Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gliosis is increased in the respiratory control area of the brainstem in victims of sudden infant death syndrome (SIDS), as it is in infants who have died of congenital heart disease. In the latter, the lesions appear to result from hypoxia or ischemia, and studies of the brainstem microvasculature of SIDS victims indicated a close relationship between the gliosis and adjacent vasculature. It is postulated that cerebral hypoperfusion may play a role in SIDS.
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PMID:Cerebral hypoperfusion in the sudden infant death syndrome? Brainstem gliosis and vasculature. 71 38

One of the few relatively consistent pathologic observations in sudden infant death syndrome (SIDS) is astrogliosis of the brain stem. Astrogliosis is a nonspecific reactive process and its cause in SIDS, although still uncertain, is postulated to be hypoxia-ischemia. In this study, the distribution of reactive astrocytes throughout the rostral-caudal extent of the medulla has been determined. Although astrogliosis was present throughout the length of the medulla, it reached a maximum at levels 50-75% of total length, with 0% at the pontomedullary junction. Counting every reactive astrocyte through serial sections of the medulla seems unwarranted in view of the nonspecificity of the astrocytic response. This report proposes a practical approach to the quantitation of reactive astrocytes in SIDS by examining a representative sample of medulla midway through its length.
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PMID:Quantitation of medullary astrogliosis in sudden infant death syndrome. 181 32

Although numerous etiological or triggering factors have been suggested in sudden infant death syndrome (SIDS), the underlying mechanism of death is ultimately cardiac and/or respiratory in nature. As there is no evidence of lung or heart abnormalities, attention has focussed on the neural control of respiration and cardiac function. It is important to appreciate the methodological limitations involved in utilizing autopsy material and the criteria for selection of appropriate controls. This report reviews the pathological evidence for developmental delay in SIDS emphasizing delay of neural maturation of both myelination and synapses. Other abnormalities of the nervous system apparently associated with hypoxia-ischemia such as brainstem astrogliosis are also discussed. The occurrence of SIDS at a precise age together with our preliminary studies indicate that neural development delay is an important link in the chain of events leading to SIDS.
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PMID:Neural maturational delay as a link in the chain of events leading to SIDS. 227 93

1. Extracellular pH (pHo) was measured in the cerebellar cortex of the rat using a recently developed liquid membrane ion-selective micropipette (ISM). pHo was determined during stimulus-evoked neuronal activity, elevated extracellular potassium concentration, [K+]o, spreading depression (SD), and complete ischemia. In many experiments [K+]o was simultaneously determined. 2. A train of local surface stimuli (LOC) produced an initial alkaline shift in pHo from a base line of 7.20-7.30 to 7.25-7.35. This was followed by a long-lasting acid phase that reached a plateau of 7.05-7.15 after 64 s of stimulation. pHo decrease was related to stimulus frequency, intensity, and duration. 3. Superfusion with Ringer solution containing manganese ions rapidly abolished parallel fiber-induced Purkinje cell synaptic depolarization together with the alkaline shifts while enhancing the acid shifts. 4. Superfusion of the cerebellar cortex with Ringer solution containing increasingly elevated [K+] progressively lowered pHo to a plateau of 6.95-7.05. The acidification occurred in the presence of ouabain but was reversed on return to the normal [K+]o or with the addition of the glycolytic blocker, fluoride. Stimulus-evoked alkaline shifts were enhanced by K+-Ringer superfusion. These experiments suggested that the acid shift was due to the metabolic production of an anion, possibly lactate. 5. Elevation of [K+]o above 8-12 mM often produced oscillation in pHo and [K+]o with a period of about 40 s. Sometimes these oscillations ended in a spontaneous SD or SD could be evoked by stimulation. Under these conditions of raised [K+]o, the SD consisted of a very pronounced alkaline transient followed by a small, long-lasting acid shift. When SD was induced by conditioning the cerebellum with proprionate or lowered NaCl, the alkaline phase was reduced and the acid enhanced. 6. Complete ischemia began with a progressive decrease of pHo and rise in [K+]o. When [K+]o reached 12 mM, a second more rapid rise in [K+]o to 40 mM or more occurred. This was correlated with 0.1-0.2 pHo transient increase similar to that seen during SD. pHo eventually reached a plateau of 6.60-6.80, close to neutrality. 7. Superfusion with Ringer solution containing acetazolamide immediately altered pHo homeostasis by increasing base-line pHo by about 0.10 and enhanced the induced pHo changes. These results suggest that carbonic anhydrase (CA) is important for acute buffering of the brain extracellular microenvironment. 8. The above results were interpreted in terms of changes in extracellular strong ion concentration differences ( [SID]o), extracellular concentration of total weak acid ( [Atot]o) and partial pressure of CO2 (Pco2) in the brain microenvironment. The results indicate that neuronal activity produces changes in many of the constituents of the microenvironment.
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PMID:Alkaline and acid transients in cerebellar microenvironment. 683 1

The cause of brain death and the physiologic sequelae of brain death may impair heart function. Pharmacologic attempts to maintain donor viability may further jeopardize myocardial performance and could only be justified if dysfunctional donor organs subsequently prove to recover normal function after transplantation. Survival data on heart transplantation with organs donated from infants with sudden infant death syndrome indicate that prolonged ischemia (cardiopulmonary resuscitation up to 60 minutes) and metabolic abnormalities a priori do not increase the risk of graft failure. To provide a donor organ to infants in immediate peril, we have used donor hearts with documented dysfunction (left ventricular shortening fraction [LVSF] < 28%, wall motion abnormalities, and mitral regurgitation). The results of heart transplantation with use of dysfunctional donor hearts (n = 22, LVSF = 24.5% +/- 3%) were compared with donors with normal left ventricular function (n = 133, LVSF > 28%). Early death (< 30 days) was similar for the dysfunctional donor group (14%) and normal function donor group (11%). Postoperative inotropic support was equally frequent in both groups. Graft function on echocardiography was normal at 30 days after transplantation for both types of donor organs. We conclude that donor hearts with decreased left ventricular function (LVSF 15% to 28% and/or asymmetric wall motion), despite massive inotropic support, can function normally in the recipient. Significant donor mitral regurgitation was seen in grafts that ultimately failed after transplantation. Research into the reversible mechanisms of myocardial dysfunction associated with brain death could enlarge the donor pool.
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PMID:Donor shortage: use of the dysfunctional donor heart. 831 34

In infants, extreme extension or rotation of the head can occlude one or both vertebral arteries. We sought to determine whether small communicating arteries or asymmetric vertebral arteries could predispose the brain stem to ischemia should such head movements occur. In 68 infants, the carotid, posterior communicating, precommunicator posterior cerebral, basilar and vertebral arteries were fixed in formalin, embedded in resin, the circumferences measured by image analysis, and the relative conductance of blood in each artery per gram of brain calculated. Conductance in the vertebrobasilar and carotid systems lagged behind increases in brain weight during the postnatal growth spurt. In 81% of infants, conductance through the communicating arteries was less than 25% of basilar artery conductance. Conductance in one vertebral artery was less than half that of the contralateral artery in 41% of infants. In conclusion, the lag in available blood flow and small communicating and asymmetric vertebral arteries may predispose the infant brain stem to ischemia if one or both vertebral arteries are occluded by head rotation or extension. Because these head movements are likely to be accentuated in the prone sleeping position (a risk factor for sudden infant death syndrome), we suggest that vertebral artery occlusion may underlie some cases of sudden unexpected infant death.
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PMID:Vulnerability of the infant brain stem to ischemia: a possible cause of sudden infant death syndrome. 873 17

Cigarette smoking during pregnancy exposes the fetus to both nicotine and hypoxia/ischemia; postnatal exposure to second-hand smoke also involves substances that cause hypoxia (CO, HCN). Although developing cardiac cells are more resistant to hypoxia-induced damage than are mature cells, we examined whether nicotine affects this resistance, either when exposure is concurrent with hypoxia, or when animals are exposed to nicotine prenatally and receive subsequent hypoxic exposure. One, 8-, or 15-day-old rats exposed to 7% O2 for 2 hr all showed inhibition of cardiac DNA synthesis. By contrast, administration of nicotine at either low (0.3 mg/kg) or high (3 mg/kg) doses failed to alter DNA synthesis. To examine effects on cells that were not undergoing mitosis, we examined ornithine decarboxylase (ODC), an enzymatic marker for cell damage. One day old rats showed inhibition of ODC by hypoxia, a response that represents preservation of cell integrity; by 8 days of age, ODC was increased by hypoxia, evidence of cell damage. The high dose of nicotine evoked an increase in ODC at all ages and the low dose exacerbated the effects of hypoxia at 8 days of age. Prenatal nicotine exposure caused a transient inhibition of cardiac DNA synthesis but did not produce evidence of cell damage (ODC, protein synthesis markers) by itself, nor did it alter the effect of a subsequent postnatal exposure to hypoxia. These results suggest that cardiac cell damage could emerge as a consequence of concurrent, repeated exposures to nicotine and hypoxia. Such effects could contribute to the elevated incidence of perinatal morbidity/mortality and Sudden Infant Death Syndrome associated with smoking.
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PMID:Does concurrent or prior nicotine exposure interact with neonatal hypoxia to produce cardiac cell damage? 883 53

Previously, high postmortem concentrations of hypoxanthine have been found in vitreous humor of children dying from sudden infant death syndrome (SIDS). We wanted to investigate further the accumulation of hypoxanthine in vitreous humor during hypoxia. Twenty-four piglets aged 9-15 days were exposed to continuous hypoxemia (180 min 11% O2, n = 6), long interval intermittent hypoxemia (60 min 11% O2, 20 min room air, n = 7) or short interval intermittent hypoxemia (10 min 9% O2, 10 min room air with (n = 6) or without (n = 5) superimposed ligation of both carotid arteries). The increase in vitreous humor Hyp was four-fold higher (p < 0.01) with ligation of the carotid arteries (14 +/- 2.4 to 38 +/- 8.9 mumol/l) than without ligation (15 +/- 2.8 to 21 +/- 5.9 mumol/l). During continuous hypoxemia, plasma Hyp (r = 0.85), Xa (r = 0.89) uric acid (UA) (r = 0.85), and base deficit (BD) (r = 0.78) increased almost linearly (p < 0.001). Plasma Hyp responded more abruptly to changes in oxygenation than base deficit (BD) and UA. Ligation of the carotid arteries had a strong impact on Hyp accumulation in vitreous humor, suggesting that vitreous humor Hyp is not merely a filtration product of plasma Hyp, but reflects local hypoxia/ischemia in the eye.
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PMID:Plasma hypoxanthine reacts more abruptly to changes in oxygenation than base deficit and uric acid in newborn piglets. 935 Jun 6

In persons with anti-Lewis antibodies, erythrocyte agglutination might take place during breathing of odors from secretors of Lewis antigens. The agglutinates occlude capillary vessels, increasing resistance to blood flow. This might lead to the sudden death of adults, sudden infant death syndrome or to diseases accompanied by tissue ischemia, such as migraine, glaucoma, epilepsy, etc.
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PMID:Lewis antigens as a possible cause of sudden death of previously healthy adults and infants and of diseases and phenomena linked to tissue ischemia. 946 79

Alz-50 antibody is immunoreactive with brain tissue of subjects with Alzheimer's disease and can also be demonstrated by immunocytochemistry in neurons of vibratome-prepared brain tissue of victims of sudden infant death syndrome (SIDS). The application of a slightly modified ImmunoMax method enabled us to demonstrate Alz-50 immunoreactivity in paraffin-embedded material. The Alz-50 epitope was detected in the hippocampus region and in nuclei of the medulla oblongata at the level of the inferior olivary protuberance in three diagnostic groups: victims of SIDS (n = 10), infants dying of subacute hypoxia/ischemia with subsequent (re-)perfusion (n = 9), and infants dying of acute ischemia without (re-) perfusion (n = 7). Quantitative evaluation of the hippocampal cortex and the nucleus olivaris inferior disclosed a significantly (P < 0.05) higher percentage of Alz-50-reactive neurons in SIDS cases than in the control groups (hippocampal cortex and the nucleus olivaris; SIDS victims: median = 100%; subacute hypoxia/ischemia: median = 33.6-81%; acute ischemia: median = 89.2-99%). Semiquantitative analysis revealed an equally pronounced preponderance of Alz-50-reactive neurons in SIDS victims versus the control groups. This greater expression in SIDS victims may be due to an ongoing hypoxia/ischemia during agony, but the present paucity of knowledge prohibits definitive elucidation. Nevertheless, the method described here appears to offer the realistic possibility of distinguishing SIDS cases from cases of sudden death in infants due to other causes, i.e., it offers for the first time a positive criterion for the diagnosis of SIDS.
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PMID:Enhanced reactivity of Alz-50 antibody in brains of sudden infant death syndrome victims versus brains with lethal hypoxic/ischemic injury. Diagnostic significance after application of the ImmunoMax technique on routine paraffin material. 954 93


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