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

Regional cerebral blood flow (rCBF) during hypertension and hypercapnia was studied in 33 patients with putaminal hemorrhage, using a single photon emission CT by means of Xenon 133 inhalation method. The results obtained were as follows: 1) A significant relationship was obtained between the impairment of autoregulation, CO2 reactivity and the degree of cerebral ischemia, i. e., in most cases, these vascular responses were impaired in cases of ischemia showing the rCBF decrease over 30 to 40% of normal values. However, there were particular cases with cerebral ischemia of over 30 to 40% in which autoregulation seemed to be preserved in the acute stage, which was considered to be the similar phenomenon as so called "false autoregulation". 2) The cerebrovascular responses such as autoregulation and CO2 reactivity were preserved in cases of less than 50 ml of hematoma volume. In cases with 50 to 74 ml of hematoma volume however, autoregulation and CO2 reactivity were mostly impaired, especially in the affected hemisphere rather than the non-affected, in the period of 1 to 2 months from the onset. Furthermore, the impairment was also involved in both hemispheres if the hematoma was over 75 ml in volume. 3) The cerebrovascular responses were markedly impaired in the region of basal ganglia of the affected hemisphere which corresponded well to the hematoma site. 4) There was a close correlation between the cerebrovascular responses and the activity of daily life (ADL), i. e, the prognosis might be poor in cases with global impairment, but which seemed to be rather good in cases with local impairment. It might be concluded, from the results mentioned above, that the study of autoregulation and CO2 reactivity is probably significant in estimating the pathogenesis and the treatment of cerebral ischemia following hypertensive putaminal hemorrhage.
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PMID:[A study of cerebrovascular autoregulation and CO2 reactivity in putaminal hemorrhage]. 310 23

Regional cerebral blood flow (rCBF), using a single photon emission CT with Xe-133 inhalation method, was measured before and after the operation in 30 patients who underwent a superficial temporal artery to middle cerebral artery (STA-MCA) anastomosis. The purpose of this study is to assess the effect of STA-MCA anastomosis from the standpoint of hemodynamics and the results obtained were as follows: rCBF at rest increased after the operation, which was approximately 10% alterations and was localized in temporal region of operated hemisphere and frontal region of non-operated hemisphere respectively. rCBF during STA compression test after surgery decreased only in temporal region (anastomotic site) of operated hemisphere. This findings might indicate that blood flow via the bypass artery become to provide mainly to the confined area. CO2 reactivity was disturbed in 6 patients before operation, but it restored in 4 patients after operation. Autoregulation was also abolished in 8 patients before operation, but it restored in 6 patients after operation. In the group of severe degree of ischemia, however, autoregulation did not show the tendency to recover after the operation, whereas CO2 reactivity somewhat recovered. Angiographical retrograde filling which indicates collateral circulation reduced or disappeared in 12 out of 14 patients, in which postoperative rCBF in temporal region increased, in addition autoregulation and CO2 reactivity tended to recover after the bypass operation. These data mentioned above probably indicated the influences of CBF increase via the bypass artery. In summary, it might be concluded that the hemodynamic change such as disappearance of collateral circulation seen on angiography, additionally postoperative rCBF increase in anastomotic site seemed to be related to the restoration of these vascular responses such as CO2 reactivity and autoregulation in ischemic brain.
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PMID:[A study of regional cerebral blood flow before and after superficial temporal artery-to-middle cerebral artery anastomosis]. 310 86

The most important premise for a successful surgical treatment of epilepsy lies in an accurate diagnosis of the focus location. The hitherto employed methods for this purpose are meticulous analysis of seizure contents and scalp EEGs, but spatial localization of the focus sites is far beyond the capacity of these diagnostic measures. With the advent of positron emission tomography (PET), in vivo observation of human brain metabolism has become possible. The indices of brain metabolism such as cerebral blood flow (rCBF), cerebral metabolic rate of glucose or oxygen (CMRG, CMRO2) are noninvasively measured by PET offering priceless information for diagnosing brain dysfunction such as ischemia, degeneration, psychosis, or epilepsy. Kuhl et al. first employed PET in assessment of epileptic foci, in which interictal foci were beautifully detected as discrete "hypometabolic zones". Many researchers have confirmed this invaluable finding, and nowadays PET seems to have acquired the citizenship as one of the most capable diagnostic measures in focus localization. We have hitherto applied PET study in 72 epileptic patients. The main contents of their seizures consists of complex partial in 32, elementary partial in 32, generalized in 6, and others in 3 cases. We administered perorally 10 mCi glucose labeled with C11 produced in the JSW Baby Cyclotron for the study of CMRG. The continuous inhalation method of CO2 and O2 labeled with O15 produced in the same cyclotron was also employed for measurement of rCBF and CMRO2. In both studies, epileptic foci were shown as well demarcated hypometabolic zones with decreased CMRG, rCBF or CMRO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Surgical treatment of convexity focal epilepsy--based on diagnosis of PET and subdural EEG]. 310 88

Common carotid artery blood flow (CCF), pulmonary gas exchange and ventilation were measured in six subjects in the supine posture (SUP I), serially during 20 min of head-down tilt at -30 degrees (HDT) and after returning to the supine posture (SUP II). CCF was approximately 6% lower during HDT, with a transient increase during the second minute, and was about 7% higher during SUP II than during SUP I. The transition from SUP I to HDT caused increases in O2 uptake (VO2), CO2 output, respiratory exchange ratio and tidal volume in the first minute. Similar responses were apparent following the HDT to SUP II transition, except for VO2, which changed little. Correction of VO2 for changes in estimated lung O2 stores indicated that about 200 ml of blood were shifted within the circulation by the tilt transitions which provided a ventilatory stimulus. HDT can cause a loss in blood and tissue O2 stores and gain in CO2 stores by shifting blood volume toward and blood flow away from the dependent headward vascular compartment and perhaps by producing ischemia in the elevated lower extremities. Cerebral venous congestion during HDT appears to cause periodic breathing and reduce CCF, the latter being partially offset by reduced flow resistance in the carotid artery.
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PMID:The effects of head-down tilt on carotid blood flow and pulmonary gas exchange. 311 16

A good result from the heart-lung transplantation depends on the quality of the preservation of cardiopulmonary transplants. To determine the functional and pathological status of the heart-lung block after preservation for several hours, we performed 10 heterologous heart-lung transplantations in Beagle dogs (weight 13.5 kg) under extracorporeal circulation. Weight and length compatibility between donor and receiver was ensured. Measurements of hemodynamics, lung mechanics and blood gases were performed in the donor and in the receiver before the transplantation, and in the receiver after heart-lung reimplantation. Histological studies were carried out by biopsy on the heart and on the lung of the donor before removal, at the beginning of the preservation at low temperature, after 3 h of ischemia in cold, and every hour after recirculation in the heart-lung block. Myocardial preservation was conducted with cold cardioplegia at 4 degrees C (Ringer lactate solution with high potassium). Lung preservation was achieved by injecting a Euro-Collins solution at 4 degrees C, with addition of dog plasma, into the pulmonary artery; during the whole ischemic phase, the lung parenchyma was maintained at 0 degrees C, and inflated at a 10 cm H2O pressure. After transplantation, we observed that cardiac output was low in all cases, with normal or subnormal pulmonary arterial pressure. Dynamic lung compliance was very low immediately after transplantation, and increased when restarting the circulation, but deteriorated again after several hours. At the same time alveolo-arterial O2 pressure difference and arterio-alveolar CO2 pressure difference progressively increased, due to the extensive gas exchange impairment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiorespiratory function and pathological findings in heart-lung block reimplanted after hypothermic preservation. 313 46

To assess whether free radicals affect the characteristic sequence of events in an in vitro model of ischemia and reperfusion, isolated canine cardiac Purkinje fibers were exposed to anti-free radical agents, superoxide dismutase 50 U/ml; catalase 600 U/ml; mannitol 2 mM and 20 mM and combined superoxide dismutase, catalase, and mannitol 20 mM. Fibers were superfused for 60 min with altered Tyrode's solution which mimicked some conditions of ischemia (glucose-free, containing lactate, equilibrated with 90% N2-10% CO2), and then re-exposed to normal, oxygenated Tyrode's solution. Anti-free radical agents alone had no electrophysiological effects. Ischemic conditions resulted in moderate depolarization in most preparations (10 control; 43 treated) but in severe depolarization, to less than -60 mV, in some (3 control, 11 treated). Re-exposure to normal, oxygenated solution resulted in prompt initial hyperpolarization followed by marked depolarization, and finally by recovery to baseline maximum diastolic potential. Anti-free radical agents had not effect on maximum diastolic potential during exposure to ischemic conditions or on initial hyperpolarization following re-exposure to oxygenated solution. Preparations that became severely depolarized during exposure to ischemic conditions were not protected by anti-free radical interventions from developing marked depolarization following re-exposure to oxygenated solution. However, in fibers only moderately depolarized by the ischemic conditions, all anti-free radical interventions except mannitol, 2 mM significantly attenuated depolarization following re-exposure to oxygenated solution. Anti-free radical interventions significantly reduced the number of preparations that became markedly depolarized (to less than -65 mV) during re-exposure to oxygenated solution (except for mannitol, 2 mM). Agents had no effect on the occurrence of abnormal automaticity; the occurrence of inexcitability was reduced, but not significantly, except when all agents were used in combination. The results suggest that free radical production may contribute to electrophysiological abnormalities when Purkinje fibers are re-exposed to oxygenated Tyrode's solution after they have been exposed to ischemic conditions.
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PMID:Electrophysiological effects of anti-free radical interventions in canine Purkinje fibers. 314 29

Intracellular pH (pHi) was measured with proton-sensitive liquid sensor microelectrodes in isolated Necturus antral mucosa, paying special attention to arranging experimental conditions to simulate conditions frequently associated with in vivo "stress ulceration." Intracellular pH in mucosas perfused under standard conditions (Ringer's solution containing HCO3-/CO2) was 7.22 + 0.02 (n = 27). Removal of Na+ and HCO3- or addition of amiloride or 4-acetamido-4-isothiocyanostillbene-2,2-disulfonic acid (blockers of Na+/H+ and Cl-/HCO3-exchangers) had no influence on steady-state pHi, suggesting that these ion exchangers do not significantly contribute to the maintenance of pHi in the presence of normal external pH. Acidification of mucosal (luminal) perfusate to pH 3 (mimicking the presence of gastric acid) had no influence on pHi, but mucosal pH 2 (10 mM HCl) acidified pHi to 6.93 +/- 0.07. Acidification of serosal (nutrient) perfusate to pH 6 (mimicking intramucosal acidosis caused by back-diffusion of luminal H+) acidified pHi to 6.72 +/- 0.10. Removal of Na+ from and addition of amiloride to the serosal perfusate during exposure to serosal pH 6.0 induced further acidification of pHi, suggesting that in this acidotic situation (with very low ambient HCO3- concentration) a Na+/H+ exchanger does contribute to the maintenance of steady-state pHi. Increased PCO2 (10% vol/vol in the gas) in a slightly acidic milieu (mimicking mucosal ischemia) likewise acidified pHi to 6.73 +/- 0.05. A combination of mucosal acid (pH 3), high PCO2 (10% CO2), and low serosal pH (pH 6) (mimicking conditions that prevail, for example, during hemorrhagic shock) acidified pHi and ultimately resulted in cell death. These derangements of intracellular acid-base balance may have pathogenetic importance also in in vivo stress ulceration.
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PMID:Intracellular pH in isolated Necturus antral mucosa in simulated ulcerogenic conditions. 316 88

Isolated rabbit hearts were perfused normoxically or ischemically using the technique of Langendorff. The hearts were perfused with a modified Krebs-Henseleit solution, perturbated with 95% O2/5% CO2 or in case of ischemia with N2 which replaced the O2. The perfusion rate was 25 ml/min under normoxic and 2.5 ml/min under ischemic conditions. The oxygen pressure was about 65 kPa in the normoxic and about 6 kPa in the ischemic medium. Reperfusion of ischemic hearts was realized in some cases normoxically. During the ischemic perfusion and reperfusion LDH was released time depended into the perfusion medium and the aortic inflow pressure increased. The LDH release and the increase of the inflow pressure are strong correlated. Both parameters direct to ischemic myocardial lesions. Amrinone applied as bolus in the start period of ischemia or as an infusion during the ischemic and reperfusion time limited the release of LDH and the increase of the inflow pressure. The results were discussed as a direct protecting effect of amrinone against a myocardial ischemic lesion, which is in correspondence with the improving effects of amrinone on the ischemia caused heart failure of canines in vivo, shown by Campbell et al.
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PMID:The effect of amrinone on LDH release and perfusion pressure in isolated ischemic rabbit hearts. 322 85

During near complete hyperglycemic brain ischemia, brain lactate levels rise in excess of 16-18 mmol/K and are associated with severe brain infarction. Analyses of pHo, Pt(CO2), and total brain lactate under these circumstances suggest that H+, HCO3, and lactate become unequally distributed between cells and the interstitial space and, perhaps, even between different types of brain cells. In addition, to whatever physiological advantages it may generate, such compartmentalization may be a factor leading to cell death in brain ischemia.
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PMID:Compartmentation of acid-base balance in brain during complete ischemia. 324 68

The determinants of reperfusion arrhythmias were investigated in 63 open-chest dogs undergoing a 25-minute coronary artery occlusion followed by reperfusion. Heart rate correlated positively with the occurrence of reperfusion ventricular tachycardia (VT) and ventricular fibrillation (VF). Collateral flow during ischemia (radioactive microspheres) exhibited a strong negative correlation with the incidence of both VT and VF upon reperfusion. Importantly, a sensitive coupling was present, whereby small differences in flow were associated with large differences in rhythm disorders. The rise in intramyocardial CO2 tension (another index of severity of ischemia) was greater in dogs exhibiting reperfusion VT (p less than 0.001) and VF (p less than 0.08); however, this variable was significantly correlated with collateral flow (r = -0.57, p less than 0.01). The size of the occluded coronary bed, determined by postmortem perfusion, was not consistently related to VT; within a given range of occluded bed sizes, the incidence of VT was inversely related to collateral flow. Thus, reperfusion-induced VT is relatively independent of the size of the occluded bed, and is determined primarily by the degree of myocardial hypoperfusion. In contrast, VF did not develop with occluded beds less than 25% of the left ventricular mass; above this critical occluded bed size, its incidence was inversely related to collateral perfusion. Reperfusion VF is therefore determined by the association of a large occluded bed with a poor collateral flow. This study identifies and systematically analyzes three major determinants of reperfusion arrhythmias: (1) the severity of antecedent ischemia, estimated either from the degree of flow reduction or the rise in intramural CO2 tension; (2) the amount of ischemic/reperfused myocardium; and (3) the heart rate. In addition to conceptual interest and clinical implications, the findings have important implications for the design of future studies aimed at evaluating antiarrhythmic interventions in experimental models.
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PMID:Factors that determine the occurrence of reperfusion arrhythmias. 333 79


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