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Biomedical subjects

A D Finck

Publications and source records attributed to A D Finck.

At least 19 recordsLinked to original sources
PubMed1996

Isolated cerebral hypothermia by single carotid artery perfusion of extracorporeally cooled blood in baboons.

OBJECTIVE: Hypothermia has been demonstrated to protect the brain from ischemic or traumatic injury. Previous efforts to induce cerebral hypothermia have relied on techniques requiring total body cooling that have resulted in serious cardiovascular derangements. A technique to selectively cool the brain, without systemic hypothermia, may have applications for the treatment of neurological disease. METHODS: After induction of general anesthesia in 12 baboons, the right common carotid artery and ipsilateral femoral artery were each occlusively cannulated and joined to a centrifugal pump. In a closed-circuit system, blood was continually withdrawn from the femoral artery, cooled by water bath, and infused through the common carotid artery with its external branches occluded. Pump flow was varied so that right carotid pressure approximated systemic blood pressure. In six animals, perfusate was cooled to decrease right cerebral temperature to < 19 degrees C for 30 minutes. In six animals, right cerebral temperature was decreased to < 25 degrees C for 3 hours. In those six animals, 133Xe was injected into the right carotid artery before, during, and after hypothermia. Peak radioactivity and washout curves were recorded from bilateral cranial detectors. Systemic warming was accomplished by convective air and warm water blankets. Esophageal, rectal, and bilateral cerebral temperatures were continuously recorded. RESULTS: In animals cooled to < 19 degrees C, right cerebral temperature decreased from 34 degrees C to 18.5 +/- 1.1 degrees C (mean +/- standard deviation), P < 0.01, in 26 +/- 13 minutes. Simultaneously, left cerebral temperature decreased to 20.7 +/- 1.6 degrees C. During 30 minutes of stable cerebral hypothermia, esophageal temperature decreased from 35.1 +/- 2.3 degrees C to 34.2 +/- 2.2 degrees C, P < 0.05. In animals cooled to < 25 degrees C, right cerebral temperature decreased from 34 degrees C to 24.5 +/- 0.6 degrees C in 12.0 +/- 6.0 minutes, P < 0.01. Simultaneously, left cerebral temperature decreased to 26.3 +/- 4.8 degrees C. After 3 hours of stable cerebral hypothermia, esophageal temperature was 34.4 +/- 0.5 degrees C, P < 0.05. Right hemispheric cerebral blood flow decreased during hypothermia (26 +/- 16 ml/min/100 g) compared to values before and after hypothermia (63 +/- 29 and 51 +/- 34 ml/min/100 g, respectively; P < 0.05). Furthermore, hypothermic perfusion resulted in a proportionally increased radioactivity peak detected in the left cerebral hemisphere after right carotid artery injection of 133Xe (0.8 +/- 0.2:1, left:right) compared to normothermia before and after hypothermia (0.3 +/- 2 and 0.3 +/- 1, respectively; P < 0.05). Normal heart rhythm, systemic arterial blood pressure, and arterial blood gas values were preserved during hypothermia in all animals. CONCLUSION: Bilateral cerebral deep or moderate hypothermia can be induced by selective perfusion of a single internal carotid artery, with minimal systemic cooling and without cardiovascular instability. This global brain hypothermia results from profoundly altered collateral cerebral circulation during artificial hypothermic perfusion. This technique may have clinical applications for neurosurgery, stroke, or traumatic brain injury.

Animals↗
PubMed1996

Selective cerebral hypothermia by means of transfemoral internal carotid artery catheterization.

Global cerebral hypothermia of 24 degrees C was induced without systemic cooling by means of selective hypothermic perfusion of a single internal carotid artery in four baboons. With a closed-circuit pump system, blood was withdrawn from the femoral artery, cooled in a water bath, and infused through an internal carotid artery catheter, which was positioned with fluoroscopic guidance. This endovascular technique may have applications in the treatment of neurologic disease in humans.

Animals↗
PubMed1995

Nitrous oxide selectively releases Met5-enkephalin and Met5-enkephalin-Arg6-Phe7 into canine third ventricular cerebrospinal fluid.

The role of the opioid receptor-endogenous opioid peptide system in mediating analgesia induced by nitrous oxide has been a controversial subject. Most previous studies provided only indirect evidence either to support or refute the involvement of opioid receptors and/or endogenous opioid peptides. To provide more direct evidence, we measured concentrations of five naturally occurring endogenous opioid peptides in third ventricular cerebrospinal fluid from eight acclimated dogs with chronically implanted ventricular catheters. Paired samples of cerebrospinal fluid were obtained from each animal when breathing room air or 66-75 vol% nitrous oxide in oxygen through a face mask. Endogenous opioid peptides were physically separated using reversed phase high-performance liquid chromatography and quantified using radioimmunoassays. Nitrous oxide inhalation increased cerebrospinal fluid concentrations of met5-enkephalin from a control value of 0.30 +/- 0.07 (mean +/- SEM, n = 8) to 42.4 +/- 8.1 pmol/mL (P = 0.0006). Increases ranged from 28 to more than 400 times the control value. Met5-enkephalin-arg6-phe7 concentrations also increased from 14.5 +/- 2.5 to 57.6 +/- 17.8 pmol/mL (P = 0.018). No significant changes were noted in concentrations of dynorphin A, dynorphin B, or beta-endorphin. These results directly support the hypothesis that nitrous-oxide-induced analgesia involves the proenkephalin-derived family of endogenous opioid peptides.

Analgesia↗
PubMed1989

Fluorescent light interferes with pulse oximetry.

Arterial oxygen saturation (SaO2) values displayed on the pulse oximeter dropped dramatically in 3 children undergoing neurosurgical procedures when a hand-held fluorescent light was used to observe the patients. Pulse rates were unchanged on both the electrocardiograph and pulse oximeter. Electromagnetic interference was excluded as the cause of desaturation. A great deal of energy was emitted by the hand-held light in the 660-nm region, which is one of the wavelengths used by the oximeter. False readings of pulse rate and SaO2 values caused by ambient light could be avoided if oximeter probes were manufactured of black opaque material that does not transmit light or enclosed in an opaque plastic housing.

Child, Preschool↗
PubMed1988

Morphine tolerance decreases the analgesic effects of ketamine in mice.

Previous studies have shown that ketamine interacts with opiate receptors, and it has been suggested that ketamine-induced analgesia is mediated through opiate receptors. If so, ketamine should produce less analgesia in morphine tolerant animals, just as morphine does. To test this hypothesis, the analgesic effects of ketamine were tested in mice implanted with placebo pellets and in mice made tolerant to morphine through implantation of morphine pellets, using the abdominal constriction test. The test consisted of ip injection of 1% acetic acid, which caused stretching of hind limbs and constriction of abdominal muscles, also called writing. The number of writhes was counted for each mouse 10-15 min following acetic acid injection. Morphine pellet implanted mice treated with saline writhed 12.2 +/- 0.8 times (mean +/- SEM), not significantly different from 9.8 +/- 0.9 times seen in placebo pellet implanted mice. Treatment of the animals with ketamine at three doses of 20, 25, and 30 mg/kg, subcutaneously (sc), reduced the number of writhes in the placebo pellet implanted group to 5.8 +/- 0.8, 4.2 +/- 0.7, and 1.3 +/- 0.3, respectively. In the morphine pellet-implanted group, with the same doses of ketamine, the numbers of writhes were 10 +/- 0.9, 9.3 +/- 1.1, and 5.2 +/- 0.9, respectively. Morphine-tolerant animals writhed significantly more at each dose of ketamine, indicating that they were cross tolerant to the analgesic effects of ketamine.

Analgesia↗
PubMed1987

Morphine and codeine are endogenous components of human cerebrospinal fluid.

We have examined cerebrospinal fluid (CSF) from twelve patients who were not on any medication and found them to contain both morphine and codeine in concentrations of 2 to 339 fmol/ml. These are comparable to the concentration of opioid peptides in spinal fluid. Both morphine and codeine are present mainly in conjugated form from which the free alkaloids can be released by acid hydrolysis.

Adolescent↗
PubMed1982

Opiate receptor mediation of ketamine analgesia.

Previous workers have noted that analgesia produced by ketamine can be antagonized by the narcotic antagonist, naloxone. In order to elaborate further the apparent similarity between ketamine- and narcotic-induced analgesia, the authors examined the effects of ketamine in three standard test systems for the opiate receptor. In a radioligand binding assay using 3H-dihydromorphine, ketamine stereospecifically bound to opiate receptors in rat brain homogenate, (+) ketamine being 2-3 times more potent than the (-) enantiomer of ketamine. In a bioassay for the opiate receptor, using the longitudinal muscle-myenteric plexus of the guinea pig ileum, ketamine inhibited the twitch-like muscular contractions, as do narcotics. However, only the inhibitory effects of (+) ketamine, which in this system also was twice as potent as (-) ketamine, could be partially antagonized by naloxone, suggesting that this enantiomer is responsible for the opiate receptor-related effects of ketamine. In vivo, the authors found that ketamine displaces 3H-etorphine, a potent narcotic, from opiate receptors in regional areas of the mouse brain, especially in the thalamic region, but not in the cortex. The results suggest that a significant mechanism of ketamine-induced analgesia is mediated by opiate receptors.

Analgesics↗
PubMed1982

Prolonged exposure to nitrous oxide decreased opiate receptor density in rat brainstem.

Groups of rats were exposed to air or 80 per cent nitrous oxide for 30 min or 18 h, following which the brainstem opiate receptor density and the apparent affinity of these receptors to the radiolabeled agonist, 3H-dihydromorphine, were assayed, Thirty-minute exposure to nitrous oxide did not change opiate receptor characteristics, immediately or 17.5 h later. However, prolonged exposure to nitrous oxide (18 h) decreased the brainstem opiate receptor density approximately 20 per cent, without a change in apparent receptor affinity. These results support the view that nitrous-oxide-induced analgesia results from release of endogenous opiate-like substances. Continued presence of these substances in turn results in a decrease in opiate receptor density and may account for the development of tolerance to the analgesic action of nitrous oxide.

Animals↗
PubMed1979

Tolerance to nitrous oxide analgesia in rats and mice.

The purpose of these experiments was to characterize the nature of tolerance to the analgesic action of nitrous oxide. Analgesia was assessed in rats using a tail-flick latency test and in mice using an abdominal constriction test. Rats and mice were exposed to nitrous oxide, 75 per cent, the balance oxygen, continuously for 16--18 hours. On re-exposure to nitrous oxide 30 min later, these animals were found tolerant to nitrous oxide in that the analgesic response was decreased by at least 50 per cent. Animals tolerant to nitrous oxide were not tolerant to morphine. Morphine (0.25--1.5 mg/kg) produced equal degrees of analgesia in control and nitrous oxide-tolerant mice and rats. In contrast, rats made tolerant to morphine by repeated daily injections of as much as 400 mg/kg subcutaneously or by subcutaneous implantation of morphine pellets (75 mg, twice) showed a decreased analgesic response to nitrous oxide. Thus the cross-tolerance between nitrous oxide and morphine appears unique in that it is unidirectional.

Anesthesia, General↗
PubMed1978

Acetylcholine concentrations and turnover in rat brain structures during anesthesia with halothane, enflurane, and ketamine.

Acetylcholine and choline concentrations in brain structures of rats during anesthesia with halothane (0.7-1.0 per cent inspired), enflurane (2.7-3.0 per cent, inspired) and ketamine (40 mg/kg, iv) were measured by gas chromatography. The turnover rate (biosynthesis) of acetylcholine in vivo was estimated by infusing phosphoryl(Me-14C)choline intravenously, determining specific activities of choline and acetylcholine, and applying principles of steady-state kinetics to compute the fractional rate constant of acetylcholine. Acetylcholine concentrations in brain structures did not change during anesthesia. Halothane decreased the acetylcholine turnover rates in all parts of the brain. Enflurane decreased the acetylcholine turnover rate in the cerebral cortex only, but not in the caudate nucleus, the hippocampus, and the hypothalamic and thalamic regions. During anesthesia with ketamine, acetylcholine turnover rates were reduced in the caudate nucleus and the hippocampus, but not in the cerebral cortex and the hypothalamic and thalamic regions. The results suggest that acetylcholine turnover rate and utilization are related to anesthetic induced electrophysiologic changes in cortical and subcortical structures.

Acetylcholine↗
PubMed1977

Antagonism of general anesthesia by naloxone in the rat.

The effect of naloxone, a narcotic antagonist, on the response of animals to painful stimuli during anesthesia was studied. Rats were anesthetized with cyclopropane, halothane, or enflurane in groups of 12. Following induction, inspired anesthetic concentration was gradually reduced to a point at which 35-60 per cent of animals responded to tail clamping. Thereafter the anesthetic concentration was held constant for 30 minutes. Rats in each group then received saline solution or naloxone, 10mg/kg, given intravenously. The response to tail clamping was retested 5 minutes later. In additional experiments EEG's were recorded from rats anesthesized with one of these anesthetics. After a stable light plane of anesthesia had been attained, each animal was given naloxone, 10 mg/kg, iv, and the EEG recorded for an additional 5 minutes. In the tail-clamping experiments, naloxone approximately doubled the number of rats responding during cyclopropane, halothane, or enflurane anesthesia. The EEG patterns of several animals anesthetized with either cyclopropane or halothane changed to patterns consistent with lighter planes of anesthesia after naloxone administration. That naloxone alters the depth of inhalational anesthesia suggests that anesthetics may release an endogenous morphine-like factor (MLF) in the central nervous system.

Anesthesia, General↗