Photochemically Induced Cortical Infarction in the Rat. 1. Time Course of Hemodynamic Consequences

Dietrich, W. Dalton; Ginsberg, Myron D.; Busto, Raul; Watson, Brant D.

doi:10.1038/jcbfm.1986.31

Cited by 96 publications

(50 citation statements)

References 45 publications

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“…The experiments were performed on 12 male Wi star rats weighing between 250 and 300 g. Photochemically induced cerebral infarction was carried out according to procedures outlined in the companion study (Dietrich et al, 1986). Following 20 min of irradiation under anes thesia to the skull region overlying the left parieto-occip ital cortex, animals were allowed to survive for either 4 h or 5 days.…”

Section: Methodsmentioning

confidence: 99%

Photochemically Induced Cortical Infarction in the Rat. 2. Acute and Subacute Alterations in Local Glucose Utilization

Dietrich

Ginsberg

Busto

et al. 1986

J Cereb Blood Flow Metab

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Summary: Local CMR g l U (LCMR g 1u) values were mea sured by [14CJ2-deoxyglucose autoradiography in the rat at 4 h and 5 days following photochemically induced cor tical infarction, and these data were compared with neu ropathological findings in adjacent serial sections. At both time periods, LCMR g lu was markedly reduced within the lesion center, and irregular regions of moderate-to marked glucose hypermetabolism were noted within the marginal zone of the developing infarct. At 4 h, the hy permetabolic zones were shown by pathological exami nation to be characterized by normal-sized, moderately hyperchromatic neurons scattered among occasional dark, shrunken neurons within preserved neuropil. In contrast, the hypermetabolic zones at 5 days coincided with foci of intense macrophage infiltration, with disso lution of the neuropil. Significant decreases in glucose utilization were also demonstrated at 4 h within brainIn the normal brain, regional metabolic activity is an important regulator of local CBF (LCBF) (Reivich, 1974). Metabolic dysfunction in areas both near and remote from the site of infarction has been demonstrated experimentally (Michenfelder and Sundt, 1971; Kogure et aI., 1974; Ginsberg et aI., 1977; Fieschi et aI., 1978; Hossmann et aI., 1985; Tanaka et aI., 1985). Kogure et al. (1974) dem onstrated an early depression of cerebral energy metabolism within both the ischemic territory and the opposite hemisphere 5 min following embolic infarction in the rat. With 2-deoxyglucose (2-DG) autoradiography, zones of markedly depressed glu-

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Section: Methodsmentioning

confidence: 99%

Photochemically Induced Cortical Infarction in the Rat. 2. Acute and Subacute Alterations in Local Glucose Utilization

Dietrich

Ginsberg

Busto

et al. 1986

J Cereb Blood Flow Metab

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“…At these sites, LCBF was either increased above con trol or elevated as compared with to the surround ing tissue (relative hyperemia). Hyperemia or "lux ury perfusion" has been observed under various experimental and clinical conditions (Lassen, 1966;Cronqvist and Laroche, 1967;H\2ledt-Rasmussen et aI., 1967;Sundt and Waltz, 197 1;Schuier et aI., 1978;Olsen et aI., 198 1;Kagstrom et al, 1983a,b;Dietrich et al, 1986Dietrich et al, , 1987. Three different types of hyperemia have been described, including border zone, postischemic, and remote hyperemia (Olsen et al, 1981).…”

Section: Discussionmentioning

confidence: 99%

“…Arterial blood was sampled at -2-s intervals from the tip of a freely flowing femoral artery catheter. Studies were terminated by decapitation and brains were frozen and sectioned as previously described (Dietrich et al, 1986, HEMODYNAMIC CONSEQUENCES OF CAROTID ARTERY THROMBOSIS 959 1989a). Densitometry of ipsilateral and contralateral hemispheres was performed by means of an automated digitizing densitometer (Optronics) interfaced to a Mi croVax minicomputer and image processor (Grinnell Sys tems).…”

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confidence: 99%

Hemodynamic Consequences of Common Carotid Artery Thrombosis and Thrombogenically Activated Blood in Rats

Dietrich

Prado

Watson

et al. 1991

J Cereb Blood Flow Metab

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Summary:We documented the hemodynamic conse quences of nonocclusive common carotid artery throm bosis (CCAT) and tested the hypothesis that vasoactive substances capable of altering local CBF (LCBF) are re leased into the systemic circulation following cerebrovas cular injury. Ten minutes after photochemically induced CCAT, an autoradiographic determination of LCBF was conducted with [14C]iodoantipyrine. In blood transfusion studies using donor and recipient rats, a I-ml sample of thrombogenically activated blood (TAB) collected down stream from the forming thrombus was reinjected into a recipient rat 15 or 60 min before CBF study. A heteroge neous pattern of abnormal LCBF was documented in the ipsilateral hemisphere of CCAT rats and recipient rats receiving TAB 15 min before CBF study. Acute hemody namic abnormalities included ischemic «35% of control) and hyperemic (> 125% of control) foci and more globalThe pathogenesis of transient ischemic attacks (TIAs) and acute ischemic stroke remains incom pletely understood. Possible mechanisms underly ing these conditions include microembolism, hemo dynamic disturbances, and platelet hyperaggrega bility (Powers and Raichle, 1985;Toole, 1990). To examine cerebral ischemic mechanisms, alterations in local CBF (LCBF) following periods of cerebral Received February 27, 1991; revised May 13, 1991; accepted May 23, 1991. Address correspondence and reprint requests to Dr. W. D. Dietrich at Department of Neurology (04-5), University of Mi ami School of Medicine, P.O. Box 016960, Miami, FL 33101, U. S. A.Abbreviations used: BBB, blood-brain barrier; CCA, common carotid artery; CCAT, CCA thrombosis; ECA, external carotid artery; LCBF, local CBF; MCA, middle cerebral artery; TAB, thrombogenically activated blood; TIA, transient ischemic at tack. 957reductions (50-80% of control) in cortical and subcortical LCBF. Border zone hyperemia exceeding 2.0 mllglmin was associated with focal sites of severe LCBF reduc tions. Although recipient rats that received TAB 15 min before CBF study displayed similar hemodynamic abnor malities, LCBF values in 60-min recipient rats were not significantly different from control despite ischemic foci. Humoral factors generated during CCAT appear to be responsible for the acute LCBF consequences of cerebro vascular thrombosis. Vasoactive substances released from a thrombotic site, capable of regionally affecting vascular reactivity in a time-dependent fashion, might be expected to participate in the pathogenesis of transient ischemic attacks and acute stroke. Key Words: Cerebral blood tlow-Platelets-Stroke-Thrombosis-Transient ischemic attacks.ischemia have been documented in various animal models. Thus, transient periods of global and focal cerebral ischemia produce consistent patterns of hemodynamic abnormalities within the postisch ernie brain, the characteristics of which are depen dent on ischemic duration and severity (Hossmann et al., 1973;Ginsberg et al., 1978;Tamura et al., 1981; Pulsinelli et a1. , 1982;Traupe et al. , 1982; Kagstrom et a...

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“…Photothrombosis (PT) is a commonly used method for the induction of focal ischemia in the brain [14][15][16][17][18][19][20] . The technique is fairly non-invasive, highly reproducible and produces a precise focal ischemic lesion in the exposed area of the brain [17][18][19][20][21] .…”

Section: Introductionmentioning

confidence: 99%

“…The technique is fairly non-invasive, highly reproducible and produces a precise focal ischemic lesion in the exposed area of the brain [17][18][19][20][21] . This is achieved by systemic administration of photoactive dyes like Rose Bengal (RB) [16][17][18][19][20]22 or erythrosine B 23 followed by localized irradiation of blood vessels with proper light source. (20 mg/ml in sterile saline) every time before the surgery.…”

Section: Introductionmentioning

confidence: 99%

Photothrombosis-induced Focal Ischemia as a Model of Spinal Cord Injury in Mice

Choudhury

Zhang

et al. 2015

JoVE

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Spinal cord injury (SCI) is a devastating clinical condition causing permanent changes in sensorimotor and autonomic functions of the spinal cord (SC) below the site of injury. The secondary ischemia that develops following the initial mechanical insult is a serious complication of the SCI and severely impairs the function and viability of surviving neuronal and non-neuronal cells in the SC. In addition, ischemia is also responsible for the growth of lesion during chronic phase of injury and interferes with the cellular repair and healing processes. Thus there is a need to develop a spinal cord ischemia model for studying the mechanisms of ischemia-induced pathology. Focal ischemia induced by photothrombosis (PT) is a minimally invasive and very well established procedure used to investigate the pathology of ischemia-induced cell death in the brain. Here, we describe the use of PT to induce an ischemic lesion in the spinal cord of mice. Following retro-orbital sinus injection of Rose Bengal, the posterior spinal vein and other capillaries on the dorsal surface of SC were irradiated with a green light resulting in the formation of a thrombus and thus ischemia in the affected region. Results from histology and immunochemistry studies show that PT-induced ischemia caused spinal cord infarction, loss of neurons and reactive gliosis. Using this technique a highly reproducible and relatively easy model of SCI in mice can be achieved that would serve the purpose of scientific investigations into the mechanisms of ischemia induced cell death as well as the efficacy of neuroprotective drugs. This model will also allow exploration of the pathological changes that occur following SCI in live mice like axonal degeneration and regeneration, neuronal and astrocytic Ca 2+ signaling using two-photon microscopy. Video LinkThe video component of this article can be found at

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Photochemically Induced Cortical Infarction in the Rat. 1. Time Course of Hemodynamic Consequences

Cited by 96 publications

References 45 publications

Photochemically Induced Cortical Infarction in the Rat. 2. Acute and Subacute Alterations in Local Glucose Utilization

Photochemically Induced Cortical Infarction in the Rat. 2. Acute and Subacute Alterations in Local Glucose Utilization

Hemodynamic Consequences of Common Carotid Artery Thrombosis and Thrombogenically Activated Blood in Rats

Photothrombosis-induced Focal Ischemia as a Model of Spinal Cord Injury in Mice

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