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Biomedical subjects

M B Weinger

Publications and source records attributed to M B Weinger.

At least 37 records · Page 2Linked to original sources
PubMed1995

Alterations in diaphragm EMG activity during opiate-induced respiratory depression.

While opiate-induced increases in thoracic muscle tone may contribute to impaired ventilation during opiate anesthesia, the effects of high-dose opiates on diaphragm muscle activity have not been elucidated. The effects of the opiate agonist alfentanil (ALF, 500 micrograms/kg subcutaneously) on diaphragm (DIA) and intercostal (IC) electromyographic (EMG) activity in spontaneously ventilating adult rats were studied. EMG segments corresponding to inspiration and expiration were selected using an impedance plethysmographic respiratory waveform. Total EMG activity over a respiratory cycle was significantly greater in the DIA than in the IC. ALF produced a decrease in inspiratory and an increase in expiratory DIA EMG activity. These changes in diaphragm function following ALF were accompanied by significant respiratory depression. The effects of the alpha-2 agonist dexmedetomidine on ALF-induced changes in diaphragm and intercostal EMG activity were also examined. While dexmedetomidine alone had minimal effects on DIA activity, it significantly attenuated the ALF-induced increase in expiratory DIA EMG. The potential etiology and implications of these opiate-induced changes in diaphragm muscle function are discussed.

Alfentanil↗
PubMed1995

Nitrous oxide produces a biphasic effect on opiate-induced muscle rigidity in the rat.

Muscle rigidity is a side effect of potent opiate agonists like alfentanil. Older clinical studies suggested that nitrous oxide (N2O) augments opiate rigidity, but this has never been rigorously examined in an animal model. Sixty-two Wistar rats were placed in a Plexiglas box through which fresh gas flowed at 4 l/min. Muscle rigidity was assessed using gastrocnemius electromyographic (EMG) activity. Rats were exposed to either 60% N2O in O2 or 100% O2, EMG was measured for 10 min, alfentanil (0, 50, 175, or 350 micrograms/kg) was administered intravenously, and data were collected for 45 min. Alfentanil produced a dose-dependent increase in EMG activity in both O2 and N2O groups (p < 0.001). At 1 min postalfentanil, N2O caused significantly more rigidity than 100% O2 (p < 0.001). However, beginning at 5 min, N2O attenuated both the magnitude and the duration of rigidity. Study of a separate group of animals breathing 30% O2 demonstrated that N2O's attenuating effect on alfentanil rigidity was not due to reduced inspired oxygen concentration. These results are described by a theoretical model of the pharmacodynamic interactions of alfentanil and nitrous oxide.

Alfentanil↗
PubMed1995

Dexmedetomidine does not modify the neuromuscular blocking action of vecuronium in the anaesthetized rat.

Dexmedetomidine is a new alpha 2 adrenergic agonist anaesthetic adjuvant. In animal studies, dexmedetomidine produced muscle flaccidity and prevented opioid-induced muscle rigidity, apparently via a central mechanism. The effect of dexmedetomidine on the neuromuscular junction or on non-depolarizing neuromuscular block during anaesthesia has not been reported. We have studied in the anaesthesized rat, the effects of dexmedetomidine on vecuronium-induced twitch depression. Wistar rats (n = 35) were anaesthetized and their lungs ventilated to maintain normocapnia. An infusion of vecuronium of 2.3 (SEM 0.1) micrograms kg-1 min-1 produced a stable twitch height (T1) depression of the tibial nerve of 53 (2)% of control in all groups. Rats were allocated randomly to receive either saline or dexmedetomidine 10, 30 or 100 micrograms kg-1 i.v. and T1 height was measured continuously for 60 min. Dexmedetomidine did not significantly affect T1 height during the first 30 min of infusion. At later times there were minor differences between groups. With cessation of the infusion of vecuronium, T1 height recovered rapidly to normal in all groups. These data suggest that the neuromuscular blocking properties of dexmedetomidine are unlikely to be produced by action at the neuromuscular junction.

Action Potentials↗
PubMed1995

Visual display format affects the ability of anesthesiologists to detect acute physiologic changes. A laboratory study employing a clinical display simulator.

BACKGROUND: Anesthesiologists use data presented on visual displays to monitor patients' physiologic status. Although studies in nonmedical fields have suggested differential effects on performance among display formats, few studies have examined the effect of display format on anesthesiologist monitoring performance. METHODS: A computer-based clinical display simulator was developed to evaluate the efficacy of three currently used display formats (numeric, histogram, or polygon displays) in a partial-task laboratory simulation. The subjects' task consisted solely of detecting any changes in the values of the physiologic variables depicted on a simulated clinical display. Response latency and accuracy were used as measures of performance. RESULTS: Thirteen anesthesia residents and five nonmedical volunteers, were enrolled as subjects. Use of either the histogram or polygon displays significantly improved response latencies and allowed greater accuracy compared with the numeric display in the anesthesia residents. Neither response latency nor accuracy improved with additional exposure to these displays. In contrast, display format did not significantly affect response latency or accuracy in the nonmedical volunteers. CONCLUSIONS: The results of this study suggest that graphic displays may enhance the detection of acute changes in patient physiologic status during anesthesia administration. This research also demonstrates the importance of assessing performance on clinical devices by studying actual users rather than random subjects. Further research is required to elucidate the display elements and characteristics that best support different aspects of the anesthesiologist's monitoring tasks.

Adult↗
PubMed1994

Atipamezole, an alpha 2 antagonist, augments opiate-induced muscle rigidity in the rat.

Atipamezole is a new, highly selective alpha2-adrenoceptor antagonist currently undergoing clinical trials as an antagonist for dexmedetomidine, a potent alpha2 agonist with sedative and analgesic properties. It has previously been demonstrated that dexmedetomidine, acting at central alpha2 adrenoceptors, antagonizes opiate-induced muscle rigidity. However, the role of endogenous alpha2-adrenergic systems in opiate-induced rigidity remains to be elucidated. The present study was designed to assess the effects of atipamezole on basal muscle tone and on alfentanil-induced muscle rigidity in the rat. Muscle tone was measured using gastrocnemius electromyography (EMG). After a 15-min baseline, saline or atipamezole (0.3 or 1.0 mg/kg) was administered, and 10 min later, saline or alfentanil (50, 150, or 300 micrograms/kg) was injected subcutaneously. Data were collected for an additional 60 min. Atipamezole (1.0 mg/kg) pretreatment (in the absence of alfentanil) produced a small increase in tonic EMG activity when compared with saline pretreatment. After saline pretreatment, significant muscle rigidity occurred in the two highest alfentanil dose groups. Atipamezole (0.3 and 1.0 mg/kg) augmented alfentanil-induced muscle rigidity. The ability of the alpha2 antagonist to potentiate both basal muscle tone and alfentanil-induced rigidity suggests that endogenous adrenergic activity and/or direct alpha2-adrenoceptor interaction with opioid receptors mediate opiate-induced muscle rigidity. These findings may be of clinical as well as basic neuropharmacological interest.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed1994

An objective methodology for task analysis and workload assessment in anesthesia providers.

BACKGROUND: Administering anesthesia is a complex task in which either human or equipment failure can have disastrous consequences. An improved understanding of the nature of the anesthesiologist's job could provide a more rational basis for improvements in provider training as well as the design of anesthesia equipment. The objective of this study was to develop a set of techniques to evaluate anesthesiologist performance and to determine what information could be obtained from performing real-time task assessment and workload analysis tests in the operating room. METHODS: The methodology used included time-motion analysis, secondary task probing, and subjective workload assessment. The time-motion data was subjected to subsequent analysis to generate quantitative measures such as task duration (time spent focused on an individual task) and task density (the number of tasks initiated per minute). The latency of response to a "vigilance light" was used as a secondary task probe. Finally, both the observer and the subjects themselves scored workload at 10-15-min intervals throughout the case. Two groups of anesthesia providers performing general endotracheal anesthesia for simple ambulatory surgical cases (1-4 h duration) were examined using this methodology. In the first group, 3rd-yr anesthesia residents and experienced certified registered nurse anesthetists (n = 11) performed cases under limited supervision by an attending anesthesiologist. In the second group, novice residents in their first 8 weeks of training (n = 11) performed similar cases under nearly constant attending supervision. RESULTS: The two groups seemed to manifest different patterns of task behavior, task density, subjective workload, and latency of response to the vigilance task. Response latency to the vigilance task increased at times of increased workload (e.g., during induction of anesthesia). The experienced (less supervised) providers spent significant amounts of time observing the monitors and the surgical field, whereas the novice subjects spent more time conversing with the supervising attending. Despite performing fewer tasks per minute (lower task densities), the novice subjects exhibited longer latencies of response to the vigilance light and increased subjective workload. Novice subjects also had longer task duration values. For example, postintubation, novices focused on their monitors for an average of twice as long as did experienced subjects (13 +/- 2 vs. 7 +/- 1 s) before moving on to another task. CONCLUSIONS: These techniques permitted an objective description of task characteristics, workload, and vigilance in anesthesia personnel under actual work conditions. This methodology could aid in understanding the factors that affect anesthesiologists' performance and may prove useful in assessing the progress of training.

Anesthesiology↗
PubMed1993

Double-blind evaluation of patient-controlled epidural analgesia during labor.

A double-blind randomized study was designed to compare the efficacy of patient-controlled epidural analgesia (PCEA) with continuous epidural analgesia (CEA) with regards to patient satisfaction with analgesia, analgesic efficacy, and local anesthetic usage. After establishing effective epidural analgesia with 8 ml of 0.25% bupivacaine, 39 parturients were randomized to 1 of 2 groups. The CEA group received a continuous infusion of 12 ml/h of 0.125% bupivacaine. The PCEA group received a background infusion of 4 ml/h of 0.125% bupivacaine and were able to self-administer additional boluses of 3 ml of 0.25% bupivacaine every 10 min up to 15 ml/h. In both groups, when patients complained of inadequate analgesia, supplemental doses of 5 ml of 0.25% bupivacaine were administered by a physician. The 2 groups were similar in age, height, weight, gravidity, labor duration, motor block, sensory block, and infant Apgar scores. The 2 groups also did not differ significantly in terms of patient satisfaction, pain assessment, or total drug usage. However, the PCEA group required significantly fewer supplemental doses (15%) compared with the CEA group (40%). The decreased need for supplemental doses in the PCEA group may suggest a potential advantage in consistency of analgesia and possibly decreased man-power needs.

Journal Article↗
PubMed1993

Effect of antagonists selective for mu, delta and kappa opioid receptors on the reinforcing effects of heroin in rats.

Antagonists selective for mu, delta and kappa-opioid receptors were evaluated for their effects on responding maintained by i.v. injections of heroin (60.0 micrograms/kg/injection) in rats during daily 3-hr sessions. Under base-line conditions, rats self-administered 10 to 20 heroin injections during each session, and injections were separated by relatively constant interinjection intervals of about 10 to 20 min. The mu-selective antagonist beta-funaltrexamine (beta-FNA; 5.0-20.0 mg/kg, s.c.) produced a dose-dependent increase in responding for heroin, with some doses of beta-FNA producing an extinction-like pattern of responding. These results were qualitatively similar to the effect obtained by lowering the unit dose per injection of heroin. The mu 1-selective antagonist naloxonazine (NXZ; 7.5-30.0 mg/kg, i.v.) and the delta-selective antagonist naltrindole (1.0-17.0 mg/kg) also produced dose-dependent increases in heroin self-administration, but neither naloxonazine nor naltrindole produced extinction-like patterns of responding. The kappa-selective antagonist nor-binaltorphimine (nor-BNI; 5.0-10.0 mg/kg, s.c.) had no effect on heroin self-administration. These results indicate that mu receptors play an important role in mediating the reinforcing effects of heroin in the rat. Delta and mu 1 receptors, but not kappa receptors, may also be involved.

Animals↗
PubMed1993

Antagonist effects of beta-funaltrexamine and naloxonazine on alfentanil-induced antinociception and muscle rigidity in the rat.

Alfentanil is a potent and short-acting mu opioid agonist that produces both antinociceptive effects and muscle rigidity. In the present study, the susceptibility of alfentanil-induced antinociception and rigidity to antagonism by the selective mu antagonist beta-funaltrexamine and the selective mu-1 antagonist naloxonazine was examined. Alfentanil (37.7-150.0 micrograms/kg) produced a dose-dependent increase both in antinociception as measured by the warm-water tail-dip assay and in rigidity as measured by electromyographic recording of the gastrocnemius muscle. Both beta-funaltrexamine (10.0 and 20.0 mg/kg) and naloxonazine (7.5 and 15.0 mg/kg) produced dose-dependent and parallel rightward shifts in the alfentanil dose-effect curves for both antinociception and rigidity. Furthermore, the alfentanil dose-effect curves for antinociception and rigidity were shifted to the right to a similar degree by any given pretreatment. These results suggest that alfentanil-induced antinociception in the warm-water tail-dip test and rigidity are mediated by pharmacologically similar populations of opioid receptors. More specifically, these results suggest that mu-1 opioid receptors mediate both alfentanil-induced antinociception and rigidity.

Alfentanil↗
PubMed1992

A widely unappreciated cause of failure of an automatic noninvasive blood pressure monitor.

Many anesthesiologists have come to depend on automatic noninvasive blood pressure monitoring to obtain blood pressure (BP) readings. A case is presented in which, during a critical phase of the anesthetic, an automatic noninvasive blood pressure (ANIBP) device not only failed to provide meaningful clinical data but, in fact, gave an error message that was misleading. At the time of the message, the patient was noted to be in ventricular trigeminy at a rate of 92 beats/min. It appears that the repetitive beat-to-beat fall in blood pressure due to the dysrhythmia "fooled" the automatic noninvasive blood pressure device's software algorithm into believing that there was an air leak in the system. Thus, in addition to pointing out an unappreciated and potentially troubling device-related critical event, the present case demonstrates the importance of good human factors design for medical devices used in the critical care setting. In particular, the issue is raised of how medical devices should deal with uncertain or potentially misleading data.

Aged↗
PubMed1992

Elucidation of dose-effect relationships for different opiate effects using alfentanil in the spontaneously ventilating rat.

In addition to producing antinociception and mild sedation, opiates diminish spontaneous movement and produce muscle rigidity. Examination of the relationship between different opiate effects may lead to a better understanding of the mechanism and sites of action of opiate anesthesia. Previous studies have compared the dose-effect relationships for morphine and fentanyl between antinociception and loss of righting reflex. However, neither muscle rigidity nor lack of spontaneous movement (as measured by catalepsy) has been fully examined or directly compared with either antinociception or loss of righting reflex. This study, therefore, compared five clinically relevant opiate endpoints (antinociception, muscle rigidity, catalepsy, loss of righting reflex, and respiratory depression) using the mu-selective agonist alfentanil in the spontaneously ventilating rat. Rats were randomized to receive alfentanil (0-500 micrograms/kg) subcutaneously. For muscle rigidity, 59 rats had electromyographic activity measured with percutaneous hindlimb electrodes. After alfentanil injection, electromyographic data were recorded for 60 min. For antinociception and catalepsy, 49 rats were studied for 120 min after alfentanil. Catalepsy was measured from the time the rat's forelimbs were placed on a 10-cm-high bar until either limb was removed. Antinociception was studied by measuring tail-flick response to hot (55 degrees C) water. For righting reflex, 40 rats were studied for 120 min. Alfentanil-induced respiratory depression was assessed in 40 rats with indwelling tail arterial catheters. Alfentanil was administered after baseline arterial blood gas measurements, and then additional samples were obtained for 45 min. For each effect, data were converted into quantal responses and were then transformed to probit-log dose-response curves for analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Alfentanil↗
PubMed1991

Brain sites mediating opiate-induced muscle rigidity in the rat: methylnaloxonium mapping study.

Previous work has demonstrated that direct injections of methylnaloxonium (MN), a hydrophilic quaternary opiate antagonist, in the area of the nucleus raphe pontis (RPn) significantly attenuated alfentanil-induced muscle rigidity in the rat. To extend these observations and to explore further the regions important for opiate-induced rigidity, rats were implanted with chronic guide cannulae aimed at discrete brain sites with an emphasis on the region from the periaqueductal grey (PAG) to the RPn. Each animal was pretreated by a blinded observer with an intracerebral injection of MN (125 ng total dose) or saline, and electromyographic (EMG) activity was recorded from the gastrocnemius muscle. Alfentanil (ALF; 500 micrograms/kg) was then administered subcutaneously and the magnitude of tonic EMG activity was assessed as a measure of hindlimb rigidity. The administration of MN into the pontine raphe nucleus (RPn) and also into the more lateral nucleus reticularis tegmenti pontis significantly attenuated ALF rigidity compared with saline-pretreated controls. Within the midbrain, MN selectively reversed rigidity when injected into the periaqueductal grey (PAG). The dorsal PAG appeared to be a more important site than the ventral PAG. There was no significant effect on ALF rigidity of MN injections into brain regions between the ventral PAG and the RPn while MN injections into the deep layers of the superior colliculus, lateral to the dorsal PAG, partially attenuated ALF rigidity. In contrast, rigidity was not consistently reversed after MN injections into the basal ganglia, the dorsal superior colliculus, or the region of the decussation of the dorsal tegmentum. This study provides strong evidence that nuclei of the reticular formation, specifically the PAG, raphe pontis, and reticularis tegmenti pontis that are known to play a role in other opioid-mediated behaviors, are important in opiate-induced muscle rigidity in the rat. These results could have implications for the prevention of this undesirable effect of high-dose opiate administration.

Alfentanil↗
PubMed1991

Methylnaloxonium diffuses out of the rat brain more slowly than naloxone after direct intracerebral injection.

The value of intracerebral injections as a means of relating brain structure and function is dependent on the degree of site specificity of the injection. The purpose of this study was to compare the distribution over time of naloxone and its quaternary derivative, methylnaloxonium, after intracerebral microinjection. One microliter of tritiated naloxone (NAL) or methylnaloxonium (MN 10.0 ng, 12.8 nCi for both drugs) was infused directly into the n. raphe pontis. Each animal was then decapitated at a specific time (2.5, 5.0, 15, 30, or 60 min), the brain was removed and dissected into hindbrain, cerebellum, midbrain and cortex. Tritium beta emissions of brain homogenates were measured 1 day later, MN remained better localized to the injection site than did the same volume of the more lipophilic NAL. Within 15 minutes, less than 5% of the NAL remained in the hindbrain compared with nearly 40% of the MN. These results that MN may be a better probe than NAL for investigating the relationship of opioid receptor anatomy and function, particularly for dependent variables requiring sustained time courses.

Animals↗