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

We superimposed extreme hypercapnia (arterial Pco2 400-450 mmHg) immediately before and during incomplete cerebral ischemia to distinguish the role of intracellular pH (pHi) and bicarbonate [( HCO3-]i) in postischemic metabolic and electrophysiological recovery. Incomplete global ischemia was produced in seven anesthetized dogs by 30 min of intracranial hypertension followed by 4 h of reperfusion. ATP, phosphocreatine (PCr), and pHi were measured with 31P magnetic resonance spectroscopy, and [HCO3-]i was calculated from the Henderson-Hasselbalch equation using the measured pHi and sagittal sinus Pco2. Cerebral blood flow was reduced to 7 +/- 1 ml.min-1.100 g-1 (+/- SE) during ischemia with extreme hypercapnia, and pHi decreased to 5.72 +/- 0.09. During normocapnic reperfusion, pHi rapidly returned to near baseline values by 14 min. [HCO3-]i fell from 12.1 +/- 0.9 to 6.0 +/- 1.2 mM by the midpoint of ischemia and recovered by 30 min of reperfusion. ATP, PCr, and O2 consumption also recovered rapidly and completely. Somatosensory-evoked potentials (SEP) recovered to 43 +/- 10% of control amplitude. These results are in marked contrast to the poor metabolic and SEP recovery previously observed in hyperglycemic dogs in which pHi decreased to the same range as with hypercapnic ischemia, but in which [HCO3-]i was much lower (1.1 +/- 0.5 mM). Therefore, [HCO3-]i depletion during hyperglycemic ischemia may be a more important factor in recovery than end-ischemic pHi per se. We speculate that higher [HCO3-]i may improve glial cell buffering capacity or decrease iron availability for hydroxyl radical production.
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PMID:Bicarbonate conservation during incomplete cerebral ischemia with superimposed hypercapnia. 190 5

This report demonstrates the feasibility of using deuterium (2H) and phosphorus (31P) nuclear magnetic resonance (NMR) spectroscopy to make multiple simultaneous determinations of changes in cerebral blood flow, brain intracellular pH, and phosphorylated metabolites for individual animals. In vivo spectra were obtained from the brains of newborn piglets immediately following an intracarotid bolus injection of deuterium oxide. Experiments were performed at magnetic field strengths of 1.9 T (2H NMR only) or 4.7 T (interleaved 2H and 31P NMR). The rate of clearance of deuterium signal was used to calculate cerebral perfusion rates (CBFdeuterium) during a stable control physiologic state and conditions known to alter blood flow. CBFdeuterium values measured at 1.9 T under conditions of control (normocarbia, normotension), hypercarbia, hypocarbia, and varying degrees of ischemia induced by hypotension showed a significant positive correlation with values measured simultaneously using radiolabeled microspheres (CBFdeuterium = 0.4 x CBFmicrospheres + 8; r = 0.8). Simultaneous interleaved 2H and 31P NMR measurements under control conditions indicate that brain energy metabolites and intracellular pH remained at constant levels during the time course of the administration and clearance of deuterium oxide. Also, brain phosphorylated metabolites and intracellular pH did not differ significantly from their preinjection levels. Under control physiologic conditions, CBFdeuterium varied by +/- 6% and phosphorylated metabolite levels did not show a significant change with time, as measured from 15 blood flow determinations collected over 4 h. The results indicate that CBFdeuterium determinations have excellent reproducibility and do not affect brain energy metabolite levels. The procedures described here have the potential to bring a novel methodology to bear on investigating the relationship between cerebral perfusion and energy status during conditions such as ischemia or asphyxia.
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PMID:Simultaneous measurement of cerebral blood flow and energy metabolites in piglets using deuterium and phosphorus nuclear magnetic resonance. 198 5

DC shifts are known to occur in association with a number of physiologic phenomena including spreading depression, hypoxia, epilepsy, and hypercapnia and possibly in migraine, closed head injury, and ischemia. Magnetoencephalography (MEG) makes it possible to record these shifts by prolonged DC monitoring of brain activity and offers several advantages over DC EEG and DC electrocorticography. Among the advantages of MEG is its non-invasive nature and the lack of impedance changes at the electrode-tissue interface that produce baseline shifts in DC EEG. In DC MEG measurements, great care must be taken in dealing with a variety of artifactual signals. Environmental noise can be reduced by magnetic shielding and recognized by use of reference magnetometers. Patient-generated artifacts are numerous and can be recognized and limited by a variety of methods.
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PMID:Techniques for DC magnetoencephalography. 205 Aug 18

We have observed that pial arteriolar dilation in response to hypercapnia and hypotension is abolished after cerebral ischemia in newborn pigs. We determined whether direct generation of activated oxygen on the brain surface (OX: xanthine oxidase, hypoxanthine, FeCl3, and FeSO4) or topical arachidonate altered pial arteriolar responsiveness in a manner similarly to cerebral ischemia. OX, which generated more brain surface superoxide than reperfusion after ischemia, dilated pial arterioles. This dilation was reversed within 10 min of the end of exposure. OX produced ultrastructural changes in pial vessel endothelium and appeared to cause intravascular aggregation of granulocytes. After OX, prostanoid-dependent pial arteriolar dilations in response to hypercapnia and hypotension were attenuated, whereas constrictor responses to norepinephrine and acetylcholine and dilator responses to prostaglandin E2 and isoproterenol were not affected. After OX, hypercapnia increased cortical periarachnoid cerebrospinal fluid prostanoids modestly, whereas acetylcholine produced the normal strong stimulation of prostanoid synthesis. Arachidonate (10(-4) M and 7 x 10(-4) M) also caused reversible pial arteriolar dilation but did not alter subsequent pial arteriolar responses. Therefore, although arachidonate did not mimic the effects of ischemia-reperfusion on pial arteriolar reactivity, OX produced alterations that are qualitatively similar, although quantitatively less, than those produced by ischemia.
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PMID:Activated oxygen and arachidonate effects on newborn cerebral arterioles. 212 Oct 51

In newborn pigs, cerebral ischemia abolishes both increased cerebral prostanoid production and cerebral vasodilation in response to hypercapnia and hypotension. Attenuation of prostaglandin endoperoxide synthase activity could account for the failure to increase prostanoid synthesis and loss of responses to these stimuli. To test this possibility, arachidonic acid (3, 6, or 30 micrograms/ml) was placed under cranial windows in newborn pigs that had been exposed to 20 min of cerebral ischemia. The conversion to prostanoids and pial arteriolar responses to the arachidonic acid were measured. At all three concentrations, arachidonic acid caused similar increases in pial arteriolar diameter in sham control piglets and piglets 1 hr postischemia. Topical arachidonic acid caused dose-dependent increases of PGE2 in cortical periarachnoid cerebral spinal fluid. 6-keto-PGF1 alpha and TXB2 only increased at the highest concentration of arachidonic acid (30 micrograms/ml). Cerebral ischemia did not decrease the conversion of any concentration of arachidonic acid to PGE2, 6-keto-PGF1 alpha, or TXB2. We conclude that ischemia and subsequent reperfusion do not result in inhibition of prostaglandin endoperoxide synthase in the newborn pig brain. Therefore, the mechanism for the impaired prostanoid production in response to hypercapnia and hypotension following cerebral ischemia appears to involve reduction in release of free arachidonic acid.
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PMID:Prostanoid synthesis and vascular responses to exogenous arachidonic acid following cerebral ischemia in piglets. 212 54

The purpose of this study was to investigate neonatal brain energy metabolism, acid, and lactate homeostasis in the period immediately following partial ischemia. Changes in brain buffering capacity were quantified by measuring mean intracellular brain pH, calculated from the chemical shift of Pi, in response to identical episodes of hypercarbia before and after ischemia. In addition, the relationship between brain buffer base deficit and intracellular pH was compared during and following ischemia. Thus, in vivo 31P and 1H nuclear magnetic resonance spectra were obtained from the brains of seven newborn piglets exposed to sequential episodes of hypercarbia, partial ischemia, and a second episode of hypercarbia in the postischemic recovery period. For the first episode of hypercarbia, brain buffering was similar to values reported for adult animals of other species (percentage pH regulation = 54 +/- 16%). During ischemia, the brain base deficit per unit change in pH was -19 +/- 5 mM/pH unit, which is similar to values reported for adult rats. By 20-35 min postischemia, brain acidosis partly resolved in spite of a net increase in lactate concentration. Therefore, the consumption of lactate could not explain acid homeostasis in the first 35 min following ischemia. We conclude that H+/HCO3- or other proton equivalent translocation mechanisms must be sufficiently developed in piglet brain to support acid regulation. This is surprising, because a substantial body of evidence implies these processes would be less active in immature brain. The second episode of hypercarbia, from 35 to 65 min postischemia, resulted in a smaller decrease in brain pH compared with the first episode, a result indicating an increase in brain buffering capacity (percentage pH regulation = 79 +/- 29%). This was associated with a parallel decrease in brain lactate content, and therefore acid regulation could be attributed to either continued ion translocation or the consumption of lactate. A mild decrease in brain pH and content of energy metabolites was observed, a finding suggesting that the metabolic consequences of severe postischemic hypercarbia are neither particularly dangerous or beneficial.
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PMID:Acid homeostasis following partial ischemia in neonatal brain measured in vivo by 31P and 1H nuclear magnetic resonance spectroscopy. 231 86

Brain circulation after 20 min of total brain ischemia was examined in unanesthetized newborn pigs. Except in the cerebrum, reactive hyperemia was observed throughout the brain, peaking by 5 min and subsiding by 20 min of reperfusion. Brain blood flow after 15 min of reperfusion matched the control. Blood flow to the cerebrum then decreased at 40 and 90 min reperfusion, while the rest of the brain was unaffected. Blood flow to the cerebrum returned to control by 24 h. Cerebral vascular resistance doubled by 15 min reperfusion, remained elevated at 90 min reperfusion, but returned to control by 24 h. Cerebral oxygen consumption followed a pattern similar to blood flow. Ninety minutes postischemia, hypercapnia-induced hyperemia was greatly attenuated in the cerebrum, reduced modestly in the diencephalon-mesencephalon, but unaffected in the rest of the brain. Thus 20 min of global brain ischemia in piglets does not produce reactive hyperemia in the cerebrum that is detectable at 5 min reperfusion but does in the remainder of the brain. Subsequent hemodynamic abnormalities apparently are confined to the cerebrum. Blood flow throughout the brain returns to normal by 24 h. Thus cerebral hemodynamic effects of total global ischemia are regionally dependent.
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PMID:Effects of ischemia on brain blood flow and oxygen consumption of newborn pigs. 251 31

The cerebral blood flow is maintained at a constant level in spite of blood pressure variations, because of a very performing auto-regulation phenomenon: vasoconstriction in case of elevated blood pressure, vasodilatation in case of blood pressure drop. The upper limit of the mean blood pressure beyond which nothing can prevent the cerebral blood flow from increasing, ranges between 150 and 170 mmHg. The lower limit, from which the dilatation of the cerebral blood vessels is not able to prevent the decreased cerebral blood flow, has been set between 50 and 70 mmHg. The auto-regulation of the cerebral blood flow is influenced by numerous factors: hypercapnia, hypoxia and ischemia complete inhibit it, making the cerebral blood flow directly related to the blood pressure; the sympathetic stimulation shifts the entire curve toward the right, because of the constriction of the pia-mater arteries, followed with a reactional vasodilatation of the small cerebral vessels. In the course of chronic arterial hypertension, the same shift of the auto-regulation curve toward high pressures is observed, related to structural alterations of the vascular wall; this make them more prone to constriction than dilatation: when these alterations are reversible, antihypertensive treatment may sometimes bring the auto-regulation curve in its initial position.
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PMID:[The brain and arterial hypertension. 1. Physiologic and physiopathologic aspects]. 266 Jul 35

CPP reflects perfusion problems related to increased ICP or inadequate MAP. CPP is a most helpful and practical management tool. The relationship of CBF and CPP depends on cerebral vascular resistance (flow equals pressure divided by resistance). At present, we do not have a practical method to measure vascular resistance or CBV. A close relationship between an increase in CBV and increase in ICP exists. However, the relationship between CBF and ICP is more complex. Whereas CBV is strongly dependent on vasodilation and venous return, CBF is influenced by CPP, vascular resistance, viscosity changes, and focally or diffusely increased ICP. For instance, in hypotensive shock one finds a low CBF with an elevated CBV (and ICP) from vasodilation related to hypercapnia, anoxia, or acidosis. Nevertheless, about two thirds of patients with increased ICP after head injury have increased CBF (hyperemia) and increased CBV. This frequent hyperemia is one rationale for the wide usage of hyperventilation to treat increased ICP. It must be recognized that a group of patients may have ischemia caused by excessive hyperventilation therapy for increased ICP. The PaCO2 must not be allowed to decrease to 20 mmHg or lower, but in some patients a PaCO2 level of 21 to 25 may be predisposing to ischemia. Strong consideration is thus given to monitoring CBF and cerebral oxygen metabolism (arteriovenous oxygen content difference [AVDO2], CMRO2) in states of coma and increased ICP. In such patients, continuous infusion of mannitol may result in improved CBF, and hyperventilation therapy can be less aggressive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonsurgical management of increased intracranial pressure. 270 May 10

Adenosine has been proposed as a metabolic factor involved in the regulation of cerebral blood flow. The evidence in support of this hypothesis, presented in this review, includes information on the adenosine receptors associated with cerebral blood vessels, the synthesis and metabolism of adenosine, and the release of adenosine from the brain. Adenosine dilates cerebral blood vessels, acting at an A2 receptor. The critical evidence implicating an involvement of adenosine in cerebrovascular regulation is derived from experiments with adenosine antagonists and potentiators. The antagonists include methylxanthine adenosine receptor antagonists and the enzyme adenosine deaminase. Potentiators include transport inhibitors, enzyme inhibitors, and adenosine precursors. Adenosine has been implicated in vascular regulation during hypoxia/ischemia, hypercapnia, seizures, severe hypotension, and hypoglycemia. Adenosine possesses a number of properties that can be used to minimize neuronal degeneration during cerebral insults, such as ischemia, including vasodilatation, reduction of excitatory transmitter release, reduction of membrane calcium permeability, inhibition of platelets, and neutrophil aggregation. Several recent studies have demonstrated that manipulation of central adenosine tone can alter the extent of cerebral ischemic damage, indicating a potential new therapeutic approach for the treatment of stroke.
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PMID:Adenosine in the control of the cerebral circulation. 270 69


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