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Biomedical subjects

V L Baughman

Publications and source records attributed to V L Baughman.

At least 37 records · Page 2Linked to original sources
PubMed1991

The 21-aminosteroid U74006F does not markedly improve outcome from incomplete ischemia in the rat.

The 21-aminosteroid U74006F reportedly decreases neuronal injury following head injury or complete cerebral ischemia. We evaluated the ability of U74006F to improve outcome following incomplete cerebral ischemia in the rat. Ischemia was induced by right carotid occlusion combined with 30 min of hemorrhagic hypotension to 30 or 35 mm Hg. Animals in groups 1 and 2 were maintained on 1.4% isoflurane in room air and rats in groups 3 and 4 were ventilated with 70% nitrous oxide (N2O) and 30% oxygen. Rectal temperature was kept at 37C and PaCO2 and pH were maintained constant during ischemia. Group 1 (n = 10) and group 3 (n = 10) received a vehicle treatment. Group 2 (n = 10) and group 4 (n = 10) received 3 mg/kg of U74006F before ischemia and a 3-h infusion of 3 mg/kg/h of the drug after ischemia. Neurologic outcome was measured for 3 days and histopathology was evaluated at the end of the study. U74006F did not significantly improve neurologic outcome or histopathology during either isoflurane or N2O compared to the vehicle-treated groups. These results suggest that U74006F does not substantially inhibit ischemic damage produced in this model of incomplete cerebral ischemia.

Journal Article↗
PubMed1991

Effects of sufentanil on cerebral blood flow, cerebral blood flow velocity, and metabolism in dogs.

The intracranial and systemic hemodynamic effects of sufentanil (20 micrograms/kg) were studied in 10 mongrel dogs. Baseline anesthesia was maintained with 0.7% end-tidal isoflurane and 50% nitrous oxide in oxygen. Catheters were inserted for blood pressure measurement, arterial and sagittal sinus blood sampling, radioactive microsphere injections, and intracranial pressure monitoring. Blood flow velocity was measured continuously in the middle cerebral artery using a transtemporal approach through a cranial window with a pulsed 8 MHz transcranial Doppler system (TCD). Cardiac output was measured using an electromagnetic flow probe on the pulmonary artery. After baseline measurements, sufentanil was injected and data were recorded at 5, 15, and 30 min. In group 1 (n = 5) blood pressure was not controlled, whereas in group 2 (n = 5) blood pressure was maintained at baseline levels with a phenylephrine infusion. Sufentanil decreased blood pressure from 120 +/- 10 mm Hg (mean +/- SEM) to 82 +/- 11 mm Hg in group 1. Cardiac output decreased 40%-50% in both groups. Intracranial pressure did not change. Cerebral blood flow (CBF) and TCD blood flow velocity decreased significantly (35%-40%) with no difference between groups. Relative decreases in CBF and TCD blood flow velocity were closely correlated (r = 0.82). The cerebral hemodynamic changes were associated with a 35%-40% decrease in cerebral oxygen consumption. We conclude that sufentanil decreases CBF in response to decreased metabolic demand without significantly affecting intracranial pressure. Relative changes in CBF can be reproducibly monitored using TCD.

Anesthesia, Inhalation↗
PubMed1991

Clonidine decreases plasma catecholamines and improves outcome from incomplete ischemia in the rat.

Clonidine decreases central sympathetic activity and anesthetic requirement. We tested whether clonidine improves outcome from incomplete ischemia of the brain in rats. Control rats were anesthetized with 25 micrograms.kg-1.h-1 of intravenous fentanyl and inhalation of 70% nitrous oxide (N2O). Clonidine-treated rats received fentanyl/N2O and 10 micrograms/kg of intravenous clonidine 10 min before ischemia, which was produced by right carotid ligation combined with hemorrhagic hypotension to 35 mm Hg for 30 min. Clonidine increased plasma glucose before ischemia and decreased blood catecholamine concentrations during ischemia compared with the control group. Neurologic outcome was evaluated daily for 3 days after ischemia and histopathology was performed at the end of this period. Clonidine significantly improved neurologic outcome on each of the 3 days after ischemia. Histopathology was severe in the control group but not enough rats survived in this group for statistical analysis. The authors conclude that clonidine decreases sympathetic activity during ischemia and that this is associated with an improvement in outcome from incomplete ischemia.

Animals↗
PubMed1990

Comparison of methohexital and isoflurane on neurologic outcome and histopathology following incomplete ischemia in rats.

Using a rat model of incomplete cerebral ischemia the effects of isoflurane (iso) and methohexital (metho) were compared with those of 70% nitrous oxide controls (N2O). Two levels of incomplete cerebral ischemia were produced by right carotid occlusion plus hypotension for 30 min: moderate = 30 mmHg, FIO2 = 0.30; severe = 25 mmHg, FIO2 = 0.20. The iso doses (1 and 2 MAC) and metho doses (0.01 and 0.1 mg.kg-1.min-1) were tested at each ischemic level. These iso and metho doses were selected because without ischemia they produced similar decreases in cerebral oxygen consumption (CMRO2) compared with that produced in N2O controls. In the absence of ischemia, the electroencephalogram (EEG) was suppressed by 0.01 mg.kg-1.min-1 metho and 1 MAC iso and showed burst-suppression with 0.1 mg.kg-1.min-1 metho and 2 MAC iso. The EEG was further depressed by ischemia under all anesthetic conditions. Neurologic outcome was evaluated for 3 days following incomplete cerebral ischemia by using a graded deficit score (0 = normal, 5 = death associated with stroke). Following moderate ischemia all four anesthetic treatments improved outcome compared with N2O controls, but after severe ischemia only 2 MAC iso significantly improved outcome. Neurohistopathology was evaluated on a scale of 0 to 40, 24 h after ischemia. The neurohistopathology score was significantly improved by all four anesthetic treatments compared with N2O following moderate ischemia and was better with 2 MAC iso compared with 0.1 mg.kg-1.min-1 metho after both moderate and severe ischemia. These results show that both iso and metho improve outcome from cerebral ischemia compared with that associated with N2O, but only 2 MAC iso resulted in an improved outcome following severe ischemia. This difference in outcome between the two anesthetics may be related to greater neuronal depression with iso, which may occur with little difference in cerebral metabolic depression.

Animals↗
PubMed1990

Cerebrovascular and cerebral metabolic effects of N2O in unrestrained rats.

There is controversy about whether N2O increases cerebral blood flow and cortical oxygen consumption (CMRO2) in rats. Cortical and subcortical blood flow and CMRO2 were measured in awake, unrestrained rats while awake and during 70% N2O administration using radioactive microspheres. In the awake state, cortical and subcortical blood flow were 126 +/- 10 and 98 +/- 7 ml.100 g-1.min-1, respectively, and CMRO2 (cortical) was 10.0 +/- 0.6 ml O2.100 g-1.min-1 (mean +/- SE). After 15 min of 70% N2O, cortical and subcortical blood flow increased 100% and 40%, respectively, while CMRO2 did not increase significantly. Cerebral blood flow remained increased after 60 min of N2O exposure, and CMRO2 did not change. These results show that N2O produces cerebrovasodilation in rats that is not related to a change in metabolic demand. Plasma catecholamines do not change during N2O administration, indicating that the increase in blood flow is not due to a general stress response.

Anesthesia, Inhalation↗
PubMed1990

Hypothermia versus ethanol: neurologic outcome after incomplete cerebral ischemia in midazolam-anesthetized rats.

We examined neurologic outcome after incomplete cerebral ischemia in rats treated with hypothermia versus ethanol, two techniques that decrease brain metabolism. All animals, including control rats, received a baseline midazolam anesthetic. Ischemia was produced by right carotid artery occlusion combined with hemorrhagic hypotension to a mean arterial pressure of 30 mm Hg for 30 min. Neurologic outcome was evaluated for 3 days after ischemia using a 5-point scale. In separate studies, cerebral blood flow (CBF) was measured using radioactive microspheres, and cortical oxygen consumption (CMRO2) was calculated from the blood flow data and the arteriovenous oxygen difference. Hypothermia to 31 degrees C decreased CBF 50% and CMRO2 52% compared with control rats, and significantly improved outcome. Although ethanol decreased CBF 35% and CMRO2 22%, it did not improve outcome from stroke compared with control rats. These results suggest that hypothermia protects the brain from ischemia and that ethanol does not, despite a decrease in CMRO2.

Journal Article↗
PubMed1989

The interaction of nitrous oxide and isoflurane with incomplete cerebral ischemia in the rat.

In rats with incomplete cerebral ischemia the effects of 70% N2O alone, isoflurane alone (0.5 and 1 MAC), and the combination of N2O + isoflurane on neurologic outcome, neurohistopathology, and EEG were compared. Moderate and severe ischemia were produced by right carotid artery occlusion combined with hemorrhagic hypotension (moderate ischemia, MAP = 30 mmHg, FIO2 = 0.30; severe ischemia, MAP = 25 mmHg, FIO2 = 0.20). Neurologic outcome was evaluated using a graded deficit score from 0 to 5 (0 = normal, 5 = death associated with stroke), and neurohistopathology was evaluated using a 40-point scale from 0 = normal to 40 = total hemisphere infarct at the level of the caudate nucleus in coronal section. Compared with N2O alone, isoflurane (0.5 and 1 MAC) improved neurologic outcome following moderate ischemia (P less than 0.05). Isoflurane also decreased histopathologic damage following moderate ischemia (N2O control = 33 +/- 1 vs. 0.5 MAC isoflurane = 11 +/- 4 and 1 MAC isoflurane = 12 +/- 3, P less than 0.05), whereas only 0.5 MAC isoflurane decreased histopathologic damage following severe ischemia (N2O control = 38 +/- 1 vs. 0.5 MAC isoflurane = 25 +/- 5; P less than 0.05) Adding N2O to 0.5 MAC isoflurane attenuated the neurologic protective effect of isoflurane alone and increased histopathologic damage following both moderate and severe ischemia (moderate = 23 +/- 5, severe = 37 +/- 2; both P greater than 0.05 compared with N2O controls). The effect of adding 70% N2O to isoflurane on cerebral blood flow (CBF) and cerebral oxygen consumption(CMRO2) was also evaluated.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1989

Effectiveness of triazolam, diazepam, and placebo as preanesthetic medications.

Eighty-three ASA Physical Status 1-2 patients were orally premedicated with triazolam (0.125, 0.25, or 0.5 mg), diazepam (5, 10, or 15 mg), or placebo to evaluate the effectiveness of these drugs and doses in reducing preoperative anxiety, providing sedation, and producing amnesia. The drug treatments were administered in a randomized, double-blind manner. The results obtained with each drug (dose) group were compared against those of the placebo group as a control. Changes in anxiety at 60 min after drug administration were evaluated: 1) by a trained anesthesia nurse clinician using an analog scale, 2) by the patient using the same analog scale, and 3) by the patient with the Multiple Affect Adjective Check List (MAACL). Changes in sedation at 60 min were also evaluated by the patient and nurse clinician using an analog scale. Amnesia was assessed by postoperative recall of picture cards shown to the patient 1 h after receiving preanesthetic medication. There were no significant differences between any drug (dose) and placebo for changes in patient-evaluated anxiety or sedation on the analog scale. With the other measures of anxiety, only triazolam (0.5 mg) reduced anxiety more than did placebo on both the patient (MAACL) and the nurse (analog) scales. With the nurse (analog) measure of sedation, only the highest doses of triazolam and diazepam were more sedating than placebo. Triazolam (0.5 mg) was the only drug dose that produced significant amnesia. The authors conclude that drug effects on anxiety, sedation, or amnesia that are statistically significant versus placebo effect are seen at only the highest doses of triazolam (0.5 mg) and diazepam (15 mg).

Adult↗
PubMed1989

Cerebral metabolic depression and brain protection produced by midazolam and etomidate in the rat.

Midazolam and etomidate have been shown to depress cerebral metabolism and may protect the brain during ischemia. However, it has been reported that etomidate may produce EEG spiking activity and seizures, which could adversely affect outcome. We compared the effects of midazolam and etomidate on EEG, cerebral blood flow (CBF), and cerebral cortical oxygen consumption (CMRO2) as well as neurologic outcome following incomplete cerebral ischemia in the rat. CBF was measured with radioactive microspheres and cortical CMRO2 was calculated by multiplying cortical CBF by the arterial-sagittal sinus oxygen content. Incomplete ischemia was produced by unilateral carotid artery occlusion combined with hemorrhagic hypotension. In low doses (0.02 mg/kg/min i.v.), both midazolam and etomidate depressed EEG, decreased CMRO2, and improved outcome from ischemia compared to nitrous oxide control rats. At a higher dose (0.2 mg/kg/min i.v.), midazolam further depressed EEG and CMRO2 and again improved outcome compared to N2O controls. In contrast, high dose etomidate (0.2 mg/kg/min) produced spiking EEG activity without further depression of CMRO2 and a worsening of outcome following cerebral ischemia. These results support previous reports that midazolam and etomidate may protect the brain from incomplete cerebral ischemia but suggest that EEG spiking activity associated with high dose etomidate may be associated with a worse outcome.

Journal Article↗
PubMed1988

Neurologic outcome in rats following incomplete cerebral ischemia during halothane, isoflurane, or N2O.

Using rats in which incomplete cerebral ischemia was induced, the authors evaluated the effects of halothane (H) and isoflurane (I) on neurologic outcome compared to nitrous oxide (N2O) controls. Incomplete cerebral ischemia was produced by right carotid artery occlusion combined with hemorrhagic hypotension. Neurologic outcome was evaluated using a graded deficit score from 0 to 5 (0 = normal, 5 = death associated with stroke). Two levels of cerebral ischemia were tested. At moderate ischemia with hypotension of 30 mmHg, an FIO2 of 0.3, and ischemic periods of 30 or 45 min, N2O produced a deficit of 4.7-5.0 and a mortality rate of 90-100%. In contrast, halothane (1 MAC) and isoflurane (1 MAC) resulted in similar deficit scores (H = 1.1-1.8, I = 1.4-1.6) and mortality rates (H = 17-30%, I = 17-20%). Cerebral blood flow (CBF) measured with radioactive microspheres showed a 60-65% decrease in the ischemic hemisphere at this level of hypotension. With severe ischemia with hypotension = 25 mmHg, FIO2 = 0.2, and a 30-min period of ischemia, deficit scores increased to 3.0 and 3.9 with 1 MAC halothane and 1 MAC isoflurane, respectively. Mortality rates also increased to 40% with halothane and 70% with isoflurane. Increasing the concentration of halothane or isoflurane to 2 MAC did not significantly improve outcome. Brain histology demonstrated extensive neuronal damage in striatal, hippocampal, and neocortical regions of N2O control treated rats, and less damage with little difference between H- and I-treated rats at each level of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1988

Effects of aerosolized and/or intravenous lidocaine on hemodynamic responses to laryngoscopy and intubation in outpatients.

A randomized, double-blind study was carried out on 40 unpremedicated, ASA I-II adult surgical outpatients to assess the effects of aerosolized lidocaine, intravenous lidocaine, both, or neither, on circulatory responses to laryngoscopy and intubation. Lidocaine (4 mg/kg) or saline was given by nebulizer in the holding area beginning at -15 minutes. The patient underwent a standardized induction of anesthesia that included IV curare (3 mg) and O2 by facemask at minute 2, followed by IV thiopental (5 mg/kg) and succinylcholine (1.5 mg/kg) at minute 5. Lidocaine (2 mg/kg) or saline was given by IV push at minute 4. Laryngoscopy was begun at 5 minutes and continued for 45 seconds before intubation. Heart rate and systolic, diastolic, and mean blood pressures were automatically recorded at 1-minute intervals from 0 to 11 minutes. The four treatment groups included: group 1, aerosolized and IV saline; group 2, aerosolized saline, IV lidocaine; group 3, aerosolized lidocaine, IV saline; and group 4, aerosolized and IV lidocaine. There were no differences among the four treatment groups (n = ten per group) in any of the four hemodynamic variables before laryngoscopy and intubation. Within each group, after intubation all four hemodynamic variables increased significantly over the corresponding baseline values for that group. However, the maximum values attained after intubation did not differ significantly among the four treatment groups for any of the four hemodynamic variables, whether those maxima were expressed as absolute values or as a percentage of baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗
PubMed1988

Neurologic outcome in aged rats after incomplete cerebral ischemia.

The effect of age on outcome after induced cerebral ischemia was tested in rats. Cerebral ischemia was produced by unilateral carotid ligation and hemorrhagic hypotension to 30 mm Hg (moderate ischemia) or 25 mm Hg (severe ischemia) in young (6 month) and old (26-28 month) rats anesthetized with 1 MAC halothane. Young rats had significantly better neurologic outcomes than old rats after similar ischemic challenges. This advantage disappears, however, when the inspired oxygen tension is altered to produce similar PaO2 in both age groups during ischemia. Measures of regional CBF with radioactive microspheres showed a 70% decrease in cortical blood flow in the ischemic cerebral hemisphere in both young and old rats. Plasma glucose concentrations increased from 150 to 250 mg/100 mL during ischemia in both age groups. Histologically, the brains showed similar signs of focal ischemic damage in striatum, hippocampus, and cortex in young and old rats. These results indicate that when blood pressure and respiratory factors are controlled experimentally during ischemia, young and aged rats have similar neurologic outcomes after cerebral ischemia.

Aging↗
PubMed1987

Cerebral vascular and metabolic effects of fentanyl and midazolam in young and aged rats.

Cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2) were measured, and electroencephalogram (EEG) was recorded in young (6-month-old) and aged (28-month-old) rats during ventilation with 70% N2O/30% O2 and following fentanyl or midazolam administration. Cerebral blood flow (CBF) was measured with radioactive microspheres, and cerebral oxygen consumption (CMRO2) was calculated from the arterial-sagittal sinus oxygen content difference and CBF measurements. Fentanyl at the highest dose used (200 micrograms/kg and 400 micrograms.kg-1.h-1) depressed the EEG and decreased CBF 49% and CMRO2 39% in young rats, whereas in old rats, this fentanyl dose decreased CBF 37% and CMRO2 34%, both significantly less than in young rats (P less than 0.05). Midazolam at the highest dose used (5.75 mg/kg) also depressed EEG in both age groups, and decreased CBF 51% and CMRO2 38% in young rats. This depression was significantly less than the 62% decrease in CBF and 59% decrease in CMRO2 produced by midazolam in old rats (P less than 0.05). These results indicate that aging attenuates the cerebrovascular and cerebral metabolic depression produced by fentanyl, but potentiates the same effects produced by midazolam. The enhanced cerebral metabolic depression produced by midazolam in the aged is similar to that seen with phenobarbital, and suggests a similar action of these drugs at the central GABA-benzodiazepine-barbiturate receptor complex.

Aging↗