenectomized dogs subjected to 35 minutes of cerebrospinal fluid compression ischemia followed by 30 minutes of recirculation to the neuraxis. The animals were all anticoagulated with heparin and were divided into 7 groups by exposure to various measures prior to induction of ischemia. Groups 1 and 2 served for comparison with the other groups and underwent, respectively, no glass-wool filtration and glass-wool filtration via an arteriovenous shunt. Post-ischemic brain blood flows in Group 1 were low and focal zones of greatly impaired reperfusion were present. In Group 2, post-ischemic brain blood flows were high and focal perfusion impairment did not occur. Groups 3-7 received 1 of several plasma fractions after glass-wool filtration in order to identify those with activity that nullified the enhancement of post-ischemic reperfusion expected after exposure to glass-wool. The infused plasma fractions included: homologous cryoprecipitate in Group 3, autologous cryoprecipitate in Group 4, autologous cryoprecipitate-poor plasma in Group 5, plasma concentrate containing molecules over 10,000 daltons in Group 6 and plasma ultrafiltrate containing molecules of less than 10,000 daltons in Group 7. Brain blood flows in Group 3,4, and 6 resembled those in Group 1 while the flows in Groups 5 and 7 were like those in Group 2. The results indicate that activity deleterious to post-ischemic reperfusion resides in the cryoprecipitate fraction of plasma and is associated with molecules exceeding 10,000 daltons.

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“…'-6 Blood constituents have also been implicated in postischemic reperfusion abnormalities. 7 - 10 In one experimental investigation, the preischemic modification of an animal's blood by exposure to glass wool greatly enhanced postischemic cerebral reperfusion. 7 Studies such as these demonstrate that cerebral ischemia can produce blood alterations that in some cases may be detrimental to postischemic brain recovery.…”

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confidence: 99%

Photochemically stimulated blood-borne factors induce blood-brain barrier alterations in rats.

Dietrich

Prado

Watson

1988

Stroke

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We have tested the hypothesis that blood-borne substances released from a site of vascular thrombosis can lead to acute alterations in the blood-brain barrier. The right common carotid artery of rats was photothrombosed using a dye/light insult. Rats were given the photosensitizing dye rose bengal and irradiated for 4 minutes with an argon laser beam focused onto the . exposed common carotid artery. During the irradiation, 3 ml of blood was taken from the right external carotid artery. After 10 minutes, the blood was infused into the external carotid artery of a recipient rat that had received horseradish peroxidase. Fifteen minutes after blood infusion, bilateral peroxidase extravasation was noted within cortical and subcortical areas of recipient rats, being most intense ipsilaterally. Ultrastructural studies demonstrated peroxidase reaction product within numerous endothelial vesicles of arteriolar segments. Infusion of blood from control rats did not produce similar changes. Thus, photoinduced vascular thrombosis of a large feeding artery leads to the formation of blood-borne factors that acutely alter cerebral vascular permeability. (Stroke 1988;19:857-862) A bnormalities of blood rheology are believed to Z A play an important role in the pathophysi-A. \~ ology of stroke. Altered platelet function, increased hematocrit, and decreased erythrocyte deformability are just a few of the changes that have been detected in patients with neurologic deficits secondary to cerebral ischemia. '-6 Blood constituents have also been implicated in postischemic reperfusion abnormalities. -10 In one experimental investigation, the preischemic modification of an animal's blood by exposure to glass wool greatly enhanced postischemic cerebral reperfusion.7 Studies such as these demonstrate that cerebral ischemia can produce blood alterations that in some cases may be detrimental to postischemic brain recovery. However, whether blood abnormalities also represent a primary event in the occurrence of acute stroke still remains unclear. For example, it is not known whether vascular injury in the absence of cerebral ischemia also leads to the Received November 17, 1987; accepted February 26, 1988. formation of blood-borne factors that acutely affect brain structure and function. Experimentally induced thrombosis of neocortical vessels can be produced in rats by means of a rose bengal dye-sensitized photochemical reaction facilitated by irradiation with a filtered xenon arc lamp. "-13 This insult leads to acute alterations in the blood-brain barrier (BBB) and to vasogenic edema within the cortical region destined to undergo ischemic infarction.12 Recently, vascular endothelial damage leading to thrombosis of the middle cerebral artery (MCA) and common carotid artery (CCA) has been accomplished using the focused beam of an argon laser as the light source.14 Photothrombosis of the MCA also resulted in rapid alterations in cerebral vascular permeability, with bilateral leakage of horseradish peroxidase (HRP) 15 minutes after thrombu...

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Anoxia of Canine Brain Without Damage

Cited by 83 publications

References 5 publications

Brain Lactic Acidosis and Ischemic Cell Damage: 1. Biochemistry and Neurophysiology

Brain Lactic Acidosis and Ischemic Cell Damage: 1. Biochemistry and Neurophysiology

Influence of several plasma fractions on post-ischemic microvascular reperfusion in the central nervous system.

Photochemically stimulated blood-borne factors induce blood-brain barrier alterations in rats.

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