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)

The possibility of measuring cerebral blood flow by mobile bedside units with the intravenous 133-Xenon technique increased the interest to monitor haemodynamic changes after head injury and subarachnoid haemorrhage in intensive care. Time course of resting CBF after trauma is variable (reduced CBF, hyperemia) and there is no strong correlation to clinical outcome. Additional studies of CBF/CO2 reactivity show normal and impaired CO2 response in the acute stage after trauma (day 1-8). A permanently impaired CO2 reactivity correlates with severe brain damage and bad outcome (GOS 1,2). A normal or improving CO2 reactivity indicates a favourable outcome (GOS 3-5). There was no significant correlation between CBF and ICP, nor between CBF and CPP. A CPP of more than 70 mmHg did not guarantee a sufficient CBF in every case indicating the variability of the limits of autoregulation. As therapeutic hyperventilation may lead to ischemia, mannitol was preferred to reduce ICP and increased low CBF to normal values. This fact should be considered in the treatment of patients with low CBF and normal CO2 reactivity. Delayed ischemic neurological deficits ("vasospasm") are well-known as significant complications of the clinical course following SAH. Immediately postoperatively performed CBF measurements enable to detect ischemia and allow to start early antiischemic therapy. During "vasospasm" CBF showed a better correlation to the neurological status than blood flow velocity in the basal arteries measured by transcranial doppler sonography. Furthermore hyperemia after SAH could only be verified by CBF measurements.
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PMID:Xenon 133--CBF measurements in severe head injury and subarachnoid haemorrhage. 790 78

Xenon-enhanced computerized tomography (CT) is well suited for measurements of cerebral blood flow (CBF) in head-injured patients. Previous studies indicated divergent results on whether inhalation of xenon may cause a clinically relevant increase in intracranial pressure (ICP). The authors employed Xe-enhanced CT/CBF measurements to study the effect of 20 minutes of inhalation of 33% xenon in oxygen on ICP, cerebral perfusion pressure (CPP), and arteriovenous oxygen difference (AVDO2) in 13 patients 3 days (mean 1 to 5 days) after severe head injury (Glasgow Coma Scale score < or = 7). The patients were moderately hyperventilated (mean PaCO2 4.3 kPa or 32.3 mm Hg). Six patients were studied before and during additional hyperventilation. All 13 patients reacted with an increase in ICP and 11 with a decrease in CPP. The mean ICP increment was 6.9 +/- 7.7 (range 2 to 17 mm Hg). The mean CPP decrement was -9.7 +/- -14.6 (range 17 to 47 mm Hg). The time course of the ICP changes indicated that ICP increased rapidly during the first 5 to 6 minutes, then declined to a plateau (peak-plateau type in four of 13 patients), remained at a plateau (plateau type in six of 13), or continued to increase in three of 13, indicating individual variance in xenon reactivity. Additional hyperventilation had no effect on the xenon-induced increments in ICP but these occurred at lower ICP and higher CPP baseline levels. The AVDO2 values, an index of flow in relation to metabolism, indicated a complex effect of xenon on CBF as well as on metabolism. This study indicates that xenon inhalation for Xe-CT CBF measurements in head-injured patients according to our protocol causes clinically significant increments in ICP and decrements in CPP. It is suggested that the effect of xenon is analogous to anesthesia induction. Individual variations were observed indicating possible individual tolerance, possible influence of type and extent of the cerebral injury, disturbances in cerebrovascular reactivity, and possible influence of medication. These effects of xenon suggest that hyperventilation should be ensured in patients with evidence of reduced compliance or high ICP. On the other hand, inhalation of stable xenon is not believed to pose a risk because no signs of cerebral oligemia or ischemia were indicated in the AVDO2 values.
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PMID:Effect of stable xenon inhalation on intracranial pressure during measurement of cerebral blood flow in head injury. 796 11

S-T segment changes have been cited as evidence for preconditioning in the human heart during repeated angioplasty inflations. Opening of preformed collaterals, however, could explain these observations. We have measured the profile of S-T segment and monophasic action potential (MAP) changes in a species with low collateralization. Open-chested pigs were subjected to two cycles of 8-min LAD occlusion and 8-min reperfusion prior to 60-min ischemia and 2-h reperfusion. Two epicardial ECGs and MAP were continuously recorded from the ischemic zone and one ECG from the normal zone. Flow was measured using Xenon washout. Infarct (IS) and risk zone (RZ) sizes were assessed after reperfusion in a subset of six pigs and confirmed profound protection with preconditioning (IS/RZ = 14 +/- 9% v 42 +/- 3% in controls, P < 0.05). S-T segment elevation was smaller early in the 2nd or 3rd (0-3 min) ischemic cycles than in the 1st. In contrast, in the 1st ischemic cycle, MAP duration after 3 min was reduced to 90 +/- 2% control and this was further reduced in the 2nd and 3rd ischemic episodes to 74 +/- 4% and 77 +/- 3% respectively. Thus, preconditioning increased APD shortening while simultaneously decreasing S-T segment elevation during the early minutes of ischemia. It therefore seems unlikely that the ability of preconditioning to limit S-T segment changes is related to limitations in APD shortening. All electrophysiological differences were lost later during ischemia. Collateral flow during the three ischemic cycles was 4.8 +/- 3.7, 5.8 +/- 2.3 and 5.6 +/- 2.9% (n = 5/grp, ns) respectively. Thus, in the absence of a significant increase in collateral flow. S-T segment and MAP changes provide an index of preconditioning but only during the first few minutes of occlusion. S-T segment changes observed during PTCA may therefore reflect genuine preconditioning in man although the contribution of ischemia-induced increases in collateral flow cannot be ignored.
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PMID:Electrophysiological characteristics of repetitive ischemic preconditioning in the pig heart. 878 75

A 69-year-old female presented with sudden onset of truncal ataxia, urinary incontinence, mental confusion, and Parinaud's sign. With conservative treatment, her ataxia and urinary incontinence resolved. Magnetic resonance (MR) imaging disclosed a round mass with laminated intramural hemorrhage in the third ventricle. Right vertebral angiography demonstrated a giant aneurysm in the distal basilar artery. Xenon-enhanced computed tomography showed that cerebral blood flow (CBF) was reduced in the thalamus bilaterally and was paradoxically decreased by acetazolamide. Two months later, MR imaging showed that the intramural hemorrhage had shrunk, and the edema in the thalamus was resolving. The CBF reduction and vascular response to acetazolamide had reversed to some extent. A partially thrombosed giant aneurysm can grow acutely as the result of fresh intramural hemorrhage. The edema is secondary to ischemia and loss of vasoresponsivity.
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PMID:Extensive edema in the thalamus caused by thrombosed basilar artery aneurysm. 964 Sep 62

Recent early cerebral blood flow (CBF) studies on severe head injury have revealed ischemia in a substantial number of patients with a variety of CT diagnoses. However, the underlying derangements causing this early ischemia are unknown, but cerebral blood volume (CBV) measurements might offer some insight into this pathology. Therefore, acute CBF and CBV measurements were performed in 51 adult severely head injured patients within 24 hours after injury. For this purpose the stable Xenon-CT procedure was used for assessment of CBF, and a dynamic CT imaging technique was used for determining CBV. All ischemic patients were found among 35 subjects studied within 4 hours after injury (31%). Based on the occurrence of regional ischemia seven patients with varying anatomical lesions on CT were selected for comparison between CBF and CBV in ischemic and non-ischemic areas. Both CBF (p < 0.02) and CBV (p < 0.02) exhibited significantly lower values in the ischemic zones. Ten patients showing a subdural hematoma (SDH) were studied preceding surgery and seven were ischemic in at least one lobe or brainstem. Ipsilateral CBF was lower than CBF in the contralateral side (p < 0.1). CBV at the ipsilateral side was significantly reduced compared to the contralateral side (p < 0.05). Follow-up studies were performed in three ischemic patients and in one borderline ischemic patient immediately after removal of SDH showing a striking increase in both CBF and CBV. In the remaining 26 subjects follow-up studies were obtained between day 2 and day 8 and all patients showed CBF values within the normal range. These data evidently support the suggestion that compromise of the microvasculature is the cause of early ischemia, rather than vasospasm of the larger conductance vessels. This has implications for acute post-traumatic therapeutical strategies and management of the severely head injured patient and may lead to testing of new drugs that are effective in interfering with processes causing this ischemia.
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PMID:Early cerebral blood volume after severe traumatic brain injury in patients with early cerebral ischemia. 977 64

Intracerebral contusions can lead to regional ischemia caused by extensive release of excitotoxic aminoacids leading to increased cytotoxic brain edema and raised intracranial pressure. rCBF measurements might provide further information about the risk of ischemia within and around contusions. Therefore, the aim of the presented study was to compare the intra- and perilesional rCBF of hemorrhagic, non-hemorrhagic and mixed intracerebral contusions. In 44 patients, 60 stable Xenon-enhanced CT CBF-studies were performed (EtCO2 30 +/- 4 mmHg SD), initially 29 hours (39 studies) and subsequent 95 hours after injury (21 studies). All lesions were classified according to localization and lesion type using CT/MRI scans. The rCBF was calculated within and 1-cm adjacent to each lesion in CT-isodens brain. The rCBF within all contusions (n = 100) of 29 +/- 11 ml/100 g/min was significantly lower (p < 0.0001, Mann-Whitney U) compared to perilesional rCBF of 44 +/- 12 ml/100 g/min and intra/perilesional correlation was 0.4 (p < 0.0005). Hemorrhagic contusions showed an intra/perilesional rCBF of 31 +/- 11/44 +/- 13 ml/100 g/min (p < 0.005), non-hemorrhagic contusions 35 +/- 13/46 +/- 10 ml/100 g/min (p < 0.01). rCBF in mixed contusions (25 +/- 9/44 +/- 12 ml/100 g/min, p < 0.0001) was significantly lower compared to hemorrhagic and non-hemorrhagic contusions (p < 0.02). Intracontusional rCBF is significantly reduced to 29 +/- 11 ml/100 g/min but reduced below ischemic levels of 18 ml/100 g/min in only 16% of all contusions. Perilesional CBF in CT normal appearing brain closed to contusions is not critically reduced. Further differentiation of contusions demonstrates significantly lower rCBF in mixed contusions (defined by both hyper- and hypodense areas in the CT-scan) compared to hemorrhagic and non-hemorrhagic contusions. Mixed contusions may evolve from hemorrhagic contusions with secondary increased perilesional cytotoxic brain edema leading to reduced cerebral blood flow and altered brain metabolism. Therefore, the treatment of ICP might be individually modified by the measurement of intra- and pericontusional cerebral blood.
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PMID:rCBF in hemorrhagic, non-hemorrhagic and mixed contusions after severe head injury and its effect on perilesional cerebral blood flow. 1145 9

Having determined that edema and not vascular engorgement is the major factor leading to traumatic brain swelling, the objective of this study was to determine which type of edema, cellular or vasogenic, is responsible for increased tissue water in patients with focal lesions. Severely head injured patients (GCS 8 or less) were transported to imaging suites for measurement of brain water and apparent diffusion coefficient (ADC) using magnetic resonance technique. Cerebral blood flow by stable Xenon method was also measured in the regions of interest. Brain water was increased significantly in the hemisphere with lesion. The increase in water was associated with reduced ADC signifying a predominant cellular edema. The ADC in the contralateral hemisphere was near normal value. Cerebral blood flow values in the regions of interest were above ischemic levels suggesting that factors other than ischemia are responsible for the cytotoxic swelling in patients with focal injury.
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PMID:Distinguishing between cellular and vasogenic edema in head injured patients with focal lesions using magnetic resonance imaging. 1145 41

Traumatic brain contusions have been associated with regional ischemia. We aimed to measure the effect of induced supra-normal values of cerebral perfusion pressure (CPP) on regional cerebral blood flow (rCBF) in the intracontusional low density area surrounding the contusional hemorrhagic core. In 7 severely head injured patients (GCS < or = 8) harbouring a contusion larger than 2 cm, the rCBF levels were measured, by means of Xenon-enhanced CT, in: 1) the intracontusional low density area: 2) contralaterally, in a normal brain symmetric area. CBF studies were performed at a baseline CPP of 65.3 mmHg +/- 7 and after 20 minutes of norepinephrine-induced CPP supernormal values (88.3 mmHg +/- 10.5) (p = 0.0013). A "paradoxical" reduction of rCBF levels was observed in both the intracontusional low density area (p = 0.07) and the contralateral "normal" area (p = 0.08). In particular, this decrease of rCBF in the intracontusional low density area (-25.7 + 10 ml/100gr/min) (p = 0.0009) was present in only 4 cases, having a mean rCBF at baseline of 25 +/- 16 ml/100gr/min. In the remaining 3 cases in which rCBF at baseline was abnormally low (12 +/- 7 ml/ 100gr/min), rCBF values improved slightly (3.6 +/- 2 ml/100gr/min) (p = 0.61). An acute increase of CPP seems to marginally affect rCBF in the intracontusional low density area having critically reduced initial values, but may greatly reduce rCBF in subjects starting from non-critical baseline values.
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PMID:Induced acute arterial hypertension and regional cerebral flow in intracontusional low density area. 1475 69

Cerebral blood flow (CBF) alterations following post-traumatic contusions have been demonstrated in recent papers. We evaluated regional CBF (rCBF) by means of Xenon-enhanced computerized tomography (Xe-CT) in 29 traumatic intracerebral hematomas, from 22 patients with severe head injury (GCS < or = 8). Fifty traumatic hematoma/Xe-CT CBF measurements were obtained from 39 Xe-CT studies performed during the acute phase (corresponding to the first 20 days post-injury). The rCBF was measured in three different regions of interest: the hemorrhagic core, the perihematoma edematous low-density area, and a 1-cm rim of perihematoma normal-appearing brain tissue, surrounding the edematous low-density area. We found a centrifugal improvement of rCBF as well as a decrease in the rates of CBF levels below 18 mL/100 g/min from the core to the periphery (p < 0.0001), which persisted over time. Ischemic rCBF values were detected in the perihematoma low-density area only in 24% of the traumatic hematomas. The time course of rCBF levels showed a reduced flow in the first 24 h, with a recovery of flow from day 2 to day 4, followed by another reduced flow (p < or = 0.0001) both in the perihematoma edematous low-density area and in the non-lesioned tissue. Our findings suggest that the only area with persistent ischemic values was the hemorrhagic core. Low rCBF levels seen in the perihematoma low-density area may only be ascribed partially to ischemia and can possibly recover over time. These results could encourage a surgical approach based on an early evacuation of the hemorrhagic core associated to a preservation of the surrounding edematous tissue.
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PMID:Centrifugal distribution of regional cerebral blood flow and its time course in traumatic intracerebral hematomas. 1525 94

Xenon is an anesthetic with minimal hemodynamic side effects, making it an ideal agent for cardiocompromised patients. We investigated if xenon induces pharmacological preconditioning (PC) of the rat heart and elucidated the underlying molecular mechanisms. For infarct size measurements, anesthetized rats were subjected to 25 min of coronary artery occlusion followed by 120 min of reperfusion. Rats received either the anesthetic gas xenon, the volatile anesthetic isoflurane or as positive control ischemic preconditioning (IPC) during three 5-min periods before 25-min ischemia. Control animals remained untreated for 45 min. To investigate the involvement of protein kinase C (PKC) and p38 mitogen-activated protein kinase (MAPK), rats were pretreated with the PKC inhibitor calphostin C (0.1 mg kg(-1)) or the p38 MAPK inhibitor SB203580 (1 mg kg(-1)). Additional hearts were excised for Western blot and immunohistochemistry. Infarct size was reduced from 50.9+/-16.7% in controls to 28.1+/-10.3% in xenon, 28.6+/-9.9% in isoflurane and to 28.5+/-5.4% in IPC hearts. Both, calphostin C and SB203580, abolished the observed cardioprotection after xenon and isoflurane administration but not after IPC. Immunofluorescence staining and Western blot assay revealed an increased phosphorylation and translocation of PKC-epsilon in xenon treated hearts. This effect could be blocked by calphostin C but not by SB203580. Moreover, the phosphorylation of p38 MAPK was induced by xenon and this effect was blocked by calphostin C. In summary, we demonstrate that xenon induces cardioprotection by PC and that activation of PKC-epsilon and its downstream target p38 MAPK are central molecular mechanisms involved. Thus, the results of the present study may contribute to elucidate the beneficial cardioprotective effects of this anesthetic gas.
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PMID:The noble gas xenon induces pharmacological preconditioning in the rat heart in vivo via induction of PKC-epsilon and p38 MAPK. 1564 76


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