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

This study was intended to investigate the effect of high arterial oxygen tension on the peripheral circulation between normal and hypoxic area by using twelve dogs. For this purpose, acute temporary ischemia was produced at the right hindlimb by an occlusion of the right external iliac artery for 1 and 2 hours, and the left hind-limb was let alone as a control. The peripheral vascular resistance and the arterio-venous difference in oxygen tension between the right and the left hind-limb were measured continuously during 1 hour from immediately after reopening of the blood flow of the right external iliac artery. They were compared between at the condition of breathing room air at 1 ATA and pure oxygen at 2 ATA. The high arterial oxygen tension causes vasoconstriction. When there exists hypoxia in the peripheral tissue, however, it does not act on as a vasoconstrictive factor until the oxygen deficit is improved.
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PMID:Effect of increased oxygen on peripheral circulation in acute, temporary limb hypoxia. 65 92

60 patients were included in a prospective study to evaluate the effectiveness of hyperbaric oxygenation (OHP) as a treatment of head injury coma. They were assigned to nine subgroups according to age, level of consciousness and eventual neurosurgical procedure, and then selected randomly for OHP or standard therapy. OHP was administered in one or several series of daily exposure at 2.5 ATA. However, the OHP therapy protocol was to be interrupted in 11 cases developing pulmonary, hyperoxic, or infectious complications. Overall mortality and mean duration of coma in survivors were not different in both groups, indicating that OHP was either ineffective or too intermittently applicated. Analysis of results in subgroups revealed that, in one subgroup (18 patients), the rate of recovered consciousness at 1 month was significantly higher when OHP was used. These patients were under 30 and had a brain stem contusion without supratentorial mass lesion. The view is defended that, besides its toxic action on the normal nervous tissue, OHP can counteract edema and ischemia in the zones of brain injuries.
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PMID:Hyperbaric oxygenation for severe head injuries. Preliminary results of a controlled study. 78 88

Human loxoscelism was modeled in albino rabbits by injection of brown recluse spider (Loxosceles reclusa) venom, and the effects of daily or twice-daily hyperbaric oxygen treatment on wound healing were investigated. Lesions similar to those seen in humans were produced in rabbits by intradermal injection of 200 microliters of a venom extract (0.21 microgram protein per microliter), including edema and erythema, ischemia and cyanosis in the first 12 hr, extensive purpura by 24 hr, and crateriform ulcer formation by day four, with induration and eschar formation. Hyperbaric oxygen treatments, consisting of two atmospheres absolute (2 ATA) for 60 min, were applied daily (n = 8) or twice daily (n = 8), while control animals (n = 8) received no treatment. Treatments were initiated 72 hr after venom injection (day 3) to duplicate typical clinical treatment delays, and were administered for seven consecutive days. No significant effects of hyperbaric oxygen treatment on lesion healing were seen as measured by lesion area. However, histologic evaluation of wound tissue collected at euthanasia on day 24 showed clear differences between rabbits receiving twice-daily treatments and those receiving daily or no treatment. The former showed complete re-epithelization or slight ulceration, while the latter usually had necrotic cavities extending into the dermis, with myonecrosis and inflammatory cell accumulation. Thus, no superficial differences were seen between groups, but twice-daily treatments resulted in enhanced recovery at the histologic level.
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PMID:Hyperbaric oxygen effects on brown recluse spider (Loxosceles reclusa) envenomation in rabbits. 194 69

In limb injuries (amputation, laceration injuries, or compartment syndrome), a circulatory insufficiency with a total or subtotal ischemia may occur and jeopardize the result of reconstructive surgery. Transcutaneous oxygen monitoring has been shown to reflect tissue perfusion and has been advocated to predict the final outcome of major vascular trauma of the limb. Unfortunately, in normal atmospheric conditions, this test is not sufficiently discriminative; we evaluate the effect of hyperbaric oxygen on the efficiency of this test. 23 patients with major vascular trauma of the limbs were evaluated by clinical examination and transcutaneous oxygen pressure (PTCO2) measurements. Sixteen had arterial repair and seven had clinical evidence of peripheral ischemia without an arterial lesion. In normal air, the transcutaneous oxygen values in the traumatized limb, of these 23 patients, were significantly lower than in the nontraumatized limb. But neither the absolute PTCO2 value nor the ratio between the traumatized limb's PTCO2 and that of the nontraumatized one can predict the final outcome (amputation). In hyperbaric oxygen (2.5 ATA), this ratio is significantly higher in the group where the surgery will succeed than in the group where final amputation will be needed (81.2 +/- 26.0 vs. 15.2 +/- 13.1; p less than 0.01). The overall sensitivity and specificity of prediction of the limb's final outcome when the bilateral PTCO2 ratio in 2.5 ATA pure oxygen is less than 0.40, are 100% and 94%, respectively. But what is perhaps more interesting is that, when considering a ratio value of less than 0.20, amputation can be predicted with a 100% true predictive value.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Post-traumatic limb ischemia: prediction of final outcome by transcutaneous oxygen measurements in hyperbaric oxygen. 231 49

By measuring near-infrared transmittance spectra, we examined the effect of HBO on cerebral Hb oxygenation in normal and ischemic brain in the anesthetized rat. The oxygenation state of Hb was around 80% in the rat brain under 1 ATA air breathing. HBO did not induce further cerebral Hb oxygenation above 2 ATA in control animals but improved tissue oxygenation in the ischemic brains. The oxidation-reduction state of cyt. aa3 in the normal brain was not affected by HBO. In the ischemic brain, however, HBO prevented ischemia-induced reduction of cyt. aa3. Non-invasive optical monitoring of COHb with visible reflectance spectrophotometry was also examined. HBO markedly accelerated dissociation of COHb. Tight correlation was found between the optical signal and COHb content determined from blood samples. These results demonstrated the usefulness of optical monitoring in vivo under hyperbaric conditions.
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PMID:The effect of hyperbaric oxygen on cerebral hemoglobin oxygenation and dissociation rate of carboxyhemoglobin in anesthetized rats: spectroscopic approach. 336 62

Nervous conduction was measured in 27 subjects before and after compression in ternary mixture (helium, nitrogen and oxygen) ranging from 5,5 to 12 ATA. Among the eleven parameters studied, three showed an acceleration of the nervous conduction in the distal part of the sensitive and motor fibers. Although no precise mechanism can be established, different factors, in particular the role of ischemia, are discussed.
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PMID:[Changes in nerve conduction velocity as a result of hyperbaria in man]. 376 38

Effects of hyperbaric oxygen (HBO) on acute cerebral ischemia were studied in spontaneously hypertensive rats, which had the carotid artery bilaterally ligated. The animals were exposed to HBO (100% 02 at 2 ATA) for 30 min at 1 or 3 h after carotid ligation (treated group). Survival time and brain tissue metabolites were measured after HBO in these animals and compared with ischemic animals without HBO exposure (nontreated group). The animals treated at 3 h after ligation survived longer (6.5 +/- 0.7 h) than did nontreated ones (4.3 +/- 0.2 h) (P less than 0.05). The cerebral lactate increased much less in these treated animals (24.60 +/- 1.67 mM/kg) than in nontreated ones (31.78 +/- 1.68 mM/kg) (P less than 0.05). Cerebral ATP levels tended to decrease less in the former (0.66 +/- 0.17 mM/kg) than in the latter (0.59 +/- 0.07 mM/kg). When HBO started at 1 h after carotid ligation, however, there were no significant differences of survival time or brain metabolites between treated and nontreated groups of animals. The present results indicate that HBO administered at 3 h after brain ischemia prevents further increase in cerebral lactate and produces a slight but significant increase in survival time.
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PMID:Hyperbaric oxygen therapy in experimentally induced acute cerebral ischemia. 377 68

It is reported that CNS hemorrhage causes membrane dysfunction and may exacerbate this damage as a result of secondary ischemia or hypoxia. Since hyperbaric oxygenation improves oxygen metabolism, it may reduce this membrane damage. The present study was conducted to reveal whether hyperbaric oxygenation influences membrane alteration after hemorrhage. Thirty minutes after subarachnoid hemorrhage induction, rats were treated with hyperbaric oxygenation 2 ATA for 1 hour. Rats were decapitated 2 hours after subarachnoid hemorrhage induction. Na+, K(+)-ATPase activity measurement and spin-label studies were performed on crude synaptosomal membranes. Subarachnoid hemorrhage decreased Na+, K(+)-ATPase activity. Spin label studies showed that hydrophobic portions of near the membrane surface became more rigid and the mobility of the membrane protein labeled sulfhydryl groups decreased after subarachnoid hemorrhage. Hyperbaric oxygenation significantly ameliorated most of the subarachnoid hemorrhage induced alterations. We conclude that hyperbaric oxygenation may be a beneficial treatment for acute subarachnoid hemorrhage.
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PMID:Effect of hyperbaric oxygenation on the Na+, K(+)-ATPase and membrane fluidity of cerebrocortical membranes after experimental subarachnoid hemorrhage. 823 20

The morphologic events in the microcirculation that lead to reperfusion injury of ischemic skeletal muscle remain incompletely understood. The purpose of this experiment was to evaluate leukocyte endothelial adherence characteristics and dynamic changes in microvessel caliber during reperfusion of an in vivo skeletal muscle ischemia preparation. In addition, the effect of hyperbaric oxygen treatment on these microcirculatory changes also was studied. An intravital microscopy preparation of a transilluminated gracilis muscle in 27 rats was used to observe a total of 101 arterioles and 63 venules (13 to 73 microns diameter). Baseline hemodynamics were videotaped for 30 minutes following muscle isolation. The animals were divided into six groups: (1) sham, no ischemia, (2) 4 hours of global ischemia only, (3) no ischemia plus hyperbaric oxygen (one 2.5 ATA/1 hour of treatment with 100% oxygen), (4) 4 hours of ischemia plus hyperbaric oxygen during ischemia, (5) 4 hours of ischemia plus hyperbaric oxygen immediately on reperfusion, and (6) 4 hours of ischemia plus hyperbaric oxygen 1 hour after reperfusion. Changes in arteriolar and venular diameters at specific times during 3 hours of reperfusion were recorded, and the number of adherent and slow-rolling leukocytes in 100-microns venular segments were counted and compared with baseline measurements. The proximity of arterioles to venules was classified as adjacent (< 15 microns) or distant (> 15 microns). No significant changes in leukocyte endothelial adherence or arteriolar diameter were noted in group 1 sham or group 3 nonischemic hyperbaric oxygen-treated rats when compared with baseline measurements. A significant increase in adherent leukocytes was observed in group 2 ischemic venules (+14.9 +/- 2.5) within 5 minutes of reperfusion, which was maintained for 3 hours. Reperfusion measurements of arteriolar diameter in group 2 ischemic muscle preparations demonstrated an initial vasodilation that was followed at 1 hour by a progressive and severe vasoconstriction (-46.9 +/- 11.3 percent at 3 hours) in arterioles adjacent to venules that was not seen in distant arterioles. The increase in adherent leukocytes seen in group 2 ischemic venules was significantly reduced by hyperbaric oxygen treatment given during ischemia (group 4) or up to 1 hour during reperfusion (groups 5 and 6). In addition, the progressive ischemic arteriolar vasoconstriction was inhibited in all groups (4, 5, and 6) treated with hyperbaric oxygen.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Morphologic analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effect of hyperbaric oxygen. 847 78

To clarify the mechanism of ischemic tolerance induced by HBO, we investigated the effect of HBO on immunoreactivity to Bcl-2 and Bax, apoptosis-regulating protein, or Mn-SOD, a radical scavenging system, in the CA1 sector of the gerbil hippocampus. Pretreatment comprising, five sessions at 2 ATA (atmosphere absolute) every other day, but not that comprising, ten sessions at 3 ATA every day, caused significant increases in Bcl-2 and Mn-SOD immunoreactivity in the CA1 sector compared with in the sham pretreatment group. No significant differences in Bax immunoreactivity and neuronal density in the CA1 hippocampal neurons was observed between the groups. These results suggest that protection against mitochondrial alterations after ischemia through Mn-SOD and/or Bcl-2 expression is related to the ischemic tolerance induced by repeated HBO pre-treatment.
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PMID:Mn-SOD and Bcl-2 expression after repeated hyperbaric oxygenation. 1145 26


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