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

University of Wisconsin and modified Euro-Collins solutions for pulmonary preservation were compared in a rat orthotopic left lung isotransplant model. Heart-lung blocks of donor rats were flushed with and preserved in one of the preservation solutions at 0 degrees C. After 6 or 12 hours of cold ischemia, the left lungs were transplanted into recipient rats and reperfused for 1 hour. Pulmonary function was assessed by measuring oxygen and carbon dioxide tensions in arterial blood after removal of the right lung. Lipid peroxide concentrations were measured as thiobarbiturate acid-reactive substances. The ratios of wet to dry weight of grafts after ischemia and after reperfusion were calculated. Histologic changes of ischemia-reperfusion injury of the lung tissue were evaluated using a graded scale. Oxygen tension after 6 hours of preservation followed by reperfusion was significantly higher with University of Wisconsin solution (308.8 +/- 81.1 mm Hg) than with Euro-Collins solution (50.8 +/- 17.8 mm Hg; p less than 0.001). Carbon dioxide tension in the University of Wisconsin solution group was also significantly lower than in the Euro-Collins solution group (28.2 +/- 2.3 versus 46.0 +/- 4.5 mm Hg; p less than 0.05). Lipid peroxide concentration after 6 hours' preservation in University of Wisconsin solution was significantly lower (0.88 +/- 0.07 mumol/g) than that in Euro-Collins solution (1.26 +/- 0.12 mumol/g; p less than 0.05). After 12 hours of preservation only lipid peroxide concentration with University of Wisconsin solution was significantly lower (1.30 +/- 0.09 mumol/g) than with Euro-Collins solution (1.71 +/- 0.15 mumol/g; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:University of Wisconsin solution for pulmonary preservation in a rat transplant model. 153 Oct 7

The amount of lactate formed during ischemia determines the rise in tissue PCO2 (PtCO2). Conflicting results exist on the relationship between lactate and PtCO2. The objective of this study was to settle this issue. We varied the preischemic plasma glucose concentration of normo- and hypercapnic rats, assessed tissue lactate and total CO2 contents, and determined the PCO2/lactate relationship over the lactate range 2-40 mmol kg-1. The results showed that whatever the equilibration time, the PCO2/lactate relationship was linear. The results obtained could be reproduced by a theoretical buffer system that mimics the buffering behavior of intracellular fluid. Our results bear on the question of whether compartmentation of H+ occurs during ischemia, with glial cells becoming more acid than neurons. A discontinuous PCO2/lactate relationship, with a constant PCO2 above a certain lactate content, would support this contention. Since our results demonstrate a linear relationship between lactate and PCO2 over the lactate range 2-40 mmol kg-1, they considerably weaken any argument for gross compartmentation of H+.
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PMID:Tissue PCO2 in brain ischemia related to lactate content in normo- and hypercapnic rats. 154 99

Ischemically sensitive abdominal visceral afferents reflexly stimulate the cardiovascular system. To explore the role of H+ contribution by lactic acid and hypercapnia, we recorded single-unit activity of ischemically sensitive abdominal afferents in anesthetized cats. The individual responses to sodium lactate, lactic acid, and hypercapnia then were examined. Abdominal ischemia significantly decreased organ tissue pH from an average of 7.21 +/- 0.03-7.05 +/- 0.03 (P less than 0.05), during which impulse activity of 13 A delta- and 32 C-fibers significantly increased. Although hypercapnia (12% CO2) induced a similar decrease in tissue pH, impulse frequency increased in 0 of 4 A delta- and only 2 of 13 C-fibers. In contrast, lactic acid decreased tissue pH significantly less than ischemia or hypercapnia but increased impulse activity in 7 of 10 A delta- and 11 of 12 C-fibers. Conversely, only 1 of 3 A delta- and 0 of 10 C-fibers responded to sodium lactate. Thus ischemically sensitive visceral afferents respond to the H+ derived from lactic acid rather than hypercapnia. However, these afferents do not respond to sodium lactate. These data suggest that ischemically sensitive abdominal visceral afferents are responsive specifically to lactic acid rather than to the dissociated ions lactate or H+ or to changes in PCO2.
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PMID:Ischemically sensitive visceral afferents: importance of H+ derived from lactic acid and hypercapnia. 155 84

Changes in middle cerebral artery flow velocity (Vmean), measured by transcranial Doppler ultrasound, were used to determine whether increases in mean arterial pressure (MAP) or brain activation enhance cerebral perfusion during exercise. We also evaluated the role of "central command," mechanoreceptors, and/or muscle "metaboreceptors" on cerebral perfusion. Ten healthy subjects performed two levels of dynamic exercise corresponding to a heart rate of 110 (range 89-134) and 148 (129-170) beats/min, respectively, and exhaustive one-legged static knee extension. Measurements were continued during 2-2.5 min of muscle ischemia. MAP increased similarly during static [114 (102-133) mmHg] and heavy dynamic exercise [121 (104-136) mmHg] and increased during muscle ischemia after dynamic exercise. During heavy dynamic exercise, Vmean increased 24% (10-47%; P less than 0.01) over approximately 3 min despite constant arterial carbon dioxide tension. In contrast, static exercise with a higher rate of perceived exertion [18 (13-20) vs. 15 (12-18) units; P less than 0.01] was associated with no significant change in Vmean. Muscle ischemia after exercise was not associated with an elevation in Vmean, and it did not provoke an increase in Vmean after static exercise. Changes in Vmean during exercise were similar to those recorded with the initial slope index of the 133Xe clearance method. The data show that middle cerebral artery mean flow velocity reflects changes in cerebral perfusion during exercise. Furthermore, they support the hypothesis that cerebral perfusion during exercise reflects an increase in brain activation that is independent of MAP, central command, and muscle metaboreceptors but is likely to depend on influence of mechanoreceptors.
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PMID:Middle cerebral artery flow velocity and blood flow during exercise and muscle ischemia in humans. 156 67

Traumatic brain injury (TBI) often causes disturbances of the cerebrovascular circulation, which contribute to the infliction of secondary injury, although the complex nature of the mechanisms involved is not fully understood. First, the role of ischemia in TBI is still controversial. Despite experimental and pathologic data suggesting important interactions between ischemia and trauma, evidence for posttraumatic ischemia with CBF measurements in patients so far had eluded most investigators. Recent data, however, indicate that low CBF and ischemia probably only occur within the first few hours after injury, yet have important impact on neurologic status and outcome. Similarly, the clinical significance of posttraumatic hyperemia is unclear. A relationship between raised intracranial pressure (ICP) and hyperemia has been suspected, but reports have not been consistent, possibly due to a dissociation between CBF and CBV in head-injured patients. Measurements of CBV in the acute stage of severe head injury now have confirmed this concept, and also suggest that increased CBV may contribute to brain stiffness and elevated ICP. Impairment of cerebrovascular CO2 reactivity and autoregulation often occurs after TBI. Although no correlation with the severity of injury or outcome has been established, it is obvious that diminished adaptive responses of the cerebral vasculature render the brain more vulnerable to additional systemic insults, such as derangements of blood pressure, altered rheology, or hypoxia. The posttraumatic status of vascular reactivity and autoregulation also has important implications with regard to the treatment of high ICP, in particular for the use of hyperventilation and pharmacologic management of blood pressure, which are discussed in detail.
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PMID:Cerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury. 158 25

The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 microL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 microL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.
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PMID:The role of bradykinin in the etiology of vasogenic brain edema and perilesional brain dysfunction. 159 96

Experiments were designed to determine whether endothelial cell injury contributes to increased coronary vascular tone after global cardiac ischemia and reperfusion. Canine hearts were exposed to global ischemia for 45 minutes and were reperfused for 60 minutes. Rings (5 to 6 mm long) of the left anterior descending coronary artery from reperfused hearts and from normal (control) hearts were suspended for isometric force measurement in organ chambers containing physiologic salt solution (37 degrees C, and 95% oxygen and 5% carbon dioxide). After contraction with prostaglandin F2 alpha, reperfused coronary arteries had significant impairment of endothelium-dependent relaxations to aggregating platelets (52% +/- 12% relaxation versus 102% +/- 11% for control segments; p less than 0.05). Reperfused arterial rings also exhibited impaired endothelium-dependent relaxations to the receptor-dependent agonist acetylcholine and the platelet-derived compounds adenosine diphosphate and serotonin. Importantly, endothelium-dependent relaxations to the non-receptor-dependent agonist A23187 were normal after ischemia and reperfusion. Quiescent (noncontracted) reperfused arterial rings lost the ability to counteract the constrictive effect of aggregating platelets on the coronary vascular smooth muscle (24% +/- 7% contraction versus 5% +/- 2% relaxation for control segments; p less than 0.05). Endothelium-independent contractions to potassium chloride and prostaglandin F2 alpha were similar in reperfused and normal arteries. Also, endothelium-independent relaxations to nitric oxide and isoproterenol were comparable in reperfused arteries and normal vessels. Thus global cardiac ischemia and reperfusion impair the normal endothelium-dependent relaxations to aggregating platelets and other receptor-dependent vasoactive drugs. This impairment of platelet-mediated coronary vasodilation may explain increased coronary vascular tone after cardiopulmonary bypass and could be an important pathophysiologic mechanism of postoperative coronary vasospasm.
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PMID:Global myocardial ischemia and reperfusion impair endothelium-dependent relaxations to aggregating platelets in the canine coronary artery. A possible cause of vasospasm after cardiopulmonary bypass. 159 79

We evaluated the CO2-induced vasomotor reactivity of the cerebral vasculature in 48 patients with high degree stenosis or occlusion of the internal carotid artery by transcranial Doppler ultrasonography measuring changes of flow velocities in the middle cerebral artery. Further, the vasomotor reactivity of the basilar artery was measured in 48 patients with vertebro-basilar ischemia. These results were compared with the findings in normal individuals. The vasomotor reactivity was significantly reduced in patients with stenosis or occlusion of the internal carotid artery as compared to normal controls. In patients with high degree ICA stenoses, undergoing to carotid surgery, CO2-test showed a significant improvement of the pathological vasomotor reactivity 6 month after the operation. In the group of patients with vertebro-basilar ischemia, the vasomotor reactivity measured in the basilar artery, was significantly reduced in patients with completed brainstem infarctions but not in patients with transient brainstem ischemia or infarctions in the posterior cerebral artery territory. We conclude that evaluation of the cerebral vasomotor reactivity by transcranial Doppler ultrasound is able to identify an inadequate cerebral blood supply and may help to estimate the hemodynamic effect of stenosis or occlusion of the extracranial brain supplying arteries.
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PMID:[CO2 test with transcranial Doppler sonography in cerebral ischemia]. 160 86

Considerable evidence has accumulated that oxygen free radicals play a major role in ischemic injury, particularly when followed by reperfusion. Few reports have demonstrated the occurrence of oxidative damage during the ischemic period, itself. Our laboratory has demonstrated that events occurring during an ischemic period with adequate oxygen supply can mimic the "oxygen paradox," using lipid peroxidation as an index of oxidative stress and lung edema as an index of tissue injury. The present study compares lipid peroxidation and oxidation of soluble (100,000g supernatant) protein during ischemia and reperfusion in isolated rat lung model perfused with artificial medium and ventilated with varying alveolar oxygen tension. Protein oxidation was determined by a modified dinitrophenylhydrazine (DNPH) method using Sephadex G-25 column chromatography to isolate the DNPH bound proteins. Global ischemia was produced by discontinuing perfusion while ventilation continued with gas mixtures containing 5% CO2 and a fixed oxygen concentration between 0 and 95%. After 1 h ischemia in the isolated rat lung ventilated with 20% oxygen, protein carbonyls and thiobarbituric acid reactive substances (TBARS) increased significantly compared with controls. These changes were more pronounced after 60 min of reperfusion with 95% oxygen in the ventilation gas. With 0% oxygen (95% nitrogen and 5% CO2) content of the ventilating gas during ischemia, TBARS and protein carbonyls remained at the control level. The wet/dry weight ratio showed changes parallel to the indices of tissue oxidation. The presence of 5,8,11,14-eicosatetraynoic, an inhibitor of cyclooxygenase and lipoxygenase pathways, in the perfusate had no effect on the generation of protein carbonyls although inhibition of lipid peroxidation was demonstrated. This implies that the oxidation of soluble protein is not mediated by the eicosanoid metabolic cascade. These data indicate that oxidative processes occur during ischemia and are dependent on the alveolar oxygen concentration. Oxidation of soluble protein can be used as an index of oxidative damage during lung ischemia and reperfusion.
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PMID:Role of oxygen in oxidation of lipid and protein during ischemia/reperfusion in isolated perfused rat lung. 160 29

Intracellular free calcium concentration ([Ca2+]i) was measured in isolated ferret ventricular papillary muscles during and after long exposures to ischemia. All experiments were performed at 37 degrees C, and the muscles were stimulated at 1 Hz. Ischemia was simulated by changing from superfusion with oxygenated Tyrode's solution to superfusion with water-saturated gas (95% N2-5% CO2), thus simultaneously stopping oxygenation and restricting the extracellular space. [Ca2+]i was measured with aequorin, which was microinjected into superficial cells of the preparation. Exposure to ischemia caused a complex series of changes in [Ca2+]i. In the first few minutes the changes in [Ca2+]i were variable; however, after approximately 5 minutes all preparations exhibited a progressive increase in amplitude and duration of the stimulated rise in [Ca2+]i (the calcium transient). The amplitude of the calcium transients peaked after approximately 18 minutes of ischemia, when they were 339% of the control value. After this peak, the calcium transients progressively failed to occur in response to stimulation and declined in amplitude; simultaneously, spontaneous oscillations of [Ca2+]i appeared and increased in size and frequency. The oscillations in turn then gradually became less frequent until a large, prolonged (5-10 minute) increase in [Ca2+]i occurred, after which [Ca2+]i returned to a low level. There were no further oscillations after this event, which was seen on average after 37 minutes of ischemia. A slowly progressive contracture often began to develop at about this time. A gradual rise in resting [Ca2+]i occurred during the remainder of the exposure to ischemia. When muscles were reperfused after long exposures to ischemia, there was a very large and prolonged increase in [Ca2+]i, which was usually associated with a contracture and failure of recovery of developed tension. The large increase in [Ca2+]i could be reduced by the inclusion of 3 mM nickel chloride in the reperfusing solution. Comparison between reperfusion with O2 gas versus reperfusion with anoxic Tyrode's solution indicated that reoxygenation was more beneficial to the muscle than resumption of bulk flow. These results reveal the complex spectrum of changes in [Ca2+]i that occur during ischemia and on reperfusion. These changes in [Ca2+]i are likely to play an important role in the generation of ischemic arrhythmias and muscle damage.
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PMID:Changes in intracellular free calcium concentration during long exposures to simulated ischemia in isolated mammalian ventricular muscle. 160 68


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