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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the effect on diastolic myocardial compliance of halothane and morphine sulfate using 15 swine placed on total cardiopulmonary and right heart bypass with controlled aortic pressure, heart rate, and left ventricular preload. The animals were divided into three equal groups: (I) regional block anesthesia, (II) morphine sulfate (10 mg/kg), and (III) halothane anesthesia at 0.5%. Myocardial performance was evaluated on right heart bypass following a 30 minute period of total cardiopulmonary bypass before and after administration of the anesthetic agent by measuring stroke volume, left ventricular end-diastolic pressure, and left ventricular end-diastolic volume. All perfusions were at normothermia, at a hematocrit level of 30%, and at a normal arterial Po2. PCO2, and pH. Neither regional block nor morphine sulfate anesthesia significantly depressed the myocardium or changed diastolic compliance. Halothane, however, significantly decreased diastolic compliance so that stroke volume was less at a given left ventricular end-diastolic pressure, but not at a given left ventricular end-diastolic volume. The depression of stroke volume with halothane following cardiopulmonary bypass at equal filling pressures appears to be due primarily to a change in compliance rather than to a change in contractility.
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PMID:Effects of halothane and morphine sulfate on myocardial compliance following total cardiopulmonary bypass. 719 84

To determine whether barbiturate administration can improve oxygenation, oxygen availability (aO2) and local cortical blood flow (ICBF) were measured in cats before and during middle cerebral artery occlusion (MCAO) using 10 platinum electrodes distributed over the cortex. Halothane/N2O anesthesia was used during the surgical preparation and N2O with a relaxant thereafter. After 15 to 30 min of MCAO, 50 mg/kg of pentobarbital was infused slowly. Measured from electrodes in severely ischemic cortex, aO2 increased if the blood pressure was maintained with dopamine. Control animals in which no pentobarbital was given showed no change in aO2 over the same period of time. In areas of cortex not affected by middle cerebral artery occlusion the aO2 did not change from control values despite a decrease in blood flow from 72.7 +/- 49.8 to 48.9 +/- 26.7 ml/min/100 g. Thus, pentobarbital appears to decrease ICBF and metabolism proportionally in well perfused cortex so that aO2 remains constant, while improving the flow to metabolism ratio in poorly perfused cortex so that aO2 rises.
Stroke
PMID:Cerebral oxygen availability and blood flow during middle cerebral artery occlusion: effects of pentobarbital. 730 77

Effective arterial elastance (Ea) and left ventricular end-systolic elastance (Ees) are used as indices of cardiac afterload and cardiac contractility, respectively. We compared the effects of two volatile anesthetics, halothane and isoflurane, on ventriculoarterial coupling using an index of Ea/Ees in 20 mongrel dogs. Ees was obtained using a single-beat estimation technique. Ea was estimated as the ratio of the mean arterial pressure to stroke volume. Basal anesthesia consisted of pentobarbital and alpha-chloralose. Dogs were further anesthetized either with halothane 1 minimum alveolar anesthetic concentration (MAC) and 2 MAC (n = 10) or with isoflurane 1 MAC and 2 MAC (n = 10). Halothane 2 MAC significantly decreased the cardiac output, Ea, and Ees by 35.5% +/- 4.9%, 18.3% +/- 12.6%, and 39.7% +/- 10.8%, respectively. Isoflurane 2 MAC significantly decreased the cardiac output, Ea, and Ees by 37.9% +/- 4.0%, 38.7% +/- 6.4%, and 43.0% +/- 6.0%, respectively. The decreases in cardiac output and Ees were not significantly different between halothane and isoflurane. Halothane increased Ea/Ees from 0.83 +/- 0.05 to 1.22 +/- 0.13, whereas isoflurane maintained the Ees/Es at a constant level. Our results suggest that mechanical efficiency is well maintained during isoflurane anesthesia because it has an equivalent effect on left ventricular contractility and arterial properties, whereas halothane can impair mechanical efficiency by depressing left ventricular contractility more than the arterial system.
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PMID:The difference of isoflurane and halothane in ventriculoarterial coupling in dogs. 794 75

Microcirculatory impairments have theoretically been proposed as a potential factor in the development of ischemic injury, but few attempts have been made to directly assess microvascular patency following stroke. To address this issue we investigated the temporal changes in microvascular perfusion induced by permanent focal ischemia. Halothane-anesthetized spontaneously hypertensive rats were subjected to middle cerebral artery occlusion (MCAO) of 5 min to 4 h duration. Two fluorescent tracers (FITC-dextran and Evans blue) were then sequentially administered i.v. and allowed to circulate for 10 and 5 s respectively. Tissue sections were examined by fluorescent microscopy, and the mean number of perfused microvessels/mm2 calculated for cortical areas representing non-ischemic (Region A), perifocal/penumbral (Region B) and core ischemic (Region C) regions. For sham-operated controls, virtually all microvessels perfused with tracer within 5 s. In contrast MCAO induced significant reductions in the number of perfused microvessels in Regions B and C. The most marked impairments in perfusion were observed in core MCA territory (e.g. 2-10% of control values for 5 s circulation period) while, initially, the deficit was less severe in penumbral cortex. However, a secondary perfusion impairment developed over time in the perifocal/penumbral region, so that the deficit was greater 4 h after MCAO than at earlier time points (e.g. 72%, 71% and 22% of control value for 0.5, 1 and 4 h MCAO respectively; 10 s circulation period). In conclusion, MCAO induced severe impairments in microcirculatory perfusion within the core ischemic region, and to a lesser extent in the penumbra. However, the development of a more severe perfusion deficit in the penumbra within 4 h of MCAO supports the hypothesis that microcirculatory failure in this region contributes to its recruitment to the ischemic infarct.
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PMID:Temporal impairment of microcirculatory perfusion following focal cerebral ischemia in the spontaneously hypertensive rat. 913 19

The anesthetic potency and cardiopulmonary effects of sevoflurane were compared with those of isoflurane and halothane in goats. The (mean +/- SD) minimal alveolar concentration (MAC) was 0.96 +/- 0.12% for halothane, 1.29 +/- 0.11% for isoflurane, and 2.33 +/- 0.15% for sevoflurane. Cardiopulmonary effects of sevoflurane, halothane and isoflurane were examined at end-tidal concentrations equivalent to 1, 1.5 and 2 MAC during either spontaneous or controlled ventilation (SV or CV). During SV, there were no significant differences in respiration rate, tidal volume and minute ventilation between anesthetics. Dose-dependent decreases in both tidal volume and minute ventilation induced by halothane were greater than those by either sevoflurane or isoflurane. Hypercapnia and acidosis induced by sevoflurane were not significantly different from those by either isoflurane or halothane at 1 and 1.5 MAC, but were less than those by halothane at 2 MAC. There was no significant difference in heart rate between anesthetics during SV and CV. During SV, all anesthetics induced dose-dependent decreases in arterial pressure, rate pressure product, systemic vascular resistance, left ventricular minute work index and left ventricular stroke work index. Systemic vascular resistance with isoflurane at 2 MAC was lower than that with sevoflurane. During CV, sevoflurane induced dose-dependent circulatory depression (decreases in arterial pressure, cardiac index, rate pressure product, systemic vascular resistance, left ventricular minute work index and right ventricular minute work index), similar to isoflurane. Halothane did not significantly alter systemic vascular resistance from 1 to 2 MAC.
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PMID:Anesthetic potency and cardiopulmonary effects of sevoflurane in goats: comparison with isoflurane and halothane. 979 97

We have investigated genetic transmission of increased sensitivity to focal cerebral ischemia and the influence of gender in the stroke-prone spontaneously hypertensive rat (SHRSP). Halothane-anesthetized, 3- to 5-month-old male and female Wistar-Kyoto rats (WKY), SHRSP, and the first filial generation rats (F1 crosses 1 and 2) underwent distal (2 mm) permanent middle cerebral artery occlusion (MCAO) by electrocoagulation. Infarct volume was measured by using hematoxylin-eosin-stained sections and image analysis 24 hours after ischemia and expressed as a percentage of the volume of the ipsilateral hemisphere. Infarct volume in males and females grouped together were significantly larger in SHRSP, F1 cross 1 (SHRSP father), and F1 cross 2 (WKY father), at 36.6+/-2.3% (mean+/-SEM, P<0.001, n=15), 25.4+/-2.4% (P<0.01, n=14), and 33. 9+/-1.6% (P<0.001, n=18), respectively, compared with WKY (14+/-2%, n=17). Male F1 cross 1 (18.9+/-2.4%, n=6) developed significantly smaller infarcts than male F1 cross 2 (32.8+/-2%, n=8, P<0.005). Females, which underwent ischemia during metestrus, developed larger infarcts than respective males. A group of females in which the cycle was not controlled for developed significantly smaller infarcts than females in metestrus. Thus, the increased sensitivity to MCAO in SHRSP is retained in both F1 cross 1 and cross 2 hybrids, suggesting a dominant or codominant trait; response to cerebral ischemia appears to be affected by gender and stage in the estrous cycle. In addition, the male progenitor of the cross (ie, SHRSP versus WKY) influences stroke sensitivity in male F1 cohorts.
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PMID:Genetic and gender influences on sensitivity to focal cerebral ischemia in the stroke-prone spontaneously hypertensive rat. 1002 27

Estrogen treatment has been shown to reduce ischemic brain damage. Because endogenous estrogen levels fluctuate markedly during the estrous cycle, we investigated the effect of stage of estrous cycle on ischemic brain damage. Halothane anesthetized 3- to 5-mo-old female Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) in proestrus (high estradiol levels) or metestrus (low estradiol levels) underwent permanent middle cerebral artery occlusion. In SHRSP, infarct volume at 24 h postocclusion was 24% smaller in proestrus compared with metestrus [208.6 +/- 9.5 mm(3) (n = 7) vs. 272.7 +/- 23.8 mm(3) (n = 7), respectively, means +/- SE; P = 0.0278, unpaired t-test]. In WKY, infarct volumes were similar in proestrus and metestrus [157.0 +/- 5.4 mm(3) (n = 5) and 131.5 +/- 16.5 mm(3) (n = 8), respectively; P = not significant (NS)]. Brain swelling (ipsilateral minus contralateral hemispheric volumes) was similar in proestrus and metestrus for SHRSP [138 +/- 9 mm(3) (n = 6) and 136 +/- 10 mm(3) (n = 7), respectively] and for WKY [103 +/- 15 mm(3) (n = 5) and 90 +/- 11 mm(3) (n = 8), respectively]. Thus the reduction in infarct size in SHRSP is caused by a true attenuation of the infarct volume and not simply by a reduction in brain edema.
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PMID:Estrogen status affects sensitivity to focal cerebral ischemia in stroke-prone spontaneously hypertensive rats. 1064 11

Transgenic murine models of cardiovascular disease offer great potential insights regarding mechanisms of human disease, but efficient and reliable methods for phenotype evaluation are necessary. We employed non-invasive echocardiography to evaluate hemodynamic parameters in mice, and evaluated statistical reliability of these parameters with respect to anesthesia regimen. Male CF-1 mice received inhaled halothane (0.25-0.75% in 95% O2) or ketamine/xylazine (80/10 mg/kg i.p.) and 2-dimensional, M-mode, and Doppler ultrasound imaging were used to assess cardiac contractility and aortic flow velocities. Halothane was more convenient and reliable with respect to rate of induction, reversal, and control of anesthetic depth. At comparable levels of anesthesia, ketamine/xylazine produced significant reductions in heart rate (308 +/- 14 vs. 501 +/- 14 bpm, p<0.001), left ventricular fractional shortening (41.7 +/- 1.3 vs. 49.3 +/- 1.0%, p<0.001), and cardiac output (7.6 +/- 0.5 vs. 11.5 +/- 0.6 ml/min, p<0.001) when compared to halothane inhalation. No change in stroke volume or peak aortic velocity was observed. Correlation analyses revealed highly significant positive relationships between heart rate and fractional shortening (r=0.61, p<0.002) and cardiac output (r=0.88, p<0.001) but no relation to stroke volume or aortic velocity. Variability of intra-animal and intragroup parameter estimation were frequently 2-fold larger for ketamine/xylazine anesthesia vs. halothane. Statistical power analysis showed the increased measurement error for ketamine/xylazine leads to much larger numbers of mice/group to achieve identical statistical sensitivity. These data further illustrate the feasibility of echocardiography for rapid, non-invasive cardiovascular assessment in mice. However, several obtainable parameters are highly sensitive to both heart rate and anesthetic used and the choice and control of anesthetic are critical for physiologically relevant performance parameters and maximal ability to detect statistical differences among groups. Thus, for these non-invasive studies, inhalation anesthesia with agents such as halothane is superior to anesthesia induced by ketamine/xylazine administration.
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PMID:Non-invasive echocardiographic studies in mice: influence of anesthetic regimen. 1144 11

We have previously shown that treatment with selective kappa-opioid receptor agonist BRL 52537 hydrochloride [(+/-)-1-(3,4-dichlorophenyl) acetyl-2-(1-pyrrolidinyl) methylpiperidine] (1) has a long therapeutic window for providing ischemic neuroprotection and (2) attenuates ischemia-evoked nitric oxide (NO) production in vivo in rats. Neuronally derived NO has been shown to be deleterious in the male, but not in the female, rodent model of focal ischemic stroke. We sought to determine if the agent fails to protect ischemic brain when neuronal NO synthase (nNOS) is genetically deleted in male, but not female, mice. Halothane-anesthetized adult male and female nNOS null mutants (nNOS(-/-)) and the genetically matched wildtype (WT) strain were subjected to transient (2 h) middle cerebral artery occlusion by the intraluminal filament technique. Vehicle or BRL 52537 treatment with continuous intravenous infusion was instituted at the onset of reperfusion and continued for 22 h. In WT male mice, infarct volumes measured at 72 h of reperfusion were robustly decreased with BRL 52537 treatment. In contrast, BRL 52537 did not decrease infarct volume in male nNOS(-/-) mice. BRL 52537 had no effect in the WT or nNOS(-/-) female mice. These data support that BRL 52537's mechanism of neuroprotection in vivo is through attenuation of nNOS activity and ischemia-evoked NO production. Neuroprotective effects of BRL 52537 are lost in the male when nNOS is not present; therefore, BRL 52537 likely acts upstream from NO generation and its subsequent neurotoxicity.
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PMID:Neuroprotective effect of selective kappa opioid receptor agonist is gender specific and linked to reduced neuronal nitric oxide. 1604 24

Osmotherapy is the cornerstone of medical management for cerebral edema associated with large ischemic strokes. We determined the effect of duration of graded increases in serum osmolality with mannitol and hypertonic saline (HS) on blood-brain barrier (BBB) disruption and regional cerebral edema in a well-characterized rat model of large ischemic stroke. Halothane-anesthetized adult male Wistar rats were subjected to transient (2-h) middle cerebral artery occlusion (MCAO) by the intraluminal occlusion technique. Beginning at 6 h after MCAO, rats were treated with either no intravenous fluids or a continuous intravenous infusion (0.3 mL/h) of 0.9% saline, 20% mannitol, 3% HS, or 7.5% HS for 24, 48, 72, and 96 h. In the first series of experiments, BBB permeability was quantified by the Evans blue (EB) extravasation method. In the second series of experiments, water content was assessed by comparing wet-to-dry weight ratios in six predetermined brain regions. Blood-brain barrier disruption was maximal in rats treated with 0.9% saline for 48 h, but did not correlate with increases in serum osmolality or treatment duration with osmotic agents. Treatment with 7.5% HS attenuated water content in the periinfarct regions and all subregions of the contralateral nonischemic hemisphere to a greater extent than mannitol did with no adverse effect on survival rates. These data show that (1) BBB integrity is not affected by the duration and degree of serum osmolality with osmotic agents, and (2) attenuation of increases in brain water content with HS to target levels >350 mOsm/L may have therapeutic implications in the treatment of cerebral edema associated with ischemic stroke.
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PMID:Effect of duration of osmotherapy on blood-brain barrier disruption and regional cerebral edema after experimental stroke. 1630 35


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