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Biomedical subjects

J C Keifer

Publications and source records attributed to J C Keifer.

12 recordsLinked to original sources
PubMed2005

The desaturation response time of finger pulse oximeters during mild hypothermia.

Pulse oximeters may delay displaying the correct oxygen saturation during the onset of hypoxia. We investigated the desaturation response times of pulse oximeter sensors (forehead, ear and finger) during vasoconstriction due to mild hypothermia and vasodilation caused by glyceryl trinitrate. Ten healthy male volunteers were given three hypoxic challenges of 3 min duration under differing experimental conditions. Mild hypothermia increased the mean response time of finger oximeters from 130 to 215 s. Glyceryl trinitrate partly offset this effect by reducing the response time from 215 to 187 s. In contrast, the response times of the forehead and ear oximeters were unaffected by mild hypothermia, but the difference between head and finger oximeters was highly significant (p < 0.0001). The results suggest that the head oximeters provide a better monitoring site for pulse oximeters during mild hypothermia.

Adult↗
PubMed2001

Postoperative sleep disturbance: influences of opioids and pain in humans.

STUDY OBJECTIVES: To test the hypothesis that opioids and pain contribute independently to postoperative sleep disturbance, 10 women undergoing surgery requiring a low abdominal incision for treatment of benign gynecologic conditions were randomized to receive either epidural opioid (fentanyl) (n=6) or epidural local anesthetic (bupivacaine) (n=4) for intraoperative and postoperative analgesia. DESIGN: N/A. SETTING: N/A. PATIENTS OR PARTICIPANTS: N/A. INTERVENTIONS: N/A. MEASUREMENTS: Polysomnography was performed in a standard patient room on the preoperative and first three postoperative nights. Pain at rest and with coughing was evaluated using a visual-analogue pain scale each evening and morning. RESULTS: On the first postoperative night, rapid eye movement (REM) sleep was abolished in all patients. On the third postoperative night, the mean +/- SE REM sleep time increased significantly (p=.003) to 9.8% +/- 3.1% in the fentanyl group, and 12.9% +/- 3.8% in the bupivacaine group. Conversely, light non-REM (NREM) sleep (%stage 1 + %stage 2) was higher on the first postoperative night and significantly lower on the third postoperative night (p=0.011). Between group comparison revealed only that the mean % slow-wave sleep (SWS) in the fentanyl group (6.0%, 2.0%, and 14.7%) was different from the bupivacaine group (7.8%, 9.1%, and 10.6%) in the postoperative period after adjusting for the preoperative night % SWS (p=0.021). Pain was well controlled in all patients, but was slightly better controlled in the fentanyl group than in the bupivacaine group on postoperative night 2 (p=0.024). There was no statistically significant association between pain score and any polysomnographically defined stage. CONCLUSION: Postoperative patients suffer a profound sleep disturbance even when opioids are avoided and pain is well controlled.

Adult↗
PubMed2000

Melatonin secretion after surgery.

Sleep disturbance is common postoperatively. We examined whether melatonin concentrations were related to this disturbance in seven postoperative patients. Nocturnal concentrations of melatonin were significantly (p=0.005) lower on the first than on the second or third nights after surgery. This finding raises the possibility that melatonin suppression and associated sleep disturbance might be prevented by melatonin replacement.

Adult↗
PubMed1996

Pontine cholinergic mechanisms modulate the cortical electroencephalographic spindles of halothane anesthesia.

BACKGROUND: Halothane anesthesia causes spindles in the electroencephalogram (EEG), but the cellular and molecular mechanisms generating these spindles remain incompletely understood. The current study tested the hypothesis that halothane-induced EEG spindles are regulated, in part, by pontine cholinergic mechanisms. METHODS: Adult male cats were implanted with EEG electrodes and trained to sleep in the laboratory. Approximately 1 month after surgery, animals were anesthetized with halothane and a microdialysis probe was stereotaxically placed in the medial pontine reticular formation (mPRF). Simultaneous measurements were made of mPRF acetylcholine release and number of cortical EEG spindles during halothane anesthesia and subsequent wakefulness. In additional experiments, carbachol (88 mM) ws microinjected in the the mPRF before halothane anesthesia to determine whether enhanced cholinergic neurotransmission in the MPRF would block the ability of halothane to induce cortical EEG spindles. RESULTS: During wakefulness, mPRF acetylcholine release averaged 0.43 pmol/10 min of dialysis. Halothane at 1 minimum alveolar concentration decreased acetylcholine release (0.25 pmol/10 min) while significantly increasing the number of cortical EEG spindles. Cortical EEG spindles caused by 1 minimum alveolar concentration halothane were not significantly different in waveform, amplitude, or number from the EEG spindles of nonrapid eye movement sleep. Microinjection of carbachol into the mPRF before halothane administration caused a significant reduction in number of halothane-induced EEG spindles. CONCLUSIONS: Laterodorsal and pedunculopontine tegmental neurons, which provide cholinergic input to the mPRF, play a causal role in generating the EEG spindles of halothane anesthesia.

Acetylcholine↗
PubMed1995

Opioid inhibition of rapid eye movement sleep by a specific mu receptor agonist.

Patients receiving opioids report feeling sleepy, but opioids actually inhibit the rapid eye movement phase of sleep (REM). Inhibition of REM sleep is followed by a rebound increase in REM sleep associated with cardiopulmonary complications. The medial pontine reticular formation (mPRF) is a brain region from which morphine can inhibit REM sleep. The present study tested the hypothesis that specific subtypes of opioid receptors within the mPRF mediate inhibition of REM sleep. Synthetic opioid agonists selective for mu, delta and kappa subtypes were microinjected into the mPRF of four awake cats and polygraphic recordings of sleep and breathing were obtained. An enkephalinase inhibitor was microinjected into the mPRF to assess the contribution of endogenous opioids to the control of sleep and breathing. Only the mu agonist significantly inhibited REM sleep, and no opioid depressed breathing. These results demonstrate that opioid-induced REM sleep inhibition is mediated by mu receptor subtypes in the mPRF.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1994

Halothane decreases pontine acetylcholine release and increases EEG spindles.

This study tested the hypothesis that halothane anesthesia would cause decreased acetylcholine (ACh) release within the medial pontine reticular formation (mPRF). ACh was collected by microdialysis and measured by high pressure liquid chromatography during wakefulness and during halothane-induced anesthesia. The electroencephalogram (EEG) showed that spindles were a reliable indicator of anesthetic depth. There was a statistically significant disease in ACh release during halothane anesthesia compared with ACh release during wakefulness. Spindles always disappeared during noxious stimulation and during emergence from anesthesia when pontine ACh levels began to increase. These results are consistent with previous data concerning brain stem cholinergic influences on thalamocortical spindle generation, and suggest that similar mechanisms generate cortical spindles during natural sleep and halothane anesthesia.

Acetylcholine↗
PubMed1993

Microdialysis of the pontine reticular formation reveals inhibition of acetylcholine release by morphine.

BACKGROUND: Systemically administered morphine inhibits rapid eye movement (REM) sleep; however, the neuronal mechanisms through which morphine disrupts REM sleep remain poorly understood. Recently, the authors have shown that morphine-mediated REM sleep inhibition is localized to a specific region of the pontine reticular formation: the gigantocellular tegmental field (FTG). Because cholinergic neurotransmission in the FTG is known to play a role in REM sleep generation, the present study examined the hypothesis that systemically administered morphine would cause decreased acetylcholine release in the FTG. METHODS: Microdialysis probes were stereotaxically positioned in the FTG of six barbiturate-anesthetized cats to measure acetylcholine release. Cholinergic input to the FTG arises from the laterodorsal (LDT) and pedunculopontine tegmental (PPT) brain stem nuclei. By electrically stimulating the LDT and PPT, it was possible to measure stimulation-evoked acetylcholine release in the FTG. Morphine sulfate (MSO4) was administered intravenously (500 micrograms.kg-1). High performance liquid chromatography with electrochemical detection was used to measure stimulation-evoked acetylcholine release in the FTG before and after the systemic administration of morphine sulfate. RESULTS: Acetylcholine release in the pontine FTG was depressed significantly (P < 0.01) by systemic morphine sulfate. Acetylcholine release without electrical stimulation of the LDT and PPT averaged 0.6 +/- 0.18 (mean +/- SD) pmol/10 min of dialysis. Before morphine sulfate was administered, electrical stimulation of cholinergic LDT and PPT neurons increased acetylcholine release within the FTG to 1.9 +/- 0.76 pmol/10 min. After morphine sulfate was administered, there was a 37% decrease in acetylcholine release within the FTG to average values of 1.2 +/- 0.63 pmol/10 min. There was no significant effect of morphine sulfate on spontaneous acetylcholine release in the absence of LDT and PPT stimulation. CONCLUSIONS: Because FTG levels of acetylcholine release increase during REM sleep, the present results are consistent with the hypothesis that diminished acetylcholine release in the pontine FTG comprises one mechanism by which morphine inhibits REM sleep.

Acetylcholine↗
PubMed1992

Sleep disruption and increased apneas after pontine microinjection of morphine.

The medial pontine reticular formation (mPRF) is a cholinoceptive brain stem region known to play a key role in regulating rapid eye movement (REM) sleep and state-dependent ventilatory depression. Numerous lines of evidence have shown that opioids inhibit both cholinergic neurotransmission and REM sleep. The present study examined the hypothesis that morphine applied to the cholinoceptive mPRF would inhibit REM sleep and alter ventilation. In six cats, guide cannulas were chronically implanted to permit pontine microinjection of morphine sulfate, naloxone, and the cholinergic agonist carbachol. After each mPRF microinjection, 2-h polygraphic recordings quantified respiratory frequency and the percent of time spent in states of wakefulness, non-REM sleep, and REM sleep. The results show that mPRF administration of morphine significantly inhibited REM sleep and that this REM sleep inhibitory effect was blocked by pretreating the mPRF with naloxone. Apneic episodes were increased after injection of morphine alone, and the apneas were decreased by the cholinergic agonist carbachol. The results also demonstrated that the ability of microinjected morphine to inhibit REM sleep was dose-dependent and site-dependent. Considered together, the site-localization, pharmacologic blocking, and dose-response data support the hypothesis that specific regions of the mPRF can contribute to the long-recognized ability of morphine to inhibit REM sleep and alter respiratory control.

Animals↗
PubMed1992

Heparin resistance after intraoperative platelet-rich plasma harvesting.

Records of anticoagulation for cardiopulmonary bypass from 58 patients who underwent elective coronary artery revascularization were analyzed to determine whether the harvesting of autologous platelet-rich plasma produces heparin resistance. The effect of preoperative heparin therapy on anticoagulation for cardiopulmonary bypass after harvesting of platelet-rich plasma was also evaluated. Patients were grouped by presence of preoperative heparin therapy and type of blood component harvested before cardiopulmonary bypass, including platelet-rich plasma, autologous whole blood, both, or neither. The dose of heparin required to initiate and to maintain anticoagulation for cardiopulmonary bypass was determined for each patient, and the groups were compared by two-way analysis of variance. Significantly more heparin was required to maintain anticoagulation for cardiopulmonary bypass in the platelet-rich plasma group than in the groups receiving autologous whole blood or no blood products. More heparin was also required to initiate and to maintain anticoagulation for cardiopulmonary bypass after preoperative heparin therapy. These results reinforce the concept that anticoagulation during cardiopulmonary bypass must be carefully monitored, and increased vigilance may be warranted in patients after harvesting of platelet-rich plasma.

Analysis of Variance↗
PubMed1983

Comparison of three methods for anaerobe identification.

In this study we evaluated the ability of three commercial methods, API 20A (Analytab Products, Plainview, N.Y.), Minitek (BBL Microbiology Systems, Cockeysville, Md.), and Anaerobe-Tek (Flow Laboratories, Inc., McLean, Va.), to accurately identify 165 recent clinical and 38 stock isolates of anaerobic bacteria without supplemental tests or gas-liquid chromatography. Strains included 89 Bacteroides spp., 12 fusobacteria, 10 gram-positive, nonsporing rods, 43 Clostridium spp., 15 Streptococcus intermedius, 18 peptococci, 6 peptostreptococci, 3 Staphylococcus saccharolyticus, and 7 Veillonella spp. The methods used were those of manufacturers, without supplemental tests. API 20A correctly identified 70.0% of strains to species and 6.4% to genus only, with 17.2% as part of a spectrum of identifications and 6.4% incorrect. Minitek, according to the current code book, yielded 69.5% correct identifications to species, 16.8% spectrum identifications, and 13.8% incorrect. Anaerobe-Tek correctly identified 64.0% of strains to species, 21.2% spectrum identifications, and 14.8% incorrect. Thirteen strains were misidentified by API 20A, 28 were misidentified by Minitek, and 30 were misidentified by Anaerobe-Tek. For laboratories without gas-liquid chromatography support and where identification of clinically significant Bacteroides fragilis and Clostridium perfringens is desired, any of the three systems would provide accurate information. For more extensive anaerobe identification, including the less frequently isolated, more unusual organisms, API 20A and Minitek are preferred at this time. All systems have identification schemes associated with a percentage of misidentifications, the most recently introduced Anaerobe-Tek system being associated with the highest error rate.

Bacteria, Anaerobic↗