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

The influence of systemic blood pressure on blood-brain barrier leakage and hemorrhage in brain ischemia was evaluated in Sprague-Dawley rats with blood pressures at the lower and upper limit normally found in these animals when anesthetized on 70% N2O:30% O2. 24 h after unilateral cerebral microembolization - when significant increases in water content and barrier permeability and decrease in blood flow is present - the extravasation of Evans Blue-albumin and inulin as well as hemorrhage in the infarcted brain area was considerably more prominent in animals with the higher blood pressure. The findings imply that attempts to elevate pressure, as well as subacute surgical circulatory reconstruction to increase perfusion of an ischemic area, may be potentially harmful.
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PMID:Influence of blood pressure on blood-brain barrier function in brain ischemia. 650 45

The authors investigated the value of high-dose thiopental (TH) therapy after 16-min complete global brain ischemia (GBI) in three groups of pigtailed monkeys, using a neck cuff model of GBI with 96 h intensive care postischemia (PI). Control group (n18): Normotension was restored within 2 min PI; paralysis/controlled ventilation was maintained for 48 h PI with 50% N2O/O2. Thiopental loading group (n13): Control treatment plus TH-loading with 90 mg/kg iv given from 5 to 65 min PI (mean peak TH plasma level 130 micrograms/ml). Thiopental anesthesia group (n14): Control treatment plus TH anesthesia with 90 mg/kg iv given over 12 h PI (sustained TH plasma levels of 25-35 micrograms/ml and EEG burst suppression). Norepinephrine requirement for blood pressure control PI was greater in the TH groups than in the control group (P less than 0.05). Lidocaine was needed for control of arrhythmias in the TH loading group. There was no significant difference in mortality or neurologic outcome between the groups. At 96 h PI seven of 11 animals were awake in the control group, compared with seven of 12 and six of 12 in the two TH groups. Neurologic deficit scores (NDS) for the survivors at 96 h PI were 23 +/- 6% (mean +/- SD) (n10) in the control group, compared with 25 +/- 9% (n11) and 26 +/- 12% (n10) in the two TH groups (NDS 100% = brain death, 0% = normal). Seizures PI (in 1-2 of each group) were associated with worse neurologic deficits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thiopental treatment after global brain ischemia in pigtailed monkeys. 669 50

We measured the relationships between changes in extracellular pH (pHe), potassium (Ke), and calcium (Cae) activities and DC potential (DCe) in progressive ischaemia of rat cerebral cortex. pHe and Ke, or Cae and Ke, were measured at the same point simultaneously, using triple-barrelled, double-ion-sensitive microelectrodes. Ischaemia was produced using bilateral carotid artery occlusion and hypotension in rats under 50% N2O-0.4% halothane anaesthesia. Unilateral carotid artery occlusion did not affect blood flow, but bilateral occlusion reduced flow to approximately 40% of normal. Autoregulation of blood pressure (BP) changes was lost after bilateral occlusion, and so progressive hypotension produced a linear decrease in flow. pHe began to decrease at high levels of flow (30-35 ml 100 g-1 min-1) and showed stepwise acidotic shifts with reductions in BP. Ke was affected at flows of approximately 15 ml 100 g-1 min-1, during which time it was critically dependent on BP. When Ke reached 6 mM, it increased rapidly to 40 mM and was associated with a negative shift in DCe. When Ke reached approximately 10 mM, Cae decreased rapidly to approximately 0.1 mM. pHe had reached 6.87 when Ke increased rapidly and showed a transient alkalotic shift of approximately 0.14 units at that time. Possible mechanisms for the sequence of ion changes described are discussed.
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PMID:Extracellular pH, potassium, and calcium activities in progressive ischaemia of rat cortex. 672 30

The objective of this study was to characterize local cerebral blood flow (CBF) in the recirculation period following incomplete forebrain ischemia. Specifically, we wished to determine whether perfusion defects developed in the immediate recirculation period, to study how initial hyperemia and delayed hypoperfusion at the local level were related to the severity of the preceding ischemia, and to find out whether reflow was influenced by the nutritional state of the animals. To that end, forebrain ischemia of 15 min duration was induced in fed and fasted ventilated rats under 70% N2O. Local CBF was measured with an autoradiographic technique at the end of ischemia, as well as at 5 and 60 min following the start of recirculation. Control experiments were performed to examine the influence of ischemia on cerebral metabolic state in fed and fasted animals. The ischemia reduced CBF to excessively low values (less than 5% of control) in many forebrain structures, including the cerebral cortices, caudoputamen, and hippocampus. In spite of this, perfusion defects failed to appear after 5 min of recirculation. Instead, moderate to marked hyperemia was present in all previously ischemic structures. After 60 min of recirculation, pronounced hypoperfusion developed. The magnitude of the initial hyperemia was poorly related to the severity of the preceding ischemia, but the latter partly determined the degree of delayed hypoperfusion. Thus, little or no hypoperfusion developed in structures whose flow rates exceeded 30-40% of control during ischemia. Fasted animals had a better preserved flow to many structures than did fed animals, indicating that the detrimental effect of feeding (or glucose infusion) is also reflected in lower perfusion rates.
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PMID:Recirculation in the rat brain following incomplete ischemia. 684 65

The cerebral metabolic effects of isoflurane suggest that it may provide a degree of cerebral protection similar to that demonstrated for barbiturates. Accordingly, the possible cerebral protection afforded by isoflurane against hypoxemia and ischemia was studied in mice and dogs, respectively. In mice breathing 5% oxygen survival time was increased significantly over control in groups exposed to 1.0% and 1.4% isoflurane. At higher concentrations (2.0% and 3.0%) it is presumed that cardiorespiratory depression contributed to shorter survival times. In six dogs the effects of 3% isoflurane on the rates of cerebral ATP and phosphocreatine depletion and lactate accumulation during incomplete global ischemia were compared with six control dogs exposed to N2O. Incomplete global ischemia was produced by acute hemorrhagic hypotension to 30 mmHg for 9 minutes, a situation that does not abolish cortical electrical activity (active EEG). In the dogs exposed to isoflurane, the cerebral energy stores of ATP and PCr and the cerebral energy charge were sustained at significantly higher levels than in dogs exposed to N2O, and the cerebral lactate accumulation was significantly less in the initial 7 minutes of hypotension. It is concluded that in the circumstances of oxygen deprivation insufficient to abolish cortical electrical activity, isoflurane, like the barbiturates, can provide some cerebral protection presumably by depressing cortical electrical activity and cerebral metabolism.
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PMID:Cerebral protection by isoflurane during hypoxemia or ischemia. 685 9

1. Cerebral energy metabolism and electroencephalogram (EEG) power spectra were evaluated before, during and after 1 minute of global compression ischemia induced in N2O anesthetized rats. 2. Before ischemia, the EEG of rats was characterized by theta and delta frequencies. During ischemia, the EEG flattened after 14 +/- 1 sec and the electrical activity reappeared 55 +/- 4 s after recirculation and was characterized by high amplitude slow waves. After ischemia, the total power showed a rapid rebound mainly due to a 10 fold increase of delta band. 10 minutes after recirculation, the EEG was normal. 3. The ischemia induced a decrease of phosphocreatine, ATP and glucose, and an increase of ADP, AMP and lactate, while pyruvate remained normal. During recirculation phosphocreatine, ATP, glucose and energy charge potential showed a rapid recovery. AMP normalized after 10 minutes, while ADP was slightly higher for up to 30 minutes. Lactate returned to normal levels after 30 minutes and pyruvate showed a high peak at 3 minutes and returned to normal values after 30 minutes. 4. The results suggest that there is not a correlation between EEG and the metabolic pattern of recovery after a short complete ischemia.
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PMID:Cerebral energy metabolism and computerized EEG. Analysis following transient ischemia in the rat. 715 67

The course of ischemic increase of extracellular potassium concentration ([K+]e) was studied in rat cerebral cortex with potassium selective microelectrodes and correlated to the preischemic functional and metabolic state. Complete cerebral ischemia was induced in artificially ventilated rats by cardiac arrest. Seven different functional states including conditions with cerebral hypermetabolism (seizures, amphetamine intoxication, hyperthermia) and hypometabolism (barbiturate anesthesia, hypothermia) were chosen in order to cover a wide range of cerebral metabolic rates (CMRO2 : 28.7--2.4 ml O2/(100 g)/min). The ischemic increase of [K+]e was delayed in conditions with low CMRO2 and accelerated in conditions with high CMRO2; the time interval to the terminal steep rise in extracellular potassium concentration varied within the extremes of 35 +/- 5 and 365 +/- 12 sec (means +/- S.E.M.), the control state (N2O-analgesia) being 116 +/- 5 sec. In groups with high CMRO2 electrocortical activity ceased within 15 sec and in groups with low CMRO2 within 22 sec. The rates of the ischemic [K+]e increase, measured as rate of change in the potassium electrode potential (mV/sec), remained high in conditions with high preischemic CMRO2 and low in conditions with low CMRO2, indicating a remaining influence of the preischemic metabolism on membrane ion permeability. These results support previous metabolic data indicating that the rate of consumption of high energy phosphates during ischemia mirrors the preischemic cerebral metabolic rate. Phenobarbital anesthesia did not change the initial rate of [K+]e increase but reduced the rate of [K+]e increase later during ischemia, suggesting a special effect of barbiturates on partly depolarized membranes.
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PMID:The increase in extracellular potassium concentration in the ischemic brain in relation to the preischemic functional activity and cerebral metabolic rate. 740 19

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
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PMID:Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection. 744 74

Certified Registered Nurse Anesthetists (CRNA) have an ethical obligation to assure the safety of the anesthetized patient. Maintenance of orotracheal tube intra-cuff pressure (IcP) in a range preventing aspiration and avoiding tracheal ischemia is one way to enhance patient safety. Currently, no standardized method of cuff inflation and IcP maintenance is used in anesthesia practice. In addition, nitrous oxide (N2O) has the ability to diffuse into and inflate a cuff. Rate of N2O induced cuff inflation in vivo, has not been clearly delineated in the current literature. This study measured IcP initially, and over time during an anesthetic including 50% to 70% N2O. The sample consisted of 44 adult subjects intubated orally. Cuff inflation technique was identified and initial IcPs were recorded. IcP was then adjusted to 19 mm Hg and was continuously monitored until increasing to 25 mm Hg. A variety of cuff inflation methods were observed none of which consistently achieved an initial IcP within the target range of 19 to 25 mm Hg. IcP rose from 19 to 25 mm Hg in all cases during N2O administration. Elapsed time for the IcP increase ranged from 2 to 52 minutes (mean = 12.34, median = 8 minutes). During anesthesia with 50% to 70% N2O, IcP will increase from initial safe levels to ischemia producing levels. Devices and approaches designed to limit N2O induced IcP increase have been described, however only direct IcP monitoring has been shown to assure safe initial and ongoing IcP.
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PMID:Orotracheal tube intracuff pressure initially and during anesthesia including nitrous oxide. 763 47

Halothane impact on cerebral blood flow, brain metabolism and its protective effect in ischemia have been assessed in 30 patients operated on for the occlusion of brachiocephalic arteries. The data obtained indicate that additional use of halothane in N2O:O2 anesthesia during reconstructive surgery on brachiocephalic arteries makes it possible to enhance collateral blood flow, increase retrograde pressure, and decrease O2 consumption by the brain, without considerable changes in systemic hemodynamics. In addition, the studies have shown that halothane decreases lipid peroxidation processes.
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PMID:[Effects of halothane on cerebral blood flow and its protective action in ischemia]. 808 Jan 25


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