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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The question of whether the carotid sinus baroreceptors modulate myocardial performance remains controversial. Several studies that have stressed their importance have been criticized because the possible role of cerebral ischemia and of other important variables was not eliminated. To reinvestigate this problem, we studied 21 dogs placed on total cardiopulmonary bypass. In each of these animals the carotid sinus regions were isolated and perfused with fully oxygenated blood at a constant flow rate; perfusion pressure was changed by varying the resistance to outflow from the isolated segments. Several indices of myocardial performance were assessed: right and left ventricular contractile force with Walton-Brodie strain gauge arches; the maximal rate of change in contractile force, dF/dt; the pressure developed within an isovolumic balloon inserted into the left ventricle; and the maximal rate of change of this pressure, dP/dt. When the pressure distending the carotid sinuses was raised from an average value of 34.1 +/-2.8 (SEM) mm Hg to 190.1 +/-4.7 mm Hg, right ventricular contractile force fell 14.9 +/-2.3% (P < 0.001); right ventricular dF/dt decreased 16.7 +/-3.0% (P < 0.01); left ventricular contractile force declined 14.9 +/-3.3% (P < 0.01); left ventricular dF/dt fell 19.3 +/-4.0% (P < 0.01); peak systolic pressure in the isovolumic balloon declined 18.2 +/-3.7% (P < 0.001); and dP/dt decreased 34.1 +/-4.0% (P < 0.01). Prior adrenalectomy and vagotomy and maintenance of heart rate at a constant level did not influence these results. The inverse relation between carotid sinus perfusion pressure and the indices of contractility that was observed in this investigation strongly suggests that the carotid sinus baroreceptors are an important regulatory mechanism in the control of myocardial performance.
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PMID:Importance of the carotid sinus baroreceptors in the regulation of myocardial performance. 557 38

The concentration of cyclic adenosine 3',5'-monophosphate (cAMP) in cerebrospinal fluid was measured in 45 samples from 45 subjects, one sample per subject. 12 of the studied persons were (control group) neurologically normal, 11 were suffering from acute cerebral ischemia with deep coma, and 22 from meningitis of different types. The mean value obtained in the control group was 21.4 +/- (SEM) 3.3 nmol/l, in the group of acute cerebral ischemic attack with deep coma it was 7.00 +/- 0.81 nmol/l and in the group of meningitis 5.5 +/- 0.4 nmol/l. These values are significantly lower than the control group (p less than 0.001). These low levels, observed in the two groups of patients, may be attributed to the altered cAMP metabolism in the central nervous system because of deep coma and bacterial infections.
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PMID:Cerebrospinal fluid cyclic adenosine 3',5'-monophosphate in cases of severe cerebral ischemia and meningitis. 630 42

To define the utility of high-dose barbiturate therapy following an episode of complete global cerebral ischemia, we investigate the effects of 60 mg/kg of thiopental given to cats five minutes after resuscitation from 12, 14, or 16 min of electrically induced ventricular fibrillation (VF). All aspects of the arrest, resuscitation, with post-arrest care were carefully controlled, with the EEG becoming isoelectric 20-25 s after the onset mean resuscitation time of 2.5 +/- 0.2 (SEM) min. For any given duration of VF, there were no differences (control vs thiopental) in any pre- or post-arrest parameters (blood pressure, blood gases, electrolytes, etc.) A total of 68 resuscitated cats were entered into various treatment and control groups, and all but one group received 20-24 h of post-resuscitation paralysis, mechanical ventilation, and ICU support before being extubated. Cats received an additional six days of aggressive nursing care, and daily examinations were performed with the assignment of a neurologic deficit score (NDS) between 0 (normal) and (brain dead). Autopsies were performed to determine the cause of death in animals which died before the end of the seven-day observation period. The early post-arrest period was marked by the occurrence of repetitive, rhythmic bursts of high-frequency electroencephalographic (EEG) activity (? seizures) in 38 per cent of control animals (16/42, all arrest times combined). Ten of these animals died as a result of severe neurologic injuries. By contrast, only 12 per cent of treated cats (3/26) developed similar EEG patterns (P less than 0.05) and there were no neurologic deaths in the thiopental groups. The differences in the incidence of neurologic deaths (control vs. thiopental) was significant (P less than 0.02). The change in overall mortality did not quite reach significance (36 per cent vs. 21 per cent), and treatment had no effect on the incidence of deaths due to cardiovascular causes (e.g., myocardial infarctions). In spite of the effects on mortality, treatment had no effect on the neurologic function of survivors (assessed by NDS). These findings suggest that thiopental improved survival rates by suppressing an unusual post-arrest EEG pattern (? anticonvulsant effect), but had no additional cerebral protective effects.
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PMID:The neurologic effects of thiopental therapy following experimental cardiac arrest in cats. 709 47

Reduction in cerebral blood flow (CBF) following global ischemia has been implicated as a pathogenetic mechanism in progressive brain damage seen after restoration of effective cardiac action and cerebral perfusion pressure. There are serious limitations to many of the techniques for measuring regional cerebral blood flow, particularly during low flow states. In 15 dogs anesthetized with thiopental, 12 minutes of total cerebral ischemia (TCI) was produced using a double balloon occlusion technique. Total and regional cerebral blood flows were sequentially measured before and after balloon release by left ventricular injection of 15 mu microspheres labelled with 5 different radionuclides. Total CBF was reduced 53 +/- 5% (mean +/- SEM) from pre-ischemic values between 1 and 3 hours after "resuscitation" despite normal perfusion pressure and arterial blood gases. CBF remained slightly reduced (24 +/- 7%) at 6 hours post-ischemia. Thirty minutes after balloon release, grey matter flow was reduced 38 +/- 8% from control values while adjacent white matter flow was increased 21 +/- 10%. However, by 1 hour after ischemia, grey and white matter flows were both reduced (60 +/- 3%, 41 +/- 5% respectively). Similar differences in brain stem and cerebellar flow were also observed. The majority (71-86%) of the reduction in total CBF seen at one hour post-TCI is due to increased cerebrovascular resistance, with 14-29% of the decrease related to arteriovenous shunting.
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PMID:Total cerebral ischemia: application of a new model system to studies of cerebral microcirculation. 722 60

Diffusion-weighted magnetic resonance imaging (DWI) can quantitatively demonstrate cerebral ischemia within minutes after the onset of ischemia. The use of a DWI echo-planar multislice technique in this study and the mapping of the apparent diffusion coefficient (ADC) of water, a reliable indicator of ischemic regions, allow for the detection of the three-dimensional (3-D) evolution of ischemia in a rat stroke model. We evaluated 13 time points from 5 to 180 minutes after occlusion of the middle cerebral artery (MCA) and monitored the 3-D spread of ischemia. Within 5 minutes after the onset of ischemia, regions with reduced ADC values occurred. The core of the lesion, with the lowest absolute ADC values, first appeared in the lateral caudoputamen and frontoparietal cortex, then spread to adjacent areas. The volume of ischemic tissue was 224 +/- 48.5 mm3 (mean +/- SEM) after 180 minutes, ranging from 92 to 320 mm3, and this correlated well with the corrected infarct volume at postmortem (194 +/- 23.1 mm3, r = 0.72, p < 0.05). This experiment demonstrated that 3-D multislice diffusion mapping can detect ischemic regions noninvasively 5 minutes after MCA occlusion and follow the development of ischemia. The distribution of changes in absolute ADC values within the ischemic region can be followed over time, giving important information about the evolution of focal ischemia.
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PMID:Multislice diffusion mapping for 3-D evolution of cerebral ischemia in a rat stroke model. 782 11

Moderate hypothermia has been shown to have therapeutic utility in the treatment of cerebral ischemia and to attenuate the rise in interstitial concentrations of the excitatory amino acid neurotransmitter L-glutamate. In this study, the influence of hypothermia on traumatic brain injury (TBI) was assessed using a controlled cortical impact model. Rats were cooled to 32.0-33.0 degrees C at least 30 min before injury and maintained at this temperature for 2 h after injury. The influence of hypothermia on the immediate increase in interstitial concentrations of aspartate and glutamate and the volume of the resultant lesion 14 days after TBI was then determined. The volume of the lesion (mean +/- SEM) in hypothermic animals (8.2 +/- 1.3 mm3, n = 9) was significantly smaller than that of normothermic animals (13.2 +/- 1.7 mm3, n = 8). By contrast, TBI-induced increases in dialysate concentrations of aspartate and glutamate were similar at the two temperatures. Thus, aspartate content (nmol/10 min) in animals maintained at 37.0-37.5 degrees C (n = 6) and 32.0-33.0 degrees C (n = 6) increased from respective mean preinjury values of 0.05 +/- 0.02 and 0.08 +/- 0.02 to much larger peak values (0.78 +/- 0.13 and 0.71 +/- 0.09, respectively). Similarly, under normothermic conditions glutamate content (nmol/10 min) increased from 0.13 +/- 0.03 to 3.08 +/- 0.52 and from 0.19 +/- 0.06 to a peak value of 3.09 +/- 0.26 under hypothermic conditions. These data clearly demonstrate the cytoprotective action of moderate hypothermia and further suggest that this action is not mediated by attenuation of the rise in interstitial concentrations of aspartate and glutamate.
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PMID:Therapeutic hypothermia is cytoprotective without attenuating the traumatic brain injury-induced elevations in interstitial concentrations of aspartate and glutamate. 790 37

Magnetic resonance diffusion-weighted imaging (MR-DWI) is sensitive to the diffusibility of water and may offer characterization and anatomical localization of stroke leading to early tailored therapeutic intervention. We compared DWI, the apparent diffusion constant (ADC), and autoradiographic cerebral blood flow (CBF) in a model of focal cerebral ischemia in the rat. Sprague-Dawley rats were embolized with a single silicone cylinder injected into the internal carotid artery. Both common carotids were permanently ligated. The animals were anesthetized (isoflurane in O2), and paralyzed (gallamine). MR-DWI were obtained with a GE 4.7 T magnet (TE = 3 s, TR = 80 msec, b = 2393.10(-3) mm2/s, slice thickness 3 mm). DWI and CBF autoradiograms were compared visually. ADC was assessed in various regions, including ischemic cortex and a region homologous to ischemic cortex. Imaging times from stroke onset were 50 +/- 6 min (mean +/- SEM) for DWI, 185 +/- 17 min for a second DWI. CBF was determined at 258 +/- 15 min. The specificity was 100% at both 50 min and 185 min, indicating that there were no false positives; in 3 animals ischemia was not present. However, the sensitivity analysis indicated that early DWI yields some false negatives; at 50 min the sensitivity was 60%. We attribute our result of low early sensitivity to small infarcts in relation to the slice thickness. Later, at 185 min, sensitivity was 100%. The first ADCs were higher than the second ADC values in ischemic cortex. For infarcts larger than the slice thickness, early MR-DWI is highly sensitive for imaging evolving ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Magnetic resonance diffusion-weighted imaging: sensitivity and apparent diffusion constant in stroke. 797 48

In a variety of recent studies, inhibitors of nitric oxide (NO) synthesis have ameliorated neuronal injury during permanent focal cerebral ischemia, suggesting that NO may contribute to ischemic damage. In other studies, however, these inhibitors increased infarct volume during permanent middle cerebral artery occlusion (MCAO). One complication in these studies was that high-dose NO synthase inhibitors increased mean arterial blood pressure (MAP) by 20-30 mm Hg. Thus, it is possible that variations in the effects of NO synthesis inhibitors on infarct volume could be related to effects of these inhibitors on MAP and cerebral perfusion during or after ischemia. The present study compared the effects of control (Ringer's lactate solution) versus low-dose NO inhibition (0.1 mg/kg bolus followed by 0.01 mg/kg/min) on cerebral infarct volume using L-NAME (NG-nitro-L-arginine methyl ester) administered during a 1-h baseline period, 3-h of MCAO, and 2 h of reperfusion in the spontaneously hypertensive rat. Infarct volume was determined using the TTC (2,3,5-triphenyltetrazolium chloride) method performed 5 h after onset of occlusion. L-NAME reduced infarct volume by 55%. In the control group (n = 7), infarct volume measured 116 +/- 4 (SEM) mm3 which was 29 +/- 1% of the left hemispheric volume (400.5 +/- 0.3 mm3). In the L-NAME group (n = 7), infarct volume measured 53 +/- 8 mm3 which was only 13 +/- 2% of the left hemispheric volume (400.4 +/- 0.5 mm3).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low dose L-NAME reduces infarct volume in the rat MCAO/reperfusion model. 825 13

Considerable evidence indicates that brain temperature during ischemia affects the extent and distribution of ischemic injury. However, only limited data have been presented concerning the influence of temperature on ischemic damage after reversible focal cerebral ischemia. Because focal ischemic events of this type resemble conditions observed in the clinic, studies were undertaken to examine the effects of mild and moderate hypothermia on the extent of cerebral infarction after focal neocortical ischemia. Under halothane anesthesia, the left middle cerebral artery and both carotid arteries were occluded reversibly for a period of 3 hours in adult Sprague-Dawley rats. The animals were killed 3 days later. Brain sections were stained with triphenyltetrazolium chloride and analyzed for infarction using a computerized image analysis system. Temporal muscle temperature and rectal temperature were monitored continuously. The following groups with different intraischemic temporal muscle temperatures were analyzed: 1) control, 35.8 to 36.2 degrees C; 2) mild hypothermia, 33.0 to 33.5 degrees C; and 3) moderate hypothermia, 27.5 to 29.2 degrees C. The volumes of infarction were 214.5 +/- 17.9, 166.5 +/- 6.8, and 108.2 +/- 5.9 mm3 (mean +/- SEM) for the control, mild hypothermia, and moderate hypothermia groups, respectively. These findings demonstrate that both mild and moderate hypothermia reduce the impact of temporary focal ischemia in Sprague-Dawley rats.
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PMID:Effects of intraischemic hypothermia on cerebral damage in a model of reversible focal ischemia. 832 2

The ability of chlormethiazole to protect against ischaemic cell damage in a rat model of permanent focal ischaemia has been examined. Chlormethiazole (1 mmol/kg) was administered intraperitoneally either 1 or 3 h after occlusion of the middle cerebral artery with an intraluminal filament. Twenty four hours after the start of occlusion there was histological evidence for ischaemic damage in both cortex and striatum. The volume of ischaemic damage in control (saline injected) animals was 310 +/- 25 mm3 (mean +/- SEM; n = 6). Chlormethiazole administered 1 h after occlusion reduced this damage by 58% (128 +/- 40 mm3; n = 6; P < 0.01), protection being observed in both brain regions. The drug was ineffective when given 3 h after occlusion (304 +/- 25 mm3; n = 5). Chlormethiazole had no effect on body temperature, mean arterial blood pressure, blood pH, pO2 or pCO2, but did induce mild bradycardia. Chlormethiazole therefore appears to be an effective neuroprotective agent in this model of permanent ischaemia, complementing previous data on the efficacy of this drug in other focal and global models of cerebral ischaemia.
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PMID:The neuroprotective effect of chlormethiazole on ischaemic neuronal damage following permanent middle cerebral artery ischaemia in the rat. 858 65


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