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Biomedical subjects

E J Heyer

Publications and source records attributed to E J Heyer.

At least 37 records · Page 2Linked to original sources
PubMed1996

Jugular venous bulb oxyhemoglobin saturation during cardiac surgery: accuracy and reliability using a continuous monitor.

Previous studies have demonstrated the feasibility of continuously monitoring jugular venous oxygen saturation (SjO2) with a fiberoptic catheter during hypothermic cardiopulmonary bypass (CPB). In the present study, with patients maintained at either moderate (28 degrees C) or mild (32-34 degrees C) hypothermia during CPB, SjO2 values obtained from a fiberoptic catheter were compared to intermittent samples analyzed by a co-oximeter. Twenty patients scheduled for elective coronary artery or valvular surgery had a 5.5 Fr Opticath catheter inserted into the left internal jugular bulb after induction of general anesthesia. The catheter was calibrated in vitro and in vivo according to the manufacturer's specifications. Catheter and co-oximetry SjO2 values obtained at four time points--1) pre-CPB, 2) target CPB temperature, 3) mid-rewarming, and 4) post-CPB--were compared using linear regression, Bland-Altman analysis, and Shrout-Fleiss interclass correlation coefficient analysis. These statistical methods revealed poor correlation between the catheter and co-oximetry SjO2 values: r = 0.44 by linear regression and 0.32 by interclass correlation coefficient analysis, and was unacceptably discrepant by Bland-Altman analysis. Oxyhemoglobin saturation values obtained continuously from a jugular venous bulb fiberoptic catheter during CPB may not accurately reflect true oxyhemoglobin saturation, and caution is warranted when interpreting SjO2 values obtained from a fiberoptic catheter during CPB.

Aged↗
PubMed1996

Intraoperative monitoring of motor evoked potentials: a review of 116 cases.

We reviewed the results of motor evoked potential (MEP) and somatosensory evoked potential (SEP) monitoring during 116 operations on the spine or spinal cord. We monitored MEPs by electrically stimulating the spinal cord and recording compound muscle action potentials from lower extremity muscles and monitored SEPs by stimulating posterior tibial or peroneal nerves and recording both cortical and subcortical evoked potentials. We maintained anesthesia with an N2O/O2/opioid technique supplemented with a halogenated inhalational agent and maintained partial neuromuscular blockade using a vecuronium infusion. Both MEPs and SEPs could be recorded in 99 cases (85%). Neither MEPs nor SEPs were recorded in eight patients, all of whom had preexisting severe myelopathies. Only SEPs could be recorded in two patients, and only MEPs were obtained in seven cases. Deterioration of evoked potentials occurred during nine operations (8%). In eight cases, both SEPs and MEPs deteriorated; in one case, only MEPs deteriorated. In four cases, the changes in the monitored signals led to major alterations in the surgery. We believe that optimal monitoring during spinal surgery requires recording both SEPs and MEPs. This provides independent verification of spinal cord integrity using two parallel but independent systems, and also allows detection of the occasional insults that selectively affect either motor or sensory systems.

Evoked Potentials, Motor↗
PubMed1995

Intraoperative data acquisition for the study of cerebral dysfunction following cardiopulmonary bypass.

As a first step in our study to document postoperative cerebral dysfunction, and to determine whether global cerebral blood flow can be implicated in the etiology of this postoperative change, we have assembled a flexible data acquisition system to acquire and record data from four independent sources, three in digital form and one analog. Each of the monitors that we use has a different requirement: One has eight channels of analog output; the other three have RS-232 digital outputs, each with a data stream with different characteristics. The central element of our data collection is a personal computer running the data acquisition and analysis program, LabVIEW for Windows (National Instruments, Austin, TX). All data are processed through separate LabVIEW global variables; the data strings are concatenated and stored on the hard disk in a spreadsheet format for further analysis. We illustrate an intraoperative recording made during cardiopulmonary bypass (CPB) by showing a graph of the mean arterial pressure (MAP), mixed venous oxyhemoglobin saturation recorded from the jugular bulb (JVO2Sat), and temperature measured from the nasopharynx. A decrease in the MAP after unclamping the aorta is accompanied by a decrease in JVO2Sat.

Blood Pressure↗
PubMed1995

Cerebral dysfunction after cardiac operations in elderly patients.

BACKGROUND: Cerebral injury remains a significant complication of cardiac operations. We determined the incidence of cerebral dysfunction in a population of elderly patients undergoing open chamber cardiac operations (group 1) as compared with a younger population (group 2) and an age-matched group of elderly patients undergoing major noncardiac operations (group 3). METHODS: Sixty-eight patients (55 for open chamber cardiac operations and 13 for noncardiac operations) were prospectively studied. Patients were evaluated preoperatively and postoperatively before hospital discharge using a complete neurologic examination and a battery of standard neuropsychometric tests, and at surgical follow-up with neuropsychometric tests only. RESULTS: Postoperative changes detected by neurologic examination consisted of the appearance of new primitive reflexes in all groups. No statistically significant differences in incidence were found. The neuropsychometric performance of group 1 patients was statistically different from that of patients in groups 2 and 3 only in the early follow-up period. CONCLUSIONS: Elderly patients having open chamber cardiac operations exhibit significantly more cerebral dysfunction in the early postoperative period than those undergoing major noncardiac operations and younger patients after open chamber procedures. These changes do not persist into the late follow-up period.

Age Factors↗
PubMed1995

Implantable cardioverter-defibrillator. Evaluation of clinical neurologic outcome and electroencephalographic changes during implantation.

During placement of implantable cardioverter-defibrillators, ventricular arrhythmias are induced to test the function of the devices. Although cerebral hypoperfusion and ischemic electroencephalographic changes occur in patients while implantable cardioverter-defibrillators are being tested, no investigation has assessed neurologic outcome in these patients. Nine patients having either implantation or change of an implantable cardioverter-defibrillator underwent neurologic examination and neuropsychometric tests before and after the operation. After induction of general anesthesia and insertion of implantable cardioverter-defibrillator leads (when needed), ventricular fibrillation, ventricular flutter, or ventricular tachycardia, was induced by means of programmed electrical stimulation. Implantable cardioverter-defibrillator testing continued until satisfactory lead placement was confirmed. The intraoperative electroencephalographic recording was analyzed for evidence of ischemic change. In all, an electroencephalogram was recorded during 50 periods of circulatory arrest. Mean duration of the arrest periods was 13.6 seconds. By means of conventional visual inspection of the raw electroencephalogram, high-amplitude rhythmic delta or theta, voltage attenuation, or loss of fast frequency activity was observed in 30 of the arrests. By means of an automated technique of electroencephalographic interpretation based on power spectral analysis, electroencephalographic changes were correctly identified in 26 of the arrests. The incidence of these electroencephalographic changes was dependent on the arrest duration. The mean interval from arrest onset to electroencephalographic change was 7.5 seconds (standard deviation +/- 1.8 seconds). In patients with electroencephalographic changes during multiple arrests, no downward trend in this interval was detected in later arrests and no evidence of persistent ischemic change was observed in electroencephalograms recorded after the conclusion of implantable cardioverter-defibrillator testing. Postoperative neurologic and neuropsychometric testing was completed in eight patients, none of whom exhibited a new neurologic deficit, exacerbation of a preexisting neurologic condition, or significant deterioration in neuropsychometric performance. We conclude that the brief arrest of cerebral circulation induced during insertion of an implantable cardioverter-defibrillator is not associated with permanent neurologic injury.

Adult↗
PubMed1995

The reliability of quantitative electroencephalography as an indicator of cerebral ischemia.

The electroencephalogram (EEG) has been used to detect episodes of cerebral ischemia during various surgical procedures. Recently, computerized systems for recording and interpreting the quantitative EEG (QEEG) have been used by anesthesiologists because of their ease of application, clarity of display, and reported ability to identify ischemic EEG changes. However, the extent to which automated techniques of QEEG interpretation reliably differentiate cerebral ischemia from the confounding effects of anesthetics and other sources of "artifact" is not completely established. In this study, EEGs were recorded before and after defibrillator testing in patients undergoing implantable cardioverter defibrillator (ICD) placement and during analogous time periods in control patients undergoing abdominal surgery. EEGs were subjected to standard visual inspection by an experienced electroencephalographer and QEEG analysis with a commercially available system was used for automated EEG interpretation in order to evaluate the reliability of this quantitative technique. The CIMON technique identified episodes which met previously defined criteria for QEEG cerebral dysfunction and ischemic pattern in both groups, despite the presumed absence of cerebral ischemia in the control patients. Since there was no evidence of cerebral ischemia in the raw EEGs of either the ICD patients or the controls, these QEEG changes were not confirmed by conventional techniques of EEG interpretation. Our results suggest that caution is warranted when using automated systems for intraoperative interpretation of EEG.

Adult↗
PubMed1993

Monitoring of intraoperative motor-evoked potentials under conditions of controlled neuromuscular blockade.

Motor-evoked potentials were recorded after electrical spinal cord stimulation in 19 patients undergoing neurosurgical or orthopedic procedures. Anesthesia was maintained with nitrous oxide, opioids, and inhaled anesthetics. Vecuronium was infused sufficient to eliminate 90% of twitch tension. The spinal cord was stimulated using either epidural or subarachnoid electrodes. Compound muscle action potentials were recorded from quadriceps and tibialis anterior muscles. Well-formed, stable motor-evoked potentials were recorded in all but one patient, in whom a preexisting myelopathy was felt to preclude recording. Intraoperative deterioration of motor-evoked potentials occurred in one patient who had a postoperative neurologic deficit. This study demonstrates the feasibility and utility of intraoperative motor tract monitoring using direct spinal cord stimulation. Controlled neuromuscular blockade permits recording of compound muscle action potentials while eliminating patient motor activity that could interfere with surgery.

Action Potentials↗
PubMed1986

Dopamine antagonists reduce spontaneous electrical activity in cultured mammalian neurons from ventral mesencephalon.

Mammalian neurons from ventral mesencephalon (VM) were grown in primary dissociated cell (PDC) culture. These neurons are predominantly non-dopaminergic. Many of these non-dopaminergic neurons have dopamine agonist and antagonist binding sites. Intracellular recordings were obtained from these neurons. When bathed in phosphate-buffered saline (PBS) solution they generated action potentials spontaneously. However, in the presence of haloperidol dissolved in PBS solution, the percentage of neurons which generated action potentials spontaneously was reduced in a dose-dependent manner (1-10 microM). This response was also obtained with (+) butaclamol (1 microM) but not with (-) butaclamol (1 microM). This neuroleptic inhibition of spontaneously generated action potentials was specific for neurons in PDC cultures of VM since neurons in PDC cultures of spinal cord did not demonstrate this phenomenon.

Action Potentials↗
PubMed1986

Characterization of dopamine receptors on neurons grown in primary dissociated cell culture from ventral mesencephalon of mouse.

Mammalian neurons from ventral mesencephalon were grown in primary dissociated cell culture. These cultures were examined for dopamine sensitive adenylate cyclase activity and specific ligand binding of [3H]spiroperidol and [3H]flupenthixol. No stimulation of adenylate cyclase activity by 10 microM dopamine was demonstrable in cell culture homogenates. [3H]Spiroperidol bound to cell culture homogenates with high affinity and was displaced by (+)-butaclamol but not by 5-hydroxytryptamine, suggesting that the [3H]spiroperidol was bound to dopamine receptors. While [3H]flupenthixol binding was also present, it could be displaced by spiroperidol indicating that the dopamine receptor was probably of the D2 subtype. Binding of spiroperidol was proportional to the amount of cell culture homogenate, and was saturable. Are these receptors autoreceptors? The toxin 1-methyl-4-phenylpyridine (MPP+) was used to destroy dopaminergic neurons; spiroperidol binding in these cultures was found to be increased, demonstrating that most of these D2 receptors are not autoreceptors.

1-Methyl-4-phenylpyridinium↗
PubMed1986

Nitrous oxide: clinical and electrophysiologic investigation of neurologic complications.

Prolonged exposure to nitrous oxide produces a recognized neurologic syndrome. We report clinical and electrophysiologic studies of nervous system involvement in a 25-year-old student who abused nitrous oxide. He developed signs of a sensorimotor polyneuropathy and of myelopathy. Routine blood studies, CSF examination, and myelogram were normal. Clinical electrophysiologic studies were performed serially. Nerve conduction studies demonstrated reduced amplitude and slowed sensory potentials, and mildly prolonged late responses. Sensory evoked potentials revealed prolonged latency of scalp-evoked potentials from tibial nerve stimulation with normal median nerve values. The foveal visual evoked potential was delayed in the right eye, with normal visual acuity, funduscopic examination, and spatial contrast sensitivity. Repeat electrophysiologic studies demonstrated improvement. Nitrous oxide produces multifocal reversible dysfunction within the nervous system similar to that described in patients with vitamin B12 deficiency.

Adult↗
PubMed1984

Electrophysiological study of mammalian neurons from ventral mesencephalon grown in primary dissociated cell culture.

Mammalian neurons from ventral mesencephalon were grown in primary dissociated cell culture. While dopaminergic neurons were found in culture and used as a marker for this area of the nervous system, our study did not segregate the neurons in terms of their dopaminergic nature. Indeed all of the results were probably from nondopaminergic neurons. Action potentials dependent on sodium and potassium could be elicited from neurons placed in a balanced salt solution. Following blockage of sodium current by tetrodotoxin, and reduction of potassium current by tetraethylammonium and 3-aminopyridine, long-duration action potentials could be elicited by intracellular stimulation. These action potentials were most probably calcium-dependent since they could not be elicited in bathing solution containing manganese, a calcium-conductance blocker.

Action Potentials↗
PubMed1982

Barbiturate reduction of calcium-dependent action potentials: correlation with anesthetic action.

Calcium-dependent action potentials were recorded from mouse spinal cord neurons in primary dissociated cell culture following addition of the potassium channel blockers tetraethylammonium ion and 3-aminopyridine. The pharmacologically active barbiturates, pentobarbital and phenobarbital, but not the pharmacologically inactive barbiturate, barbituric acid, produced reversible, dose-dependent reduction of action potential duration at sedative-hypnotic and anesthetic concentrations. Pentobarbital reduced action potential duration at concentrations from 25 to 600 microM (50% reduction at 170 microM) while phenobarbital reduced action potential duration at concentrations from 100 to 5000 microM (50% reduction at 900 microM). The barbiturate concentrations which reduced calcium-dependent action potential duration in this study correlate with reduction of neurotransmitter release from other neuronal preparations and with reduction of calcium uptake by synaptosomes. The results suggest that barbiturates may produce anesthesia in part by reduction of presynaptic calcium entry and consequent reduction of neurotransmitter release in addition to postsynaptic increase of membrane chloride ion conductance. Barbiturate anticonvulsant actions are probably due to postsynaptic augmentation of GABA-mediated inhibition and depression of excitatory synaptic transmission. The major difference between anticonvulsant (phenobarbital) and anesthetic (pentobarbital) barbiturates was the dose-dependency of these actions. Phenobarbital produced postsynaptic modulation of neurotransmitter responses at low concentrations and decreased calcium-dependent action potential duration and increased chloride ion conductance at high concentrations. In contrast, pentobarbital produced all actions at low concentrations. Thus for phenobarbital there would be a large therapeutic index for anticonvulsant activity compared to anesthetic activity but for pentobarbital there would be a small therapeutic index.

Animals↗
PubMed1982

Membrane depolarization and prolongation of calcium-dependent action potentials of mouse neurons in cell culture by two convulsants: bicuculline and penicillin.

The convulsant compounds bicuculline (BICUC) and penicillin (PCN) are antagonists of GABA-mediated synaptic inhibition. In addition, we have shown that BICUC and PCN produced membrane depolarization of mouse spinal cord neurons in primary dissociated cell culture by blocking a potassium conductance, a non-synaptic direct effect. Both compounds also prolonged calcium-dependent action potentials of mouse dorsal root ganglion and spinal cord neurons in cell culture. Thus, BICUC and PCN had both synaptic and non-synaptic actions. The possibility that both synaptic and non-synaptic actions of BICUC and PCN are involved in their convulsant mechanism of action is discussed.

Action Potentials↗
PubMed1981

Calcium-dependent action potentials in mouse spinal cord neurons in cell culture.

Following blockade of membrane potassium conductance with tetraethylammonium ions or 3-aminopyridine, long-duration action potentials were recorded from mouse spinal cord neurons in primary dissociated cell culture. The action potentials were calcium-dependent since they: (1) were not blocked by the sodium-channel blocker tetrodotoxin, (2) could be recorded in sodium-free, calcium-containing medium (3) could not be evoked in sodium-containing, calcium-free medium, (4) were blocked by calcium channel blockers manganese and cobalt and (5) had overshoot amplitudes that varied linearly with the log of the extracellular calcium concentration (slope of 27.5 mV/decade change in calcium concentration).

Action Potentials↗
PubMed1981

Nortriptyline therapy in elderly patients: dosage prediction from plasma concentration at 24 hours after a single 50 mg dose.

Ten depressed elderly female patients in hospital (mean age 82 years) received a single oral dose of 50 mg nortriptyline prior to commencing treatment with this drug. The nortriptyline concentration in a plasma sample obtained 24 hours afterwards was used to predict the daily dose required to achieve a steady-state concentration within the range of 50-150 micrograms. l-1. The mean daily dose prescribed was 50 mg (range 20-100 mg). These dosage regimes provided a mean observed steady-state nortriptyline concentration of 104 micrograms. l-1, with a range of 76-180 microgram. l-1 (S.D. 30 microgram. l-1). Use of this prediction test can prevent the development of toxic plasma concentrations and enhance the possibility of therapeutic success.

Aged↗
PubMed1981

Bicuculline: a convulsant with synaptic and nonsynaptic actions.

The convulsant bicuculline (BICUC) had both synaptic and nonsynaptic actions on mouse spinal cord neurons in primary dissociated cell culture. BICUC antagonized postsynaptic responses to the inhibitory neurotransmitter GABA (a synaptic action) and produced direct membrane depolarization by blocking a membrane potassium conductance and directly prolonging calcium-dependent action potentials (nonsynaptic actions). In cultured spinal cord neurons, BICUC also produced paroxysmal depolarizing events (PDE), which might be equivalent to in vivo convulsant-induced bursting in spinal cord neurons or paroxysmal depolarizing shifts (PDS) in cortical neurons. Thus, the concentrations of BICUC producing both synaptic and nonsynaptic actions overlapped those producing paroxysmal activity. The results suggest that in addition to antagonism of GABA-mediated synaptic inhibition, direct nonsynaptic actions of BICUC may be required for some neurons to develop PDS.

Action Potentials↗
PubMed1976

Inactivation of monazomycin-induced voltage-dependent conductance in thin lipid membranes. I. Inactivation produced by long chain quaternary ammonium ions.

The voltage-dependent conductance induced in thin lipid membranes by monazomycin undergoes inactivation upon the introduction of quaternary ammonium ions (QA) having a long alkyl chain (e.g. dodecyltrimethylammonium [C12]) to the side containing monazomycin. That is, in response to a step of voltage the conductance rises to a peak and then falls to a much lower steady-state value. We demonstrate that the basis of this phenomenon is the ability of QA to pass through the stimulated membrane and bind to the opposite surface. As a consequence, the surface potential on that side becomes more positive, thus reducing the voltage across the membrane proper and turning off the monazomycin-induced conductance. Because the flux of QA through the membrane increases linearly with conductance, we believe that these ions pass through the monazomycin channels. QA permeability increases with alkyl chain length; remarkably, in spite of its much larger size, C12 is about 150 times more permeant than K+. It appears, therefore, that there is a hydrophobic region of the cahnnel that favors the alkyl chain; we propose that this region is formed by the hydrophobic faces of the monazomycin channels in lipid bilayers to QA inactivation of potassium channels in the squid giant azon, and suggest that there may be a common structural feature for the two channels. It is possible that some of the inactivation phenomena in excitable cells may arise from local field changes not measurable by the recording electrodes.

Anti-Bacterial Agents↗