Suitability of the lumbar test dose for the thoracic epidural space.
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Aged, 80 and over↗
Biomedical subjects
H Mayumi Homi
Publications and source records attributed to H Mayumi Homi.
Xenon and the inflammatory response to cardiopulmonary bypass in the rat.
OBJECTIVE: The purpose of this study was to investigate the effect of xenon on the inflammatory response to cardiopulmonary bypass. DESIGN: Prospective, randomized experimental study. SETTING: University research laboratory. PARTICIPANTS: Sprague-Dawley rats. INTERVENTIONS: After surgical preparation, rats were randomly divided into 4 groups: (1) SHAM rats were cannulated but did not undergo cardiopulmonary bypass; (2) cardiopulmonary bypass rats were subjected to 60 minutes of cardiopulmonary bypass using an oxygenator receiving a 30% O(2), 65% N(2), and 5% CO(2) gas mixture; (3) MK801 rats received MK801 (0.15 mg/kg intravenous) 15 minutes before 60 minutes of cardiopulmonary bypass with the same gas mixture; and (4) xenon rats underwent 60 minutes of cardiopulmonary bypass receiving a 30% O(2), 60% xenon, 5% N(2), and 5% CO(2) gas mixture. MEASUREMENTS AND MAIN RESULTS: All bypass groups showed elevations in both cytokines compared with the SHAM-operated group. However, the inflammatory response to cardiopulmonary bypass in the group receiving xenon was no different from the other bypass groups. CONCLUSIONS: Xenon appears to have no effect on the inflammatory response to cardiopulmonary bypass, making its previously described neuroprotective effect during cardiopulmonary bypass likely independent of any inflammation modulation.
Anesthesia, Inhalation↗
Cognitive dysfunction after cardiac surgery: revisiting etiology.
Cognitive dysfunction remains a frequent complication of cardiac surgery. Despite many years of research, few preventive strategies and no definitive therapeutic options exist for the management of this troublesome clinical problem. This shortcoming may be secondary to an incomplete understanding of the pathophysiology and etiology of cognitive loss after cardiac surgery; a better understanding of the etiology is essential to finding new therapies. The etiology of cognitive dysfunction after cardiac surgery is multifactorial and includes cerebral microembolization, global cerebral hypoperfusion, systemic and cerebral inflammation, cerebral temperature perturbations, cerebral edema, and possible blood-brain barrier dysfunction, all superimposed on genetic differences in patients that may make them more susceptible to injury or unable to repair from injury once it has occurred. This review expands on these potential etiologies in detailing the evidence for their existence.
Blood-Brain Barrier↗
Cardiopulmonary bypass reduces the minimum alveolar concentration for isoflurane.
OBJECTIVE: The purpose of this investigation was to determine the influence of cardiopulmonary bypass (CPB) on the minimum alveolar concentration (MAC) of isoflurane in a rat model of CPB. DESIGN: Prospective. SETTING: University research laboratory. PARTICIPANTS: Sprague-Dawley rats. INTERVENTIONS: Using tail-clamp methodology, the pre- and post-CPB MAC for isoflurane was studied. METHODS AND MAIN RESULTS: Rats were anesthetized with isoflurane, intubated, ventilated, and surgically prepared for CPB, after which they were randomized to either Sham-operated or CPB groups. The CPB group (n = 10) underwent 90 minutes of normothermic nonpulsatile CPB. The Sham group (n = 13) were cannulated but did not undergo CPB. Pre- and post-CPB MAC determinations were compared within groups using a paired Student t test. The CPB group had a pre-CPB baseline isoflurane MAC of 1.09% +/- 0.11% versus 1.09% +/- 0.08% in the Sham group (p = 0.90). Twenty minutes after CPB, the CPB group exhibited a decrease in MAC to 0.98% +/- 0.14% (p = 0.0026, compared with baseline). The MAC in the Sham group was unchanged (p = 0.5852, compared with baseline). Two hours after CPB, the MAC in the CPB group remained lower compared with baseline at 0.99% +/- 0.14% (p = 0.0032). CONCLUSIONS: CPB resulted in a small (10%) but significant reduction in the MAC for isoflurane. The mechanism behind this reduction in MAC is not clear but may be related to CPB-induced cerebral injury.
Anesthetics, Inhalation↗
"Other" neurologic complications after cardiac surgery.
Compared to the neurologic morbidity of stroke and cognitive dysfunction, "other" neurologic complications involving injuries to the brachial plexus, phrenic nerve, cranial nerves, other peripheral nerves, as well as the visual pathways, have been disproportionately underrepresented in the cardiac surgery and anesthesiology literature. These injuries are often missed in the early postoperative period when attention is focused principally on recovery from the acute trespass of cardiac surgery and cardiopulmonary bypass. However, when these problems do become apparent, they can cause considerable discomfort and morbidity. An overview of the current concepts of injury mechanisms/etiology, diagnosis, prognosis, and when possible, prevention of these injuries is presented.
Blindness, Cortical↗
Hemodilution during cardiopulmonary bypass increases cerebral infarct volume after middle cerebral artery occlusion in rats.
Although the optimal hematocrit during cardiopulmonary bypass (CPB) is not defined, excessive hemodilution may lead to organ ischemia via a reduction in oxygen-carrying capacity uncompensated by autoregulatory and/or rheologic increases in organ blood flow. As a result, the consequences of hemodilution in patients at risk for cerebral ischemia are not clearly understood. We designed this study to evaluate the effects of hemodilution in the setting of focal cerebral ischemia during CPB. Wistar rats surgically prepared for CPB were randomized to either hemodilution (hemoglobin (Hb), 6 g/dL; n = 9) or control (Hb, 11 g/dL; n = 8) groups and subsequently exposed to focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO). Immediately after the onset of MCAO (maintained for 90 min), 65 min of hypothermic (28 degrees C) CPB was initiated. Twenty-four hours later, functional neurological outcome and cerebral infarct volume were determined. Compared with controls, the hemodilution group had worse neurological performance (new score = 8 [2], hemodilution; versus 10 [2], control; P = 0.030) and larger total cerebral infarct volumes (182 +/- 84 mm(3), hemodilution; versus 103 +/- 58 mm(3), control; P = 0.043). In this experimental model of CPB with reversible MCAO-induced focal cerebral ischemia, hemodilution worsened neurological function and increased cerebral infarct volume.
Animals↗
Intraischemic nitrous oxide alters neither neurologic nor histologic outcome: a comparison with dizocilpine.
N-Methyl-D-aspartate receptor antagonism contributes to the anesthetic action of nitrous oxide (N(2)O). We examined the effects of the N-methyl-D-aspartate antagonists N(2)O and dizocilpine on outcome from filament occlusion of the middle cerebral artery (MCAO). Rats breathed 70% nitrogen/30% oxygen or 70% N(2)O/30% oxygen during MCAO. A third group breathed 70% nitrogen/30% oxygen and was given dizocilpine (0.25 mg/kg IV). After 75 min of MCAO, the rats recovered for 3 or 14 days. Pericranial temperature was maintained at 37.5 degrees C +/- 0.2 degrees C during ischemia and for 20 h postischemia. N(2)O did not alter neurologic scores at 3 days (N(2)O, 21 +/- 6; nitrogen, 22 +/- 8; P = 0.95; 0 = normal; 48 = maximal deficit; mean +/- sd; n = 15) or 14 days (N(2)O, 13 +/- 6; nitrogen, 12 +/- 6; P = 0.93; n = 15-16) postischemia. N(2)O had no effect on infarct size at 3 days (N(2)O, 162 +/- 45 mm(3); nitrogen, 162 +/- 61 mm(3); P > 0.99) or 14 days (N(2)O, 147 +/- 56 mm(3); nitrogen, 151 +/- 62 mm(3); P = 0.99) postischemia. Dizocilpine treatment caused smaller infarcts (3 days: 66 +/- 49 mm(3), P < 0.0001 versus nitrogen; 14 days: 84 +/- 50 mm(3), P < 0.006 versus nitrogen) and reduced the neurologic deficit (3 days: 10 +/- 10, P = 0.002 versus nitrogen; 14 days: 6 +/- 7, P = 0.006 versus nitrogen). N(2)O (70%) had no effect on either behavioral or histologic outcome from transient focal cerebral ischemia when compared with results in rats breathing 70% nitrogen. These results indicate that normobaric N(2)O does not alter the response of rat brain to a focal ischemic insult.
Animals↗
The neuroprotective effect of xenon administration during transient middle cerebral artery occlusion in mice.
BACKGROUND: Xenon has been shown to be neuroprotective in several models of in vitro and in vivo neuronal injury. However, its putative neuroprotective properties have not been evaluated in focal cerebral ischemia. The purpose of this study was to determine if xenon offers neuroprotection in a mouse model of middle cerebral artery occlusion. METHODS: C57BL/6 mice underwent 60 min of middle cerebral artery occlusion. The animals (n = 21 per group) were randomized to receive either 70% xenon + 30% O2, 70% N2O + 30% O2, or 35% xenon + 35% N2O + 30% O2. After 24 h, functional neurologic outcome (on three independent scales: four-point, general, and focal deficit scales) and cerebral infarct size were evaluated. RESULTS: The 70% xenon + 30% O2 group showed improved functional outcome (median [interquartile range], four-point scale: 2 [2], 70% xenon + 30% O2 versus 3 [2], 70% N2O + 30% O2, P = 0.0061; general deficit scale: 9 [6], 70% xenon + 30% O2 versus 10 [4], 70% N2O + 30% O2, P = 0.0346). Total cerebral infarct volumes were reduced in the 70% xenon + 30% O2 group compared with the 70% N2O + 30% O2 group (45 +/- 17 mm3 versus 59 +/- 11 mm3, respectively; P = 0.0009). CONCLUSIONS: In this model of transient focal cerebral ischemia, xenon administration improved both functional and histologic outcome.
Administration, Inhalation↗
Severe hypotension is not essential for isoflurane neuroprotection against forebrain ischemia in mice.
BACKGROUND: Volatile anesthetics provide protection in experimental models of global cerebral ischemia. To date, all models evaluated have included profound systemic arterial hypotension as a component of the ischemic insult. This study was designed to determine if isoflurane protection persists in a global insult devoid of hypotension. METHODS: C57BL/6J mice having a high incidence of posterior communicating artery atresia were anesthetized with isoflurane (1.2%) or fentanyl/N2O and subjected to bilateral carotid artery occlusion for 15 min or 20 min with normotension (80-110 mmHg mean arterial pressure) or for 10 min with hypotension (35 mmHg mean arterial pressure). Three days later, neurologic function and histologic damage were assessed. Other mice underwent measurement of intraischemic cerebral blood flow (4-iodo-N-methyl-[14C]antipyrine autoradiography) or plasma norepinephrine. RESULTS: Isoflurane reduced the percentage of hippocampal CA1 dead neurons (e.g., 10 min bilateral carotid occlusion + hypotension: 43 +/- 18 (isoflurane) vs. 67 +/- 20 (fentanyl/N2O), P = 0.003; 20 min bilateral carotid occlusion + normotension: 49 +/- 27 (isoflurane) vs. 71 +/- 22 (fentanyl/N2O), P = 0.003). Isoflurane also reduced CA3 damage and improved neurologic function under all conditions. Intraischemic forebrain blood flow was similar during bilateral carotid occlusion plus normotension for the two anesthetic states. Plasma norepinephrine values were greater when hypotension was added to the ischemic insult. CONCLUSIONS: Isoflurane resulted in improved neurologic function and reduced histologic damage regardless of the presence or absence of systemic hypotension during the ischemic insult. This indicates that beneficial effects of isoflurane are most likely attributable to direct effects at the neuronal level as opposed to indirect effects resulting from interactions with profound hypotension.
Anesthetics, Inhalation↗