Cerebral blood flow in the monkey after focal cryogenic injury.

Abstract

SUMMARY A focal cryogenic lesion was made in the left superior frontal gyms of the anesthetized macaque brain. Cerebral blood flow (CBF) was determined by the hydrogen clearance technique before and during the 4 hours following trauma. Local CBF in tissue adjacent to the lesion increased in the first half hour after the lesion was made and then decreased during the ensuing 3'/i hours. Local CBF in the contralateral superior frontal gyrus, as well as total CBF and oxygen consumption, were unchanged by cryogenic trauma. The spread of vasogenic edema into uninjured tissue probably accounts for the observed decrease in local CBF. This experimental model may assist in discovering therapy to alter favorably the spatial and temporal profile of pathologic CBF changes in tissue surrounding an acute lesion of the brain.IT HAS BEEN proposed that injury to the brain initiates an autodestructive process that enlarges the lesion beyond its original limits.

Cerebral Blood Flow, Metabolism, and Head Trauma

“…They found that a brief period of hyperemia was observed in the rim of the tissue closest to the lesion, but after the fi rst hour post-injury it was replaced by progressive ischemia. This supported the results of earlier investigations into the effects of cryogenic trauma on CBF, but failed to shed light on the role of vasospasm produced by biogenic amines released from injured tissue (Martins and Doyle 1978 ) . An interesting aspect of this publication goes beyond the results and lies within the discussion when the authors admit, "this model may be criticized on the grounds that cryogenic trauma lacks clinical relevance."…”

“…Injured neurons and blood vessels would release vasoactive biogenic amines that spread through the tissue surrounding the original lesion and constrict vessels enough to decrease blood fl ow and induce tissue necrosis (Meyer et al 1974(Meyer et al , 1976Wurtman and Zervas 1974 ) . To test this theory and better understand the fl uctuations in cerebral blood fl ow, Martins and Doyle ( 1978 ) performed experiments on young adult macaques. Using standard microsurgical techniques, they performed a 3 cm by 3 cm craniotomy and applied a brass cylinder which had been immersed in liquid nitrogen to create a cryogenic lesion.…”

Changes of Cerebral Blood Flow during the Secondary Expansion of a Cortical Contusion Assessed by14C-Iodoantipyrine Autoradiography in Mice Using a Non-Invasive Protocol

“…The craniectomy necessary for the induction of CCI was carefully resealed after trauma allowing the subsequently evolving brain edema to cause pathologically elevated intracranial pressure (Zweckberger et al, 2003). Therefore, this model resembles many features of contusions found in patients and seems to have a higher relevance for the clinical condition of TBI as compared to previous experimental TBI models used for post-traumatic CBF measurements lacking a kinetic component or significant increases in intracranial pressure (Martins et al, 1978;Pollay et al, 1980;Zhuang et al, 1992;Bryan, Jr. et al, 1995).…”

“…Changes of CBF following experimental TBI were reported in non-human primates (Martins et al, 1977(Martins et al, , 1978, pigs (Madsen, 1990;Zhuang et al, 1992), cats (Lewelt et al, 1980;Wei et al, 1980;Dewitt et al, 1986Dewitt et al, , 1992Tornheim et al, 1990), rats (Nilsson et al, 1977;Pollay et al, 1980;Ishige et al, 1987;Yuan et al, 1988), and mice (Liu et al, 2002;Lundblad et al, 2004;Zweckberger et al, 2006) by hydrogen clearance (Martins et al, 1977(Martins et al, , 1978Zhuang et al, 1992), 14 C-iodoantipyrine autoradiography (Nilsson et al, 1977;Pollay et al, 1980;Ishige et al, 1987;McIntosh et al, 1987), labeled microbeads (Yuan et al, 1988;Yamakami et al, 1989;Madsen, 1990;Tornheim et al, 1990;Dewitt et al, 1992), laser-Doppler fluxmetry (Muir et al, 1992;Cherian et al, 1994;Nilsson et al, 1996;Maeda et al, 1997;Liu et al, 2002) and MRI (Hendrich et al, 1999). Despite this wealth of information on changes of CBF after TBI, only few clinical (Bouma et al, 1991;Bullock et al, 1992;Schroder et al, 1995;Garnett et al, 2001;von Oettingen e...…”

SUR1‐TRPM4 and AQP4 form a heteromultimeric complex that amplifies ion/water osmotic coupling and drives astrocyte swelling

“…To study astrocyte swelling in vivo, we utilized a cold injury model of brain edema. Cold injury is a well-characterized model of brain edema (Murakami et al, 1999) that creates highly reproducible lesions (Strungs et al, 2013) that closely resemble many of the molecular, histopathological and functional changes that occur following arterial occlusion (Darby et al, 1993;Itabashi et al, 2001;Martins and Doyle, 1978;O'Quinn et al, 2011;Pollay and Stevens 1980;Remond et al, 2011). Cold injury results in an area of frozen tissue immediately below the probe, with a surrounding area of reduced cerebral blood flow (<15/100g min) (Darby et al, 1993), blood-brain barrier disruption, and brain edema formation (Murakami et al, 1999).…”