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11. |
Transtentorial diaschisisreduction of cerebellar blood flow caused by supratentorial local cerebral ischemia in the gerbil. |
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Stroke,
Volume 14,
Issue 2,
1983,
Page 213-218
Naritomi H,
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摘要:
To assess the effect of supratentorial cerebral ischemia on infratentorial brain function, changes in regional cerebellar blood flow (rCeBF), after right carotid occlusion for 4 hours, were studied in 30 mongolian gerbils. The regional cerebral blood flow (rCBF) in the occluded cerebral hemisphere and rCeBF in both cerebellar hemispheres were measured simultaneously by hydrogen clearance methods. Before carotid occlusion, rCBF was 0.44 +/− 0.07 ml/g brain/min, and rCeBF in the left and right cerebellar hemispheres was 0.37 +/− 0.09 and 0.40 +/− 0.09 ml/g brain/min, respectively. After carotid occlusion, rCBF decreased in all animals showing levels of above 0.20 ml/g brain/min in 14 (group A), between 0.10 and 0.19 ml/g brain/min in 7 (group B) and below 0.10 ml/g brain/min in 9 (group C). rCeBF exhibited no changes in group A and a mild reduction in group B after carotid occlusion. In group C, rCeBF was significantly reduced 30 min after carotid occlusion in the left cerebellar hemisphere followed subsequently by bilateral reduction. In groups B and C, supratentorial brain edema was observed 4 hours after occlusion, but the degree of edema was moderate. The results of the present study suggest that depression of infratentorial brain function may occur after supratentorial local cerebral ischemia, presumably due to diaschisis.
ISSN:0039-2499
出版商:OVID
年代:1983
数据来源: OVID
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12. |
Pathophysiology of ischemic cell deathI. Time of onset of irreversible damage; importance of the different components of the ischemic insult. |
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Stroke,
Volume 14,
Issue 2,
1983,
Page 219-226
Ames A,
Nesbett F,
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摘要:
Rabbit retina was used as an example of organized central nervous tissue in in vitro experiments designed to characterize the onset of cell death from ischemia. Retinas were subjected to progressively longer periods of different types of ischemic insult and then given an opportunity to recover before being tested for irreversible damage, using failure to reinstitute protein synthesis as the principal criterion. Anoxia was more damaging than substrate deprivation, but they were synergistic in combination. Restricting the volume of extracellular fluid during the combined deprivation, to simulate complete circulatory arrest in vivo, caused irreversible damage to occur even sooner. The cells were able to recover from 20 min of the complete ischemia, but it took them more than 2 h to do so. After 30 min, there was extensive irreversible damage. Loss of viability was usually associated with failure to reinstitute energy metabolism, as assessed by 2-deoxyglucose uptake. Under some circumstances loss of viability may have been the consequence of the failed energy metabolism. Increasing medium Mg++, prior to ischemia, to levels that greatly reduce energy requirements caused a significant improvement in the recovery of 2-deoxyglucose uptake.
ISSN:0039-2499
出版商:OVID
年代:1983
数据来源: OVID
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13. |
Pathophysiology of ischemic cell deathII. Changes in plasma membrane permeability and cell volume. |
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Stroke,
Volume 14,
Issue 2,
1983,
Page 227-233
Ames A,
Nesbett F,
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摘要:
Isolated rabbit retinas were subjected for various durations to several types of ischemic insult, and then returned to control medium for periods of up to 4 3/4 h before measurements were made of total water, inulin-free water, and plasma membrane permeability as assessed by mannitol penetration into the inulin-free water. Neither anoxia nor substrate deprivation alone, for as long as 50 min, caused significant irreversible swelling, but they were synergistic in combination. Restricting the volume of extracellular fluid during the combined deprivation caused the changes responsible for swelling to occur much sooner. There was a progressive increase in membrane permeability, with a delayed increase in intracellular water beginning about 2 h after the ischemic insult. Cell swelling correlated closely with loss of viability as evidenced by failure to reinstitute protein synthesis, but the swelling appeared to be the consequence rather than the cause of the initial irreversible damage.
ISSN:0039-2499
出版商:OVID
年代:1983
数据来源: OVID
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14. |
Pathophysiology of ischemic cell deathIII. Role of extracellular factors. |
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Stroke,
Volume 14,
Issue 2,
1983,
Page 233-240
Ames A,
Nesbett F,
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摘要:
The purpose of this study was to determine the effect on cell survival of extracellular changes that occur during ischemia, over and above the depletion of O2 and substrate. Rabbit retinas were deprived in vitro of both O2 and substrate, and then returned to control medium for 4 h before recovery was assessed by measuring protein synthesis, glucose utilization, and tissue water. Experimental conditions were altered in various ways during the period of O2 and substrate deprivation in order to modify the changes taking place in the interstitial fluid as a result of the failure of energy metabolism. When O2-free, substrate-free extracellular electrolyte solution was added to the retinas to reduce the ischemia-induced changes in the interstitial fluid, there was marked reduction in irreversible damage. But when energy-deprived retinas were exposed to retinas that had already been ischemic, or to interstitial fluid from ischemic retinas, there was an increase in irreversible damage. Removing Ca++ from the extracellular fluid during the period of energy deprivation increased the damage due to short deprivations in a restricted volume of extracellular fluid, but reduced the damage from longer deprivations in a large volume of extracellular fluid. The results demonstrate that several changes occur in the extracellular fluid during ischemia that significantly affect recovery.
ISSN:0039-2499
出版商:OVID
年代:1983
数据来源: OVID
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15. |
The angiopathy of subarachnoid hemorrhageangiographic and morphologic correlates. |
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Stroke,
Volume 14,
Issue 2,
1983,
Page 240-245
Smith R,
Clower B,
Peeler D,
Yoshioka J,
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摘要:
In patients with subarachnoid hemorrhage, particularly hemorrhage due to aneurysmal rupture, there was a positive significant relation between angiographic vessel constriction and vessel pathology (angiopathy). Furthermore, there was a positive relationship between post-hemorrhage survival time and the severity of angiopathy. Factors such as age, sex, operations, steroid and CSF pressure seemed to have little affect on angiopathy following hemorrhage. Pathological changes were primarily limited to the involved major cerebral vessels themselves, with their branches rarely being affected. While intramural vascular hemorrhage was a common pathological feature in vessels showing severe pathology, the mere presence of blood surrounding an artery seemed to have little influence on vessel alterations.
ISSN:0039-2499
出版商:OVID
年代:1983
数据来源: OVID
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16. |
Auscultation of cervical and ocular bruits in extracranial carotid occlusive diseasea clinical and angiographic study. |
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Stroke,
Volume 14,
Issue 2,
1983,
Page 246-249
Pessin M,
Panis W,
Prager R,
Millan V,
Scott R,
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摘要:
The clinical and angiographic features of cervical and ocular bruits were correlated in 50 consecutive patients with severe extracranial internal carotid artery occlusive disease. Cervical bruits, generally localized to the carotid bifurcation, were highly associated (P = 0.004) with “tight” (residual lumen less than or equal to 2 mm) internal carotid artery stenosis, but significantly less often with a widely patent or occluded internal carotid artery. Angiographic features of a “slow-flow” state through a patent, but “tight” stenosis were identified as the apparent explanation for the absence of bruit in some patients. A unilateral ocular bruit contralateral to the side of internal carotid artery occlusion occurred in 9 of 10 patients, more often than an associated cervical bruit, and was interpreted as a sign of augmentation flow.
ISSN:0039-2499
出版商:OVID
年代:1983
数据来源: OVID
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17. |
Effects of vasoconstriction and distal dilation on carotid stenoses in the dog. |
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Stroke,
Volume 14,
Issue 2,
1983,
Page 249-255
Santamore W,
Wood J,
Bove A,
Lawner P,
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摘要:
Traditionally, arterial stenoses have been assumed to be inflexible, static obstructive lesions that could not acutely change their configuration or cross-sectional area. However, recent clinical and experimental observations have shown that coronary arterial stenoses can respond to vasoconstriction and intraluminal pressure changes. This experimental study evaluated whether similar dynamic changes could occur in a carotid artery stenosis. The effects of dilation distal to a circumferential snare were examined in 6 mongrel dogs. To eliminate collateral flow, the distal carotid artery was occluded and blood flow diverted through a 16 or 20 gauge needle. With no stenosis, distal dilation increased flow from 29.0 +/− 2.0 to 90.1 +/− 3.8 ml/min, (p less than 0.01). With moderate stenosis, the flow increase (25.5 +/− 1.3 to 56.4 +/− 3.7 ml/min, p less than 0.01 following dilation was attenuated. With severe stenosis, flow paradoxically decreased (20.4 +/− 1.0 to 11.4 +/− 1.0 ml/min, (p less than 0.01). This flow decrease was associated with a large stenotic resistance increase (2.13 +/− 0.51 to 18.93 +/− 5.58 mm Hg/ml · min-1, (p less than 0.01). In eight additional experiments, an in vitro preparation was used to examine the effects of vasoconstriction on stenotic severity. Vasoconstriction, induced by ergonovine, methoxamine, angiotensin, or vasopressin, resulted in a significant flow decrease and stenotic resistance increase. Thus, both vasoconstriction and intraluminal pressure were shown to affect stenotic severity, and thereby influence blood flow. These data illustrate hemodynamic factors which may be important in patients with severe carotid artery stenosis.
ISSN:0039-2499
出版商:OVID
年代:1983
数据来源: OVID
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18. |
Measurement of carotid blood flow in man and its clinical application. |
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Stroke,
Volume 14,
Issue 2,
1983,
Page 256-266
Uematsu S,
Yang A,
Preziosi T,
Kouba R,
Toung T,
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摘要:
With the use of a new ultrasonic volume flow meter (VFM), over 8000 measurements of common carotid blood flow were made in 120 normal control subjects and 550 patients with various neurological disease. The accuracy of the flow meter in measuring blood flow on an experimental model ranged from 93 to 97%. In normal subjects, common carotid blood flow varies with age. It increased from newborn to age 20 and gradually decreased thereafter. In normal healthy subjects, the flow varies within +/− 6.7% (2SD) at one sitting (intrasession) and +/− 21.2% (2SD) from week to week (intersession study). Carotid blood flow varies linearly with PaCO2 and increased markedly in response to endotracheal intubation. In healthy adults, the flow ratio between the two common carotid arteries is 1.07 +/− 0.052. This ratio increases in patients with transient ischemic attacks to 1.28 +/− 0.23 (p less than 0.05) and in patients with intracranial space occupying lesions to 1.46 +/− 0.39, (p less than 0.01). In 26 consecutive cases of carotid endarterectomies, the preoperative common carotid blood volume flow was 5.1 +/− 1.0 cc/sec. All cases preoperatively had at least 30% stenosis and ranged from 30 to 100% stenosis. The carotid blood volume was significantly increased post-operatively (p less than 0.001). The overall accuracy in detecting carotid and cerebral arterial disease is 89% with sensitivity of 96% and the specificity of 71%. Our clinical experience indicates that this device is not only a valuable noninvasive diagnostic tool for evaluation of carotid disease but also appears to be useful in assessing cerebral blood flow.
ISSN:0039-2499
出版商:OVID
年代:1983
数据来源: OVID
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19. |
CSF enzymes in lacunar and cortical stroke. |
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Stroke,
Volume 14,
Issue 2,
1983,
Page 266-269
Donnan G,
Zapf P,
Doyle A,
Bladin P,
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摘要:
Cerebrospinal fluid enzyme levels of creatine kinase (CK), lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (GOT) and angiotensin converting enzyme (ACE) were studied in 40 acute stroke patients comprising 20 lacunar strokes and 20 cortical strokes. A marked elevation of at least one of the enzymes CK, GOT or LDH was seen in 80% of cases of cortical strokes. No elevation was seen in lacunar stroke with CK, GOT or ACE and only a slight elevation with LDH. Within the cortical group, there was a correlation between the site, size of infarction seen on CT scan and enzyme level. These findings may help to explain the previously noted unpredictability of rises in CSF enzymes in stroke patients. In certain instances, a study of CSF enzymes may be of use to distinguish cortical from lacunar stroke. A precise diagnosis of lacunar infarction is important for management purposes, entry into stroke treatment trials or description of new syndrome types.
ISSN:0039-2499
出版商:OVID
年代:1983
数据来源: OVID
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20. |
Mechanisms of relaxant action of nicardipine, a new Ca++‐antagonist, on isolated dog cerebral and mesenteric arteries. |
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Stroke,
Volume 14,
Issue 2,
1983,
Page 270-275
Yamamoto M,
Ohta T,
Toda N,
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摘要:
In helically-cut strips of cerebral and mesenteric arteries contracted with prostaglandin (PG) F2 alpha, carbocyclic thromboxane A2 (cTxA2) or K+, the addition of nicardipine caused a dose-related relaxation. Nicardipine-induced relaxation was greater in cerebral than in mesenteric arteries when contracted with PGF2 alpha and cTxA2, but did not appreciably differ in the arteries contracted with K+. Cerebral arteries contracted with hemolysate and PGF2 alpha relaxed in response to nicardipine to a similar extent. The contractile response to PGF2 alpha was attenuated by pretreatment with nicardipine, the attenuation being greater in cerebral than in mesenteric arteries. Ca++-induced contractions in cerebral and mesenteric arteries previously exposed to Ca++-free media and depolarized by excess K+ were attenuated by nicardipine to a similar extent. PGF2 alpha-induced contractions of cerebral arteries exposed to Ca++-free media were attenuated by nicardipine, whereas those of mesenteric arteries were unaffected. Attenuations by nicardipine of the Ca++-induced contraction in PGF2 alpha-treated cerebral arteries were greater than those seen in mesenteric arteries. It may be concluded that nicardipine produces a greater relaxation of cerebral arteries than mesenteric arteries, possibly due to a greater inhibition of the Ca++-influx and to a decrease in the release of Ca++ from intracellular storage sites in cerebral arteries. As far as the concentrations used are concerned, nicardipine appears to attenuate the inward movement of Ca++ across cell membrane in mesenteric arterial smooth muscle, but not the release of intracellularly stored Ca++.
ISSN:0039-2499
出版商:OVID
年代:1983
数据来源: OVID
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