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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study we examined the reactions of cerebral vessels to hypercapnia and hypoxia during the recovery period following cerebral ischemia. We used ventilated, lightly anesthetized rats and induced complete ischemia by CSF compression, incomplete ischemia by bilateral carotid occlusion combined with hypotension. After 15 min of ischemia and 60 min of recirculation the animals were rendered hypercapnic or hypoxic for 2-3 min and local CBF was then measured autoradiographically with 14C-iodoantipyrine. Following complete ischemia vascular CO2 responsiveness was abolished or attenuated in most structures analysed. However, there was a considerable interstructural heterogeneity. For example, in the cerebellum and the red nucleus flow rates were observed which approached values obtained in hypercapnic control animals, whereas CO2 responsiveness was abolished in several cortical areas and hippocampus. The response to CO2 following incomplete ("forebrain") ischemia varied considerably. In the cerebral cortices areas with low flow rates were often mixed with hyperemic zones, and in most structures that had very low flow rates during ischemia, CO2 responsiveness was lost or grossly attenuated. Structures that had suffered moderate or only mild ischemia had better retained or completely preserved CO2 response. The cerebrovascular reaction to hypoxia was found to be attenuated in most, but not abolished in any of the structures examined. In general, the vascular response to hypoxia was better preserved than that to hypercapnia. Reactivity was similar following complete and incomplete ischemia. As observed during hypercapnia, there were pronounced interstructural variations with considerable increases in flow rates e.g. in the substantia nigra and the cerebellum.
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PMID:Cerebral circulatory responses to hypercapnia and hypoxia in the recovery period following complete and incomplete cerebral ischemia in the rat. 641 51

A critical review of the literature of retrolental fibroplasia indicates that the cause of this disease is not yet known. Oxygen is certainly a critical factor but it is still not possible to make precise recommendations as to the amount or the duration of therapy that is safe. We have overemphasized the role of oxygen in the past, and as a result of this the false impression has been created that RLF is a disease that can be prevented. This gross oversimplification of a complex disease with multiple causes has resulted in many unjustified malpractice claims. A study of the present epidemic indicates that excessive oxygen administration probably plays a minor role, in contrast to the first epidemic in which prolonged oxygen administration was clearly a major factor. A reasonable working hypothesis is that the developing retina is highly sensitive to any disturbance in its oxygen supply, either hyperoxemic or hypoxemic. The retinal circulation is subject to the same wide fluctuations as the cerebral circulation in newborn infants. The very low-birth-weight, sick premature infant suffers from a number of conditions, many of which can seriously disturb the retinal circulation, resulting in hypoperfusion and ischemia. These factors (immaturity, hyperoxia, hypoxia, blood transfusions, intraventricular hemorrhage, apnea, infection, hypercarbia, hypocarbia, patent ductus arteriosus, prostaglandin synthetase inhibitors, vitamin E deficiency, lactic acidosis, prenatal complications, genetic factors) may all be present in an infant. They may interact to produce various degrees of retinal damage. Nearly all of these factors cannot be prevented or controlled by our present methods of care. Unfortunately, this means that RLF is an extremely difficult disease to prevent, treat, or investigate. A disease of this complexity with multiple causes will require very large numbers of infants in any controlled study of a therapy. Retrolental fibroplasia should not be considered an avoidable iatrogenic disease in very low-birth-weight infants. Its cause in these infants is not known.
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PMID:A reexamination of the role of oxygen in retrolental fibroplasia. 641 99

Reactive hyperemia has been characterized in many vascular beds, but little is known about quantitative characteristics of reactive hyperemia in the cerebral circulation. We measured velocity of blood flow and pial artery diameter to characterize the time course of reactive hyperemia and used microspheres to study regional blood flow in the brain. Cerebral ischemia was produced by raising intracranial pressure or by arterial occlusion with a cuff around the neck. Five seconds of ischemia produced virtually maximal peak reactive hyperemia, and 30 s of ischemia produced maximal peak reactive hyperemia. During reactive hyperemia after 30 s of cerebral ischemia, there was a three- to fourfold increase in cerebral blood flow. The magnitude of reactive hyperemia was greater in gray matter than in white matter. Minimal resistance during reactive hyperemia, after ischemia produced by arterial occlusion, is similar to minimal resistance during seizures or hypercapnia, which suggests that reactive hyperemia produces maximal vasodilatation. Oxygen saturation of cerebral venous blood increased almost twofold during reactive hyperemia, which indicates that factors in addition to venous (and presumably tissue) oxygen are important determinants of reactive hyperemia. In summary, 1) we have characterized the time course of reactive hyperemia in the cerebral circulation; 2) reactive hyperemia after arterial occlusion produces maximal cerebral vasodilatation; and 3) there is marked heterogeneity of the response, with much larger increases in flow in cortical gray matter than white matter.
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PMID:Characteristics of reactive hyperemia in the cerebral circulation. 669 88

The existence of treatable postischemic (PI) changes which influence neurological outcome has been documented by this group before. A global brain ischemia model without cardiac arrest was developed in monkeys. It includes high-pressure neck tourniquet inflation plus hypotension for a reproducible ischemic insult; survival with reproducible neurological deficit (ND) under continuous PI life-support for 7 days with control of extracranial variables; and new ND and histopathological damage scoring systems. Hypoxemia, hypercarbia, hypotension, uremia, sepsis, and other extracranial complications PI in 50 unsatisfactory experiments led to immediate worsening in ND and brain death (ND = 100%) in most of these monkeys. In contrast, all monkeys with the same initial insult, with life-support according to protocol, survived with a 7 day ND of 60% or less. In 46 experiments of seven treatment groups, after 16 or 18 min ischemia, life support was according to protocol for 7 days. The control 1 protocol (spontaneous breathing when feasible) resulted in a mean 7-day ND score of 53% (including quadriplegia). Immobilization with pancuronium and controlled ventilation ameliorate deficit to an ND score of 19% (P less than 0.05) (including quadriparesis); this became control 2 protocol. Immobilization resulted in less neuronal damage in the neocortex. Severe repetitive hypertension worsened ND to 46%, versus 19% in controls (P less than 0.05). In separate series, neither heparinization over 72 hours PI, nor hemodilution to hematocrit 25% with dextran 40, changed final ND significantly from that of their control groups. Histopathological damage scores correlated with ND scores.
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PMID:Effect of postcirculatory-arrest life-support on neurological recovery in monkeys. 676 78

Cerebral vasodilator responses to hypercarbia were tested during inhalation of 5% CO2 in air by normal volunteers with and without risk factors for cerebral atherosclerosis. The results were compared with those of patients with hemispheric infarction or ischemia or vertebrobasilar arterial insufficiency (VBI). Regional cerebral blood flow was measured by the 133Xe inhalation method before and during hypercarbia. Responsiveness to CO2 was expressed as the percentage increase of gray matter flow per mm Hg of end-tidal CO2 tension. Cerebral vasodilator responsiveness is mildly impaired by the atherosclerosis of normal aging, is moderately impaired in normal subjects with risk factors for cerebral atherosclerosis, and is greatly impaired in patients with symptomatic hemispheric ischemia and VBI. Testing regional cerebral blood flow with CO2 appears to be a useful, harmless screening test for cerebral atherosclerosis.
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PMID:Aging and cerebral vasodilator responses to hypercarbia: responses in normal aging and in persons with risk factors for stroke. 677

Following 5 minutes of global ischemia, local cerebral blood flow (LCBF) was shown to have an initial reactive hyperemia that was followed, within the first hour, by persistent hypoperfusion (Part I). Intracranial pressure (ICP) was never elevated during the period of poor reperfusion. These experiments attempted to reverse the state of subnormal LCBF by inducing hypercarbia or hyocarbia or maintaining normocarbia. Although hypocarbia did increase LCBF at several electrode sites, neither the intracerebral steal syndrome nor the "squeeze" syndrome are a dominant consequence of hypercarbia in this model of global ischemia. Hypercarbia was consistently more effective in elevating LCBFs and in recovery of the electrocorticogram. It appears that, in the absence of raised ICP, hypercarbia may be preferred to normal or low PACO2,. Even though hypercarbia was superior to normocarbia or hypocarbia, hypercarbia was not a completely satisfactory regimen for reversing the state of poor reperfusion.
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PMID:Local cerebral blood flow following transient cerebral ischemia. II. Effect of arterial PCO2 on reperfusion following global ischemia. 677 97

Combined hypertension and hypercarbia, which was found to improve post-traumatic spinal cord hypoxia and presumably ischemia in our previous study, was used in dogs subjected to experimental spinal cord injury to determine its therapeutic effects against acute spinal cord trauma. Intermittent hypertension and hypercarbia therapy, in which 15 minutes of hypertension and 95% O2:5% CO2 gas ventilation were alternated with 10 minutes of air ventilation, was given for 3 hours beginning 3 hours after injury. The treated dogs and untreated control dogs were checked neurologically and electrophysiologically at weekly intervals for up to 8 weeks. The treated dogs showed higher grades of neurological function within 1 week, but the results were statistically insignificant. Both groups demonstrated steady neurological improvement for the next 2 weeks and remained paraparetic thereafter with no group difference. The size of the intramedullary lesion was identical in both groups. Recovery of the somatosensory evoked potentials coincided well with neurological improvement, with again no difference between the two groups.
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PMID:Therapeutic trial of combined hypertension and hypercarbia on experimental acute spinal cord injury. 677 24

The effects of hypercapnia on enhancement of reduced cerebral perfusion were re-evaluated in areas of ischemia produced by occlusion of the canine middle cerebral artery. Perfusion was measured by 85Kr (beta-ray) and 133Xe (gamma-ray) clearances, fluorescein angiography and diameter measurement of arteries. Between 45 and 55 mm Hg of PaCO2 rCBF measured with both isotopes increased significantly. When PaCO2 was elevated above 55 mm Hg, there was a remarkable dissociation in the rCBF measured by both isotopes. Cortical blood flow measured by 85Kr clearance decreased and, conversely, rCBF measured by 133Xe continued to increase. Arteries of less than 50 mu in diameter in areas of ischemia dilated significantly during hypercapnia. At PaCO2 above 65 mm Hg, progressive sub-pial hemorrhage and extravasation of dye were observed as side effects of hypercapnia. The use of mannitol combined with hypercapnia appeared to be harmful. A PaCO2 level between 45 and 55 mm Hg increases perfusion in areas of mildly reduced rCBF.
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PMID:Effects of hypercapnia on enhancement of decreased perfusion flow in non-infarcted brain tissues. 678 86

In case of quick physiological variations or in pathological conditions, it is impossible to measure the deoxyglucose consumption by means of the deoxyglucose technique and we propose a method for the study of the deoxyglucose uptake by the cerebral tissue. It is simultaneously measured with the blood flow, 3 min following the intravenous administration of deoxyglucose (2-deoxyglucose-14C). Hypercapnia induces an increase in the flow but does not modify the deoxyglucose uptake and moderate hypoxia results in a decrease in the deoxyglucose uptake without modifying the flow. In pathological conditions such as ischemia or stricture, the blood flow and deoxyglucose uptake variations are not parallel. These results show that the 2-deoxyglucose uptake does not follow the blood flow and that it depends on the cell activity. It is therefore possible to use this method when the consumption studies cannot be implemented.
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PMID:Deoxyglucose uptake in pathological conditions. 726 9

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 clamping 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 mumol g-1 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 mumol g-1. 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 mumol g-1 (normoglycemic animals) to 20-30 mumol g-1 by preischemic hyperglycemia and, in separate animals, combined 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 deleterious than complete brain ischemia.
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PMID:Brain lactic acidosis and ischemic cell damage: 1. Biochemistry and neurophysiology. 732 45


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