Selective posterior cerebral artery amobarbital test in patients with temporal lobe epilepsy for surgical treatment.
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PURPOSE: To evaluate whether the selective posterior cerebral artery amobarbital test (PCAAT) can predict postoperative memory function in patients with temporal lobe epilepsy (TLE) for surgical treatment and its clinical safety. METHODS: The database included adult patients with intractable TLE undergoing presurgical evaluation at Taipei Veterans General Hospital between 1995 and 2002. The PCAAT was carried out on patients who had failed conventional intracarotid amobarbital test (IAT) or had IAT results that evoked a concern of postoperative memory function decline. A battery of learning and memory testing was performed immediately before and after injection of amobarbital into the peduncular segment of the posterior cerebral artery (PCA) on the presumed hemisphere of epileptogenicity. Neuropsychological assessments were followed in surgically treated patients. RESULTS: A total of 16 patients completed PCAAT successfully and underwent anterior temporal lobectomy (ATL). Four patients failed PCAAT angiographic procedures due to technical difficulty in one patient, transient signs of vasospasm in two patients, and subarachnoid hemorrhage in one patient. Of the 12 patients who performed well in PCAAT learning and memory testing items by free recall or recognition, only 1 patient demonstrated postoperative memory decline in follow-up neuropsychological assessments. In contrast, two of the four patients with a deficit in PCAAT memory testing showed postoperative memory decline. Regarding subjective memory function (not necessarily associated with objective memory decline), patients not seizure-free after ATL were more likely to have memory complaints (in 3 out of 6 patients) than patients with seizure-free outcomes (in 1 out of 10 patients). CONCLUSIONS: The PCAAT memory test reliably predicts postoperative memory function in patients with TLE for surgical treatment. However, the inherent risks of PCAAT must be considered and it should be used judiciously. (+info)
A repeated dose comparison of dichloralphenazone, flunitrazepam and amylobarbitone sodium on some aspects of sleep and early morning behaviour in normal subjects.
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1 Seven normal subjects were given three different hypnotics (flunitrazepam 1 mg, amylobarbitone sodium 100 mg and dichloralphenazone 1300 mg) for four consecutive nights each. 2 All three substances improved subjective assessment of the ease of getting to sleep. Flunitrazepam was rated as better than eithr dichloralphenazone or amylobarbitone sodium in this respect. 3 The perceived quality of induced sleep was not altered by any of the preparations. 4 There was a disturbance of the subjective ratings of getting to sleep following cessation of treatment with dichloralphenazone, giving tentative support to the existence of a 'rebound' effect. 5 Dichloralphenazone produced an impairment in psychomotor performance as measured on a complex reaction time test following four nights medication with the drug. (+info)
Safety of cerebral digital subtraction angiography in children: complication rate analysis in 241 consecutive diagnostic angiograms.
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BACKGROUND AND PURPOSE: Catheter-based cerebral angiography remains an important diagnostic tool in the pediatric population, particularly considering the currently growing interest in diagnosing and treating cerebrovascular disorders in children. There are no recent estimates of the complication rate associated with modern diagnostic digital subtraction angiography (DSA) in the pediatric population. The purpose of this study was to estimate the rate of complications occurring during cerebral angiography in children. METHODS: Data from 241 consecutive pediatric cerebral angiograms performed at a single institution were entered into an institutional review board-approved database. Information on patient demographics, DSA indication, neurovascular diagnosis, and intra procedural and postprocedural complications was collected. RESULTS: Our population included 115 boys and 90 girls, with age ranging from 1 week to 18 years (mean+/-SD, 12+/-5 years). All angiograms were technically successful. No intraprocedural complication was noted; in particular, there was no occurrence of iatrogenic vessel injury (dissection) and no transient or permanent neurological deficit secondary to a thromboembolic event. One child with a complex dural arteriovenous fistula experienced a fatal intracranial rehemorrhage secondary to a posterior fossa varix rupture 3 hours after completion of an uneventful diagnostic angiogram. The rates of intraprocedural and postprocedural complications were therefore 0.0% (95% CI, 0.0% to 1.4%) and 0.4% (95% CI, 0.012% to 2.29%), respectively. CONCLUSIONS: The rate of immediate complications occurring during diagnostic cerebral angiography in children is very low. No intraprocedural complication was documented in the reported series. DSA performed by experienced angiographers is a safe procedure that can provide critical diagnostic information. (+info)
Reversible blockade of electron transport during ischemia protects mitochondria and decreases myocardial injury following reperfusion.
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Cardiac mitochondria sustain damage during ischemia and reperfusion, contributing to cell death. The reversible blockade of electron transport during ischemia with amobarbital, an inhibitor at the rotenone site of complex I, protects mitochondria against ischemic damage. Amobarbital treatment immediately before ischemia was used to test the hypothesis that damage to mitochondrial respiration occurs mainly during ischemia and that protection of mitochondria during ischemia leads to decreased cardiac injury with reperfusion. Langendorff-perfused Fischer-344 rat hearts were treated with amobarbital (2.5 mM) or vehicle for 1 min immediately before 25 min of global ischemia. Both groups were reperfused for 30 min without additional treatment. Subsarcolemmal (SSM) and interfibrillar (IFM) populations of mitochondria were isolated after reperfusion. Ischemia and reperfusion decreased state 3 and increased state 4 respiration rate in both SSM and IFM. Amobarbital treatment protected oxidative phosphorylation measured following reperfusion and improved the coupling of respiration. Cytochrome c content measured in SSM and IFM following reperfusion decreased in untreated, but not in amobarbital-treated, hearts. H(2)O(2) release from SSM and IFM isolated from amobarbital-treated hearts during reperfusion was markedly decreased. Amobarbital treatment before ischemia improved recovery of contractile function (percentage of preischemic developed pressure: untreated 51 +/- 4%, n = 12; amobarbital 70 +/- 4%, n = 11, p < 0.01) and substantially reduced infarct size (untreated 32 +/- 2%, n = 7; amobarbital 13 +/- 2%, n = 7, p < 0.01). Thus, mitochondrial damage occurs mainly during ischemia rather than during reperfusion. Reperfusion in the setting of preserved mitochondrial respiratory function attenuates the mitochondrial release of reactive oxygen species, enhances contractile recovery, and decreases myocardial infarct size. (+info)
Pyridine nucleotide redox state parallels production of aldosterone in potassium-stimulated adrenal glomerulosa cells.
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Extracellular potassium ions (K+) raise the intracellular concentration of free Ca2+ ([Ca2+]i) by gating voltage-dependent Ca2+ channels and stimulate aldosterone production in adrenal glomerulosa cells. The pathway leading from calcium influx to increased steroid synthesis has not been completely elucidated. In the present study we demonstrate that the reduction of pyridine nucleotides known to be required for steroid hydroxylation is enhanced by K+ (4.1-8.4 mM) in single rat glomerulosa cells. The action of K+ was strictly dependent on the presence of extracellular Ca2+. Amytal, a blocker of site I of the mitochondrial respiratory chain, abolished the K+ effect, indicating a mitochondrial origin for the recorded changes. Supraphysiological K+ concentration (18 mM) resulted in a further increase in [Ca2+]i, while steroidogenesis was decreased as measured in cell suspensions. However, a possible explanation for this dichotomy is provided by the finding that the level of reduced pyridine nucleotides also decreased at supraphysiological K+ concentration. (+info)
Inhibited mitochondrial respiration by amobarbital during cardiac ischaemia improves redox state and reduces matrix Ca2+ overload and ROS release.
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AIM: Damage to the mitochondrial electron transport chain (ETC) occurs during ischaemia. Blockade of electron flow in the ETC just before ischaemia with the reversible complex I inhibitor amobarbital protects isolated mitochondria against ischaemic damage and preserves oxidative phosphorylation and cytochrome c content. We hypothesized that brief amobarbital perfusion just before ischaemia would improve cardiac recovery and decrease infarct size after ischaemia and reperfusion (IR) by preserving the mitochondrial redox state and reducing mitochondrial superoxide (O(2)(-*)) generation, in turn would decrease mitochondrial Ca(2+) accumulation (mt[Ca(2+)]). METHODS: Guinea pig Langendorff-perfused hearts were treated with Krebs Ringer solution (KR; untreated) or amobarbital (2.5 mM) in KR for 1 min immediately before 30 min of no flow, global ischaemia, followed by reperfusion without additional treatment. Cardiac function, mitochondrial NADH, FAD, mt[Ca(2+)], and O(2)(-*) levels were assessed during the 1 min perfusion period and throughout IR. RESULTS: Amobarbital perfusion alone before ischaemia significantly increased O(2)(-*) levels and NADH, without altering FAD, and decreased mt[Ca(2+)]. During ischaemia, mitochondrial NADH was higher, O(2)(-*) levels were lower, and mt[Ca(2+)] was less elevated in the amobarbital group. On reperfusion O(2)(-*) levels and mt[Ca(2+)] were significantly reduced, NADH-FAD redox state was preserved and cardiac function was markedly improved in the amobarbital group; infarct size was smaller in the amobarbital group compared to the untreated group. CONCLUSION: Temporary blockade of mitochondrial complex I activity by amobarbital protects hearts by reducing production of O(2)(-*) and mtCa(2+) loading during IR injury. (+info)
A relation between (NAD+)/(NADH) potentials and glucose utilization in rat brain slices.
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Changes in several parameters involved in the control of metabolism were correlated with changes in glucose utilization in rat brain slices incubated under conditions which reduced glucose oxidation by 40 to 70%. The parameters included: the concentrations of ATP, ADP, AMP, and the adenylate energy charge; the cytoplasmic oxidation-reduction state ([NAD+]/[NADH]), determined from the [pyruvate]/[lactate] equilibrium; the mitochondrial oxidation-reduction state, determined from the [NH4+] ]2-oxoglutarate]/[glutamate] Equilibrium; the cytoplasmic and mitochondrial oxidation-reduction potentials (in volts), calculated from the respective [NAD+]/ [NADH] ratios using the Nernst equation; and the difference between the cytoplasmic and mitochondrial [NAD+]/[NADH] potentials. The conversion of [3, 4-14C] glucose to 14CO2 and of [U-14C] glucose to acetylcholine and to lipids, proteins, and nucleic acids by the brain slices were also determined. The values obtained by subtracting the mitochondrial from the cytoplasmic [NAD+1/[NADH] potentials correlated more closely with glucose utilization than did other parameters, under the conditions studied. For the synthesis of acetylcholine, the correlation coefficient was 0.96, and for the production of 14CO2 from [3, 4-14C] glucose it was 0.82. (+info)
Enigmatic effect of cellular ATP on fatty acid biosynthesis. Stimulation by moderate decrease and inhibition by increase of cellular ATP.
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