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Biomedical subjects

H M Shapiro

Publications and source records attributed to H M Shapiro.

At least 19 recordsLinked to original sources
PubMed1992

Comparison of lymphocyte immunophenotypes obtained simultaneously from two different data acquisition and analysis systems on the same flow cytometer.

Immunophenotyping of different lymphocyte populations was carried out in parallel on 113 consecutively received specimens of human peripheral blood using 2 different data acquisition and analysis systems (EPICS C and 4Cyte-Acmecyte) on the same flow cytometer (EPICS C). The phenotypes analyzed were CD3+, CD4+, CD8+ CD56+ CD16+ CD3-, TCR-gamma delta+ CD8-, and TCR-gamma delta+ CD8+. Both HIV- and HIV+ specimens were used for this study, including some with CD4 levels as low as 2% of all lymphocytes. Despite differences in gating procedures and shapes of bitmap (rectilinear vs. "amorphous"), the 2 methods agreed to within 2% positive cells in 97% of the cases. Although some statistically significant biases in the methods were observed, these were small and not biologically important. We conclude that both methods of data acquisition and analysis, as employed by experienced operators on the EPICS C flow cytometer, gave essentially equivalent results for lymphocyte sub-populations in peripheral blood preparations.

Electronic Data Processing↗
PubMed1992

Epidural blood patch in the HIV-positive patient. Review of clinical experience. San Diego HIV Neurobehavioral Research Center.

To characterize the natural history of autologous epidural blood patch (EBP) in human immunodeficiency virus (HIV)-seropositive patients, records from an ongoing longitudinal study of the neuropsychological manifestations of HIV infection were retrospectively reviewed. Of 252 participants (218 HIV-seropositive, 34 HIV-seronegative) who underwent at least one diagnostic lumbar puncture, 9 (7 seropositive, 2 seronegative) required EBP for post-dural puncture headache. After EBP, 6 of the seropositive subjects underwent serial neuropsychological evaluations over periods ranging from 6 to 24 months; none of these six subjects had a decline in neurocognitive performance or other adverse neurologic or infectious sequelae. We were unable to identify morbidity attributable to EBP in the HIV-seropositive patient followed for as long as 2 yr.

Adult↗
PubMed1992

Effects of levemopamil on neurologic and histologic outcome after cardiac arrest in cats.

BACKGROUND AND METHODS: A study was performed to examine the effects of the calcium-channel blocker levemopamil on neurologic outcome and neuropathology in a clinically relevant model of complete global cerebral ischemia (ventricular fibrillation in cats). Levemopamil was administered to cats starting 5 mins after resuscitation from 14 mins of cardiac arrest. In a "blinded" manner, 46 animals received levemopamil 1 mg/kg over 15 mins followed by 10 micrograms/kg.min for 16 hrs or vehicle. In a nonblinded manner, eight additional animals were pretreated with levemopamil beginning 45 mins before cardiac arrest. After resuscitation, levemopamil was infused at 10 micrograms/kg.min for 16 hrs. Animals in all three groups remained sedated, paralyzed, and mechanically ventilated for 24 to 30 hrs after resuscitation. Neurologic examinations were performed at 2, 4, and 7 days after resuscitation. Thirty-five cats were entered into data analysis (16 levemopamil posttreated, 14 vehicle-treated, and 5 levemopamil pretreated). RESULTS: Neurologic deficit scores and over-all neuropathologic scores did not differ among groups at any interval after resuscitation. However, the occipital cortex and CA1 region of the pretreated animals showed less severe damage than was observed in the animals that received levemopamil or vehicle, starting after resuscitation (p less than .01). CONCLUSIONS: Postarrest administration of levemopamil was not associated with improved neurologic or neuropathologic outcome. However, the data suggest that prearrest administration may result in regionally selective improvement in neuropathology.

Animals↗
PubMed1991

Failure of nimodipine to improve neurologic outcome after eighteen minutes of cardiac arrest in the cat.

The calcium entry blocker nimodipine was administered to cats following resuscitation from 18 min of cardiac arrest to evaluate its effect on neurologic and neuropathologic outcome in a clinically relevant model of complete cerebral ischemia. Cardiac arrest (ventricular fibrillation) was maintained for 18 min and resuscitation was performed by a standardized protocol in 40 cats. Beginning at 5 min post-resuscitation, nimodipine, 10 micrograms/kg over 2 min followed by 1 microgram/kg per min for 10 h, or the same volume of placebo was administered in a randomized, blinded fashion. Neurologic deficits were scored at 2, 4, and 7 days post-resuscitation by observers blinded to the treatment group. Thirty cats were evaluated neurologically at 7 days post-resuscitation and were entered into data analysis (n = 15 per group). Neither neurologic deficit scores nor neuropathologic scores were significantly different between groups. The authors conclude that nimodipine administration in the manner and doses stated does not improve neurologic outcome in cats following resuscitation from cardiac arrest.

Animals↗
PubMed1990

A reversible component of cerebral injury as identified by the histochemical stain 2,3,5-triphenyltetrazolium chloride (TTC).

The extent of histochemical change following middle cerebral artery occlusion was quantitatively determined in three groups of Sprague-Dawley rats with 2,3,5-triphenyltetrazolium chloride (a marker of mitochondrial oxidative enzyme function). In group I (n = 7) occlusion was maintained for 3 h, with immediate sacrifice. In group II (n = 7) occlusion was maintained for 5 h, with immediate sacrifice. In group III (n = 7) occlusion was maintained for 3 h, followed by a 2-h period of reperfusion prior to sacrifice. The area of injury was significantly larger (P less than 0.05) in the 5-h occlusion group [15 +/- 4% (mean +/- SD)] compared to the 3-h occlusion group (9 +/- 2%); indicating a time-dependent worsening of the histochemical detection of injury. However, the area of injury was significantly less in the reperfusion group (5 +/- 2%) compared to the group that was evaluated after 3 h of occlusion without reperfusion (9 +/- 2%); indicating that some component of the injury revealed by 2,3,5-triphenyltetrazolium chloride is potentially reversible. These data suggest that contrary to previous understanding, the histochemical abnormality revealed by 2,3,5-triphenyltetrazolium chloride is reversible in some circumstances and does not necessarily represent inevitable infarction.

Animals↗
PubMed1990

Spinal tetracaine decreases central nervous system metabolism during somatosensory stimulation in the rat.

The influence of spinal tetracaine on central nervous system (CNS) metabolism was determined during nociceptive stimulation. Rats were divided into a halothane group in which the sciatic nerve was stimulated during 0.5 per cent halothane anaesthesia, a tetracaine group in which the sciatic nerve was stimulated during a simultaneous tetracaine spinal and 0.5 per cent halothane anaesthetic, or an awake group. Autoradiographic determination of local spinal cord and cerebral glucose utilization was performed using 14C-2-deoxyglucose. Central nervous system metabolism was greater in the halothane group than the tetracaine and awake groups (P less than 0.05). The only meaningful differences between the tetracaine and awake groups were in two lumbar grey areas at the site of drug administration where metabolism was decreased in the tetracaine/stimulated group. These results indicate that spinal tetracaine effects a decrease in metabolism locally, and attenuates increases in metabolism throughout the CNS observed during somatosensory stimulation.

Analysis of Variance↗
PubMed1990

Influence of hypotension and hypotensive technique on the area of profound reduction in cerebral blood flow during focal cerebral ischaemia in the rat.

We have studied the effect of induced hypotension on reduction in regional cerebral blood flow (CBF) during middle cerebral artery occlusion (MCAO). Rats were anaesthetized with 2% isoflurane. MCAO was performed during four conditions: normotension (mean arterial pressure (MAP) 107 (SD 15) mm Hg); hypovolaemic hypotension (blood withdrawn to reduce MAP to 43 (2) mm Hg); nitroprusside (SNP) hypotension (MAP reduced to 45 (3) mm Hg); isoflurane hypotension (MAP reduced to 44 (3) mm Hg with 3.5 (0.48)% isoflurane). Hypotension was established before MCAO and was maintained for 10 min, at which time the dimension of the brain areas with zero CBF was determined autoradiographically. All hypotensive regimens were associated with significantly larger areas of extreme CBF reduction. In a coronal section at the centre of the MCA distribution, the area with zero CBF (expressed as a percentage of the area of the entire coronal section) was: normotension 4.7 (4.5)%; hypovolaemic hypotension 10.1 (2.8)%; nitroprusside hypotension 13.5 (2.0)%; and isoflurane hypotension 11.8 (3.9)%. There were no differences between the three hypotensive regimens. The data indicate that, when focal cerebral ischaemia occurs during hypotension (MAP 45 mm Hg) induced by any of the three regimens evaluated, extreme CBF reduction occurs over larger areas than are observed during normotension. These data confirm the importance of arterial pressure as a determinant of collateral flow during focal cerebral ischaemia.

Animals↗
PubMed1990

Glucose administration before cardiac arrest worsens neurologic outcome in cats.

The effects of glucose on neurologic and neuropathologic outcome following global cerebral ischemia were examined in 20 cats subjected to 14 min of cardiac arrest, followed by closed chest resuscitation and intensive care monitoring. Beginning 30 min prior to cardiac arrest, 15 ml/kg of 5% dextrose in 0.45% saline or the same volume of 0.9% saline was administered in a blinded fashion over 15 min. Ventricular fibrillation was electrically induced and cardiac resuscitation was performed according to a standardized protocol, which included closed chest cardiac compressions, epinephrine, lidocaine, sodium bicarbonate administration, and electrical defibrillation. Animals not resuscitated within 4 min were excluded from further study. Resuscitated animals were managed in an intensive care setting for 24 h postresuscitation. Neurologic deficits were scored at 2, 4, and 7 days postresuscitation. Subsequently, the animals' brains underwent histologic examination. Nine cats were excluded from data analysis. Three did not meet protocol criteria and six could not be resuscitated within 4 min. As a result of a technical error, the brain of one glucose-treated cat was not analyzed. Six saline-treated and five glucose-treated animals met all protocol criteria and survived for 7 days postresuscitation. Plasma glucose concentration before cardiac arrest was 118 +/- 24 mg/dl (mean +/- SD) in the saline group and 269 +/- 21 mg/dl in the glucose group (P less than 0.01). Neurologic outcome rank at 2, 4, and 7 days postresuscitation was significantly worse in glucose-treated cats (P less than 0.01, P less than 0.01, and P less than 0.01, respectively). The neuropathologic score did not differ between glucose- and saline-treated groups (P = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The nonlinear potency of sub-MAC concentrations of nitrous oxide in decreasing the anesthetic requirement of enflurane, halothane, and isoflurane in rats.

The effect of nitrous oxide (N2O) on the MAC of enflurane, halothane, and isoflurane was determined in male rats. Each rat received either enflurane, halothane, or isoflurane, along with 0%, 15%, or 75% N2O. Anesthetic equilibration was verified by mass spectrometry sampling of end-tidal gases. MAC was determined at each N2O concentration by the standard tail clamp method. The N2O dose-response data for each animal were fit by a second-order polynomial equation to estimate the value of a second-order coefficient. A linear dose-response would result in a value of zero, whereas the extent to which the data deviate from nonlinearity would be reflected by an increase in the value of this coefficient. The null hypothesis, that the second-order coefficient should be zero, was tested by a one-sample two-tailed t test. The volatile anesthetic requirement decreased as the N2O concentration increased; however, it did not do so linearly. For each of the three volatile anesthetic groups, the second-order coefficients were consistently greater than zero (P less than 0.05). These data are not consistent with the accepted presumption that the summation of N2O with volatile anesthetics is linear.

Anesthesia, Inhalation↗
PubMed1989

MK-801, an excitatory amino acid antagonist, does not improve neurologic outcome following cardiac arrest in cats.

The excitatory amino antagonist MK-801 was administered to cats following resuscitation from cardiac arrest to evaluate its effect on neurologic and neuropathologic outcome in a clinically relevant model of complete cerebral ischemia. In 29 cats studied, cardiac arrest (ventricular fibrillation) was maintained for 18 min and resuscitation was successfully performed in 21 cats. Four animals underwent a sham arrest. MK-801 or placebo was administered in a blinded, randomized manner. Beginning at 5 min post resuscitation (PR), MK-801 330 micrograms/kg over 2 min followed by 73 micrograms/kg/h for 10 h or the same volume of placebo was administered. Resuscitated animals remained paralyzed and sedated in an intensive care setting for 24-30 h PR. Neurologic examinations were performed at 2, 4, and 7 days PR by observers blinded to the treatment groups. Seventeen cats were entered into data analysis (nine MK-801-treated and eight placebo-treated). MK-801-treated animals had a significantly greater neurologic deficit score (NDS) rank (0 = normal, 100 = brain death) 2 days PR (mean rank 12.1 vs. 5.6; p = 0.008). This difference is most likely due to ongoing sedative actions of MK-801. There were no significant differences in NDS rank at 4 (10.3, MK-801 vs. 7.5, placebo) and 7 (9.6, MK-801 vs. 8.3, placebo) days PR. There were no significant differences in frontal cortex, hippocampus, occipital cortex, or cerebellar neuropathology between groups. Sham-arrested cats had normal neurologic and neuropathologic evaluations. In the circumstance of complete cerebral ischemia as employed in the current study, MK-801 had no beneficial effect upon neurologic or neuropathologic outcome.

Animals↗
PubMed1989

Insufficient anesthetic potency of nitrous oxide in the rat.

Nitrous oxide (N2O) is frequently used for maintenance of anesthesia in research animals because of its minimal effect upon circulatory variables and the ability to rapidly alter its anesthetic concentration. However, N2O's low anesthetic potency may result in inadequate levels of anesthesia under experimental conditions; thus, the ability of N2O to provide adequate anesthesia during tracheal stimulation in rats, following withdrawal of halothane was evaluated. Twenty rats of similar ages and weights were anesthetized with halothane (1.44% inspired) and their tracheas orally intubated. Ten minutes prior to the conclusion of a 90-min halothane stabilization period, either 70% N2O (n = 10) or 70% nitrogen (n = 10) was added to the inspired anesthetic gas mixture. The halothane was discontinued at the conclusion of the 90-min period and each rat was observed for spontaneous motor behavior while end-expiratory anesthetic gases were intermittently measured with mass spectrometry. The halothane concentrations present at the times of four specific, consistently occurring behaviors were measured, and comparisons were made between the N2O and nitrogen groups by a mean t test. There were no significant differences (P less than 0.05) in the halothane concentration between the N2O and nitrogen groups in three of the four behaviors compared: 1) change in respiratory pattern, 2) purposeful movement of the torso, and 3) purposeful self-extubation. In the fourth behavior (purposeful movement of an extremity) the halothane concentration was higher in the N2O group than in the nitrogen group. A mean halothane concentration of 0.49% was required to prevent the purposeful behaviors in the presence of N2O.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1989

Different 1.2 MAC combinations of nitrous oxide-enflurane cause unique cerebral and spinal cord metabolic responses in the rat.

The effect of three different 1.2 MAC combinations of nitrous oxide (N2O) and enflurane upon glucose metabolism in the central nervous system was evaluated in male rats (n = 30). Anesthesia was induced with enflurane and N2O prior to tracheal intubation and mechanical ventilation. Physiologic variables (temperature, blood pressure, pH, PaO2, PaCO2, serum glucose, and hematocrit) were maintained within normal limits. Each rat was randomly assigned one of the following 1.2 MAC anesthetic regimens: 1) control--0% N2O/2.76% enflurane, 2) treatment 1--30% N2O/2.26% enflurane, or 3) treatment II--60% N2O/2.12% enflurane. Following anesthetic equilibration, an autoradiographic evaluation of local cerebral and spinal cord glucose utilization was performed. There were no differences in the physiologic data. As enflurane was partially replaced by an equivalent MAC fraction of N2O (0-30%), a heterogeneous activation of cerebral metabolism was observed in selected sensory input structures, and in components of the limbic system. The values tended to return to control when N2O was increased to 60% (and the enflurane was appropriately reduced). At all spinal cord levels, a homogeneous increase in metabolism was observed in both white and grey matter when enflurane was replaced by the 0-30% N2O change, with a return to control when the N2O was further increased from 30-60%. Thus, in rats, increasing the N2O concentration (while concurrently decreasing enflurane) produced a biphasic metabolic response. Metabolism was activated when N2O was increased from 0-30%, with a relative depression in metabolism when N2O was further increased from 30-60%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Halothane, fentanyl/nitrous oxide, and spinal lidocaine protect against spinal cord injury in the rat.

Little information is available regarding the interaction of anesthesia and spinal cord injury. In this study male, Sprague-Dawley rats (n = 140) of similar weights underwent a graded lumbar spinal cord injury by inflation of an epidural balloon, to determine the effect of anesthesia upon the severity of injury. One of three different anesthetic regimens (halothane, fentanyl/nitrous oxide, or spinal lidocaine) were administered during the time of injury, and the neurologic outcome was compared to an awake control group. Physiologic variables (pH, PaCO2, PaO2, hematocrit, mean arterial pressure, serum glucose, and temperature) were maintained within normal ranges. Dose-response curves were constructed evaluating the relationship between the duration of balloon inflation versus the percentage of animals with a sustained neurologic deficit. The dose-response curves were analyzed for differences by use of a group t test. The incidence of clinical spinal cord injury (hindlimb paralysis) was lower in all three anesthetic groups as compared to awake controls (P less than 0.05). The balloon inflation time required to produce a sustained neurologic deficit in 50% of rats for each group was (minutes [mean +/- SD]): 1) awake--10.0 +/- 2.3; 2) spinal lidocaine-19.6 +/- 11.6, 3) halothane--19.8 +/- 6.7; and 4) fentanyl/nitrous oxide--37.9 +/- 18.7. This observation demonstrates that, in this model of spinal cord injury, various anesthetics improve neurologic function as compared to the awake state. It does not indicate any one technique as being either more favorable or deleterious in determining the final neurologic outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1989

The effect of fentanyl anesthesia and intrathecal naloxone on neurologic outcome following spinal cord injury in the rat.

Whereas opiate receptor agonists have resulted in spinal cord damage; opiate receptor antagonists have demonstrated protection against spinal cord injury. Because opioids are used in clinical anesthesia, the effect of an opiate antagonist was evaluated on neurologic outcome in a rat model of spinal cord injury occurring during opioid anesthesia. One day prior to spinal cord injury, a catheter was inserted into the spinal subarachnoid space with the tip at T8. On the day of spinal cord injury a balloon tipped catheter was inserted in the epidural space with the tip at the thoracolumbar junction. Spinal cord injury was produced by balloon inflation during one of the following states: 1) group 1 (A/S), injury was produced in awake rats and saline was administered in the subarachnoid space immediately following injury; 2) group 2 (F/S), injury was produced during a fentanyl/nitrous oxide (N2O) anesthetic, and subarachnoid saline administered; and 3) group 3 (F/Nx), injury was produced during a fentanyl/N2O anesthetic, and subarachnoid naloxone (1 mg/kg) was administered immediately following injury. Dose-response curves describing the relationship between the duration of balloon inflation and the percentage of animals with a persistent neurologic deficit were constructed and compared for differences by use of a group t test. The duration of balloon inflation required to produce a neurologic deficit was greater in both the F/S and F/Nx groups than in the A/S group (P less than 0.05). There was no difference between the F/S and F/Nx groups. In summary, in rats receiving a fentanyl/N2O anesthetic, neurologic outcome was improved compared with the awake state.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia Recovery Period↗
PubMed1989

The effect of hypervolemic hemodilution with and without hypertension on cerebral blood flow following middle cerebral artery occlusion in rats anesthetized with isoflurane.

The effect of hypervolemic hemodilution or hypervolemic hemodilution with dopamine-induced hypertension on cerebral blood flow (CBF) was investigated during 1.2 MAC isoflurane anesthesia in rats (n = 24) subjected to middle cerebral artery occlusion (MCAO). Prior to MCAO each animal was randomized to one of the following groups: 1) control, mean arterial pressure (89 +/- 10 mmHg [mean +/- SD]), blood volume, and hematocrit (46 +/- 1) were not manipulated; 2) hypervolemic hemodilution (HH), 30 min before MCAO, 5% albumin was administered to reduce the hematocrit to 29-32%; or 3) hypervolemic hemodilution/dopamine hypertension (HH/Dop), hemodilution was accomplished and dopamine (10 micrograms.kg-1.min-1) was infused during the ischemic period to achieve a mean arterial pressure of 111 +/- 10 mmHg (mean +/- SD). Ten minutes after occlusion of the left middle cerebral artery, CBF was determined using 14C-iodoantipyrine. Five coronal brain sections were analyzed to determine the area within each brain section with CBF ranges of 0-15 ml.100 g-1.min-1 and 15-23 ml.100 g-1.min-1. The area of 0-15 ml.100 g-1.min-1 CBF was less in both the HH and HH/Dop groups compared with control (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗