strychnine and Hypoxia

This article reviews recent studies on the importance of glycine receptors for both the spontaneous and the reflex respiratory modulation of the laryngeal abductors and adductors. Our findings show that strychnine blockade of glycine receptors within the brainstem changes the eupneic three-phase respiratory pattern into two phases. This has major implications for glottal control: (i) the inspiratory glottic abduction and early expiratory adduction were both compromised--a finding mimicked by 5% hypoxia; (ii) closure of the glottis during defensive upper airway reflexes became intermittent and the reflex apnoea reversed to sustained inspiratory discharge. Based on these data, we predict that periods of prolonged hypoxia, such as those that occur during sleep apnoeas, will constrain inspiratory glottic abduction thereby impeding inhalation.

Topics: Airway Resistance; Animals; Brain Stem; Glottis; Humans; Hypoxia; Mammals; Pulmonary Ventilation; Receptors, Glycine; Sleep Apnea Syndromes; Strychnine

Topics: Aminobutyrates; Animals; Choline; Epilepsy; Humans; Hydroxybutyrates; Hypertension; Hypoxia; Mental Disorders; Mice; Nervous System Diseases; Oxygen; Psychopharmacology; Seizures; Sound; Strychnine

In different region of Saudi Arabia Acacia tortilis (Fabaceae) is present but still the medicinal properties of Acacia tortilis have not been studied. However, in Zimbabwe different species of Acacia are already used for the treatment of convulsions and dizziness. In the present study, the anticonvulsant and neuroprotective effects of the Acacia tortilis, were evaluated by using different paradigms. For extraction, the leaves of acacia were blended with distilled water at 40°C and filtered. Two different doses of the extracts (400 and 800mg/kg) were administered in the mice once orally (p.o.) and after 30 min occurrence of seizures (strychnine at the dose of 1mg/kg, i.m.) were monitored. In the present work, acute toxicity and neurotoxicity of the extracts were also assessed by inducing hypoxic stress. The Acacia tortilis leaves AAq (400 and 800 mg/kg) produced a dose dependent increase in time of onset of seizures (197.8±32.4 and 338.2±40.6 respectively) when compared with its respective control (184.0±13.8sec). The anticonvulsant effect after administration of AAq (800mg/kg: 338.2±40.6 sec) was more pronounced than diazepam (290.6±1.38 sec). The high dose (800mg/kg) of AAq administered orally prolonged the onset of convulsion and latencies for death following hypoxic stress. The present study suggested that Acacia have anticonvulsant property and may probably be affecting the inhibitory mechanism of glycine. It is also concluded that chemical constituent of acacia might act on BZD or 5-HT(1A) receptor and decrease the oxidative brain membrane damage process induced by psychological/hypoxic stress. Further experiments will be required to identify the active molecules (s) and their mechanism (s) of action.

Topics: Acacia; Animals; Anticonvulsants; Diazepam; Female; Hypoxia; Male; Mice; Neuroprotective Agents; Plant Extracts; Plant Leaves; Strychnine

The presympathetic neurons in the rostral ventrolateral medulla (RVLM) are considered to be the source of the sympathetic activity, and there is experimental evidence that these cells present intrinsic autodepolarization. There is also evidence that an important respiratory neuronal population located in the RVLM/Bötzinger complex (BötC) corresponds to augmenting expiratory neurons (aug-E), which send projections to the phrenic nucleus in the spinal cord. However, the pacemaker activity of presympathetic neurons and the intrinsic properties of aug-E neurons had not been evaluated in brainstem slices of juvenile rats (postnatal day 35). Chronic intermittent hypoxia (CIH) is a sympathetic-mediated hypertension model, which seems to produce an associated increase in the activity of aug-E neurons. In this study, we evaluated the effects of CIH on the intrinsic properties of RVLM/BötC presympathetic and phrenic nucleus-projecting neurons (aug-E) in brainstem slices of juvenile rats (postnatal day 35). We observed that all presympathetic neurons presented spontaneous action potential firing (n = 18), which was not abolished by ionotropic receptor antagonism. In addition, exposure to 10 days of CIH produced no changes in their intrinsic passive properties, firing pattern or excitability. Most aug-E neurons presented spontaneous firing in control conditions (13 of 15 neurons), and this characteristic was preserved after blocking fast synaptic transmission (12 of 15 neurons), clearly demonstrating their intrinsic pacemaker activity. Chronic intermittent hypoxia also produced no changes in intrinsic passive properties, frequency and pattern of discharge or excitability of the aug-E neurons. The present study shows that: (i) it is possible to record the electrophysiological properties of RVLM/BötC presympathetic and aug-E neurons in brainstem slices from juvenile rats; (ii) these neurons present characteristics of intrinsic pacemakers; and (iii) their intrinsic properties were not altered by chronic intermittent hypoxia.

Topics: 2-Amino-5-phosphonovalerate; Action Potentials; Animals; Bicuculline; Cervical Cord; Hypoxia; Male; Medulla Oblongata; Membrane Potentials; Neurons; Patch-Clamp Techniques; Quinoxalines; Rats, Wistar; Spinal Cord; Strychnine; Sympathetic Nervous System

In this letter, (R)-muscone and (S)-muscone were prepared by optical resolution of dl-muscone using N,N'-dibenzyl-l-tartaramide or N,N'-dibenzyl-d-tartaramide, according to the method reported by Kunihiko Takabe. But we separated the diastereomers using EtOH instead of MeOH in the recrystallization step to get the goal product with higher optical purity and yield. The regulatory effect of muscone and its enantiomer on the neural system showed that they could prolong mouse hypoxia tolerance and dose-dependently enhance mouse spinal cord stimulation induced by strychnine nitrate. (R)-muscone and (S)-muscone had a synergistic action on shortening sleep time induced by sodium pentobarbital in mice.

Topics: Animals; Cycloparaffins; Dose-Response Relationship, Drug; Hippocampus; Hypoxia; Mice; Molecular Structure; Nervous System; Neurons; Phenobarbital; Stereoisomerism; Strychnine

Hypoxia elevates splanchnic sympathetic nerve activity (SNA) with differential effects during inspiration and expiration by unresolved central mechanisms. We examined the hypothesis that cardiovascular-related neurones in the caudal ventrolateral medulla (CVLM) contribute to the complex sympathetic response to hypoxia. In chloralose-anaesthetized, ventilated, vagotomized rats, acute hypoxia (10% O2, 60 s) evoked an increase in SNA (103 +/- 12%) that was characterized by a decrease in activity during early inspiration followed by a prominent rise during expiration. Some recorded baro-activated CVLM neurones (n = 13) were activated by hypoxia, and most of these neurones displayed peak activity during inspiration that was enhanced during hypoxia. In contrast, other baro-activated CVLM neurones were inhibited during hypoxia (n = 6), and most of these neurones showed peak activity during expiration prior to the onset of hypoxia. Microinjection of the glutamate antagonist kynurenate into the CVLM eliminated the respiratory-related fluctuations in SNA during hypoxia and exaggerated the magnitude of the sympathetic response. In contrast, microinjection of a GABA(A) antagonist (bicuculline or gabazine) into the CVLM dramatically attenuated the sympathetic response to hypoxia. These data suggest the response to hypoxia in baro-activated CVLM neurones is related to their basal pattern of respiratory-related activity, and changes in the activity of these neurones is consistent with a contribution to the respiratory-related sympathetic responses to hypoxia. Furthermore, both glutamate and GABA in the CVLM contribute to the complex sympathetic response to acute hypoxia.

Topics: Animals; Bicuculline; Blood Pressure; Excitatory Amino Acid Antagonists; GABA Agonists; GABA-A Receptor Antagonists; Glutamic Acid; Hypoxia; Kynurenic Acid; Male; Medulla Oblongata; Models, Neurological; Muscimol; Neurons; Phrenic Nerve; Pyridazines; Rats; Rats, Sprague-Dawley; Receptors, Glycine; Respiratory Mechanics; Sodium Cyanide; Splanchnic Nerves; Strychnine; Sympathetic Nervous System; Vagotomy

Although oxidative stress and reactive oxygen species generation is typically associated with localized neuronal injury, reactive oxygen species have also recently been shown to act as a physiological signal in neuronal plasticity. Here we define an essential role for reactive oxygen species as a critical stimulus for cardiorespiratory reflex responses to acute episodic hypoxia in the brain stem. To examine central cardiorespiratory responses to episodic hypoxia, we used an in vitro medullary slice that allows simultaneous examination of rhythmic respiratory-related activity and synaptic neurotransmission to cardioinhibitory vagal neurons. We show that whereas continuous hypoxia does not stimulate excitatory neurotransmission to cardioinhibitory vagal neurons, acute intermittent hypoxia of equivalent duration incrementally recruits an inspiratory-evoked excitatory neurotransmission to cardioinhibitory vagal neurons during intermittent hypoxia. This recruitment was dependent on the generation of reactive oxygen species. Further, we demonstrate that reactive oxygen species are incrementally generated in glutamatergic neurons in the ventrolateral medulla during intermittent hypoxia. These results suggest a neurochemical basis for the pronounced bradycardia that protects the heart against injury during intermittent hypoxia and demonstrates a novel role of reactive oxygen species in the brain stem.

Topics: Animals; Animals, Newborn; GABA Antagonists; Glutamic Acid; Glycine Agents; Hypoxia; In Vitro Techniques; Inhalation; Medulla Oblongata; Membrane Potentials; Nerve Net; Neurons; Oxygen; Patch-Clamp Techniques; Pyridazines; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Strychnine

Deficiency in energy supply, such as occurs during hypoxia, anoxia, metabolic stress and mitochondrial failure, strongly affects the excitability of central neurons. Such lowered energy supply evokes various changes in spontaneous synaptic input to the hippocampal and cortical neurons. However, how this energy deprivation affects synaptic input to motor neurons, which are also vulnerable to energy deprivation, has never been addressed. Here we report for the first time the effect of metabolic stress on synaptic input to motor neurons by recording postsynaptic currents in the hypoglossal nucleus. Chemical anoxia with NaCN (1 mm) and anoxia with 95% N(2) induced a persistent inward current and a marked and robust increase in action potential-independent synaptic input. This increase was abolished by strychnine, but not by picrotoxin, CNQX or MK-801, indicating glycine release facilitation. Blockade of voltage-dependent Ca(2+) channels and extracellular Ca(2+) deprivation strongly attenuated this facilitation. The amplitude of inward currents evoked by local application of NMDA to the motor neurons in the presence of strychnine was significantly increased during NaCN application. A saturating concentration of d-serine occluded this potentiation, suggesting that released glycine activated the glycine-binding sites of NMDA receptors. By contrast, neurons in the dorsal motor nucleus of the vagus showed no detectable change in synaptic input in response to NaCN. These data suggest that increase in synaptically released glycine in response to metabolic stress may play an exacerbating role in NMDA receptor-mediated excitotoxicity in motor neurons.

Topics: Analysis of Variance; Animals; Animals, Newborn; Cyanates; Drug Interactions; Excitatory Amino Acid Agents; Glycine; Glycine Agents; Hypoxia; In Vitro Techniques; Inhibitory Postsynaptic Potentials; Membrane Potentials; Motor Neurons; Patch-Clamp Techniques; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate; Solitary Nucleus; Strychnine

The most ubiquitous form of arrhythmia is respiratory sinus arrhythmia in which the heart beat slows during expiration and heart rate increases during inspiration. Whereas respiratory sinus arrhythmia benefits pulmonary gas exchange respiratory dysfunction presents a major challenge to the cardiorespiratory system. Hypoxia evokes a pronounced bradycardia mediated by increases in parasympathetic cardiac activity. It has been hypothesized that the fatal events in sudden infant death syndrome (SIDS) are exaggerated cardiorespiratory responses to hypoxia. This study tests whether premotor cardiac vagal neurons receive rhythmic respiratory-related excitatory synaptic inputs during normoxia and hypoxia, and if animals exposed to nicotine in the prenatal period have exaggerated responses to hypoxia. Premotor cardiac vagal neurons in the nucleus ambiguus were identified in rats by the presence of a fluorescent tracer in medullary slices that generate rhythmic inspiratory-related motor discharge. Respiratory activity was recorded from the hypoglossal nerve and excitatory synaptic events in cardiac vagal neurons were isolated using patch clamp techniques. Adult female rats were implanted with osmotic minipumps that delivered nicotine at a level approximately equivalent to those that occur in moderate to heavy smokers. During normal eupneic respiration, as well as during hypoxia, premotor cardiac vagal neurons from control animals did not receive any rhythmic respiratory-related excitatory inputs. However in animals exposed to nicotine throughout the prenatal period respiratory bursts during hypoxia dramatically increased the frequency of excitatory synaptic events in cardiac vagal neurons. In summary, in animals exposed to nicotine throughout the prenatal period, but not in unexposed animals, respiratory bursts that occur during hypoxia dramatically increase the frequency of excitatory synaptic events in cardiac vagal neurons. This study establishes a likely neurochemical mechanism for the heart rate responses to hypoxia and a link between prenatal nicotine exposure and exaggerated bradycardia responses during hypoxia that may contribute to sudden infant death syndrome.

Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; Action Potentials; Animals; Animals, Newborn; Brain Stem; Drug Interactions; Excitatory Amino Acid Antagonists; Excitatory Postsynaptic Potentials; GABA Antagonists; Glycine Agents; Hypoxia; Neural Pathways; Neurons; Nicotine; Nicotinic Agonists; Picrotoxin; Rats; Rats, Sprague-Dawley; Respiration; Strychnine; Valine

This study evaluated possible neuronal mechanisms responsible for the transition from normal breathing (eupnea) to gasping. We hypothesized that a blockade of both inhibitory glycinergic synaptic transmission and potassium channels, combined with an increase in extracellular concentration of potassium, would induce a switch from an eupneic respiratory pattern to gasping. Efferent activities of the phrenic, vagal, and hypoglossal nerves were recorded during eupnea and ischemia-induced gasping in a perfused in situ preparation of the juvenile rat (4-6 wk of age). To block potassium channels, 4-aminopyridine (4-AP, 1-10 microM) was administered. Strychnine (0.2-0.6 microM) was used to block glycinergic neurotransmission. After administrations of 4-AP, excess extracellular potassium (10.25-17.25 mM), and strychnine, the incrementing pattern of eupneic phrenic activity was altered to a decrementing discharge. Hypoglossal and vagal activities became concentrated to the period of the phrenic burst with expiratory activity being reduced or eliminated. These changes in neural activities were similar to those in ischemia-induced gasping. Results are consistent with the concept that the elicitation of gasping represents a switch from a network-based rhythmogenesis for eupnea to a pacemaker-driven mechanism.

Topics: 4-Aminopyridine; Age Factors; Animals; Brachial Plexus; Brain Stem; Glycine; Glycine Agents; Hypoglossal Nerve; Hypoxia; Phrenic Nerve; Potassium Channel Blockers; Potassium Channels; Potassium Chloride; Rats; Respiratory Mechanics; Strychnine; Synaptic Transmission; Vagus Nerve

We evaluated the hypothesis that the neurogenesis of gasping is not dependent upon inhibitory synaptic transmission involving GABA(A) or glycine receptors. Activity of the phrenic nerve was recorded in a perfused juvenile rat preparation. The pattern of phrenic activity was altered from eupnea to gasping in severe hypoxia or ischaemia. To block GABA(A) receptors, bicuculline or picrotoxin was administered. Strychnine was used to block transmission by glycine. Following administrations of bicuculline, picrotoxin or strychnine, the eupneic rhythm was greatly distorted whereas the decrementing pattern of the gasp was maintained. At high concentrations of these antagonists, the frequency of gasps was increased and the peak height of gasps fell. We conclude that the neurogenesis of gasping is not dependent upon fast, chloride-mediated inhibitory synaptic transmission.

Topics: Animals; Bicuculline; Dose-Response Relationship, Drug; GABA Agonists; GABA Antagonists; GABA-A Receptor Agonists; GABA-A Receptor Antagonists; Glycine Agents; Hypoxia; In Vitro Techniques; Muscimol; Neural Inhibition; Perfusion; Phrenic Nerve; Picrotoxin; Rats; Receptors, GABA-A; Receptors, Glycine; Respiration; Statistics, Nonparametric; Strychnine

The 'switching model' for generation of respiratory rhythms holds that gasping represents the release of a rostral medullary pacemaker mechanism from the pontomedullary neuronal circuit that generates eupnea. In a perfused preparation of the decerebrate juvenile rat, exposure to ischemia or hypoxic-hypercapnia caused an alteration in integrated phrenic activity from the incrementing pattern of eupnea to the decrementing pattern of gasping. The time required to elicit gasping was not altered by multiple exposures to ischemia or hypoxic-hypercapnia. Furthermore, this time to gasping was not altered following addition to the perfusate of increasing concentrations of bicuculline or picrotoxin; both block GABA(A) receptors. Addition to the perfusate of strychnine, a glycine antagonist, significantly shortened the duration of ischemia or hypoxic-hypercapnia required to elicit gasping. These results support the concept that a loss of inhibitory glycinergic transmission is a critical factor in release of pacemaker mechanisms for gasping from the pontomedullary neuronal circuit for eupnea.

Topics: Animals; GABA-A Receptor Antagonists; Hypercapnia; Hypoxia; In Vitro Techniques; Ischemia; Rats; Receptors, GABA-A; Receptors, Glycine; Respiration; Strychnine

The present study was designed to investigate the mechanism of NMDA receptor activation as a function of brain maturation by studying the development of the glycine binding site of the NMDA receptor and its modification by in-utero hypoxia in the guinea pig fetus brain during gestation. Measurements of Bmax (number of functional receptors) and Kd (apparent receptor affinity) of glycine binding sites of the NMDA receptor were performed in eleven (45 days, n = 5; 60 days, n = 6) synaptosomal membranes from normoxic (control) fetuses and ten (45 days, n = 4; 60 days, n = 6) synaptosomal membranes constituted the hypoxic (experimental) group. In the experimental group, fetuses were exposed to maternal hypoxia (FiO2 0.07) for 1 h. Synaptosomal membranes were prepared and strychnine-insensitive specific [3H]glycine binding was determined During development, the number of glycine binding sites increased (Bmax:392 +/- 30 vs. 583 +/- 30 fmol/mg protein at 45 and 60 days respectively, P < 0.05) where as the affinity remained unchanged (Kd: 190 +/- 9 vs. 211 +/- 30 nM at 45 and 60 days respectively). Following hypoxia, glycine binding sites increased at 45 days (Bmax:392 +/- 30 vs. 561 +/- 96 fmol/mg protein, P < 0.005) but decreased at 60 days (Bmax:583 +/- 85 vs. 411 +/- 65 fmol/mg protein, P < 0.005) with change in Kd only at 60 days (Kd:211 +/- 30 vs. 149 +/- 52 nM, P < 0.05). The data show that there are alterations in the characteristics of the glycine binding site during development and following hypoxia. We conclude that developmental changes in the glycine binding site might modulate NMDA receptor activation as a function of brain maturation. Furthermore, hypoxia-induced modification of the glycine binding site might be a potential mechanism of neurotoxicity and might increase susceptibility of the fetal brain to excitotoxicity at term.

Topics: Animals; Binding Sites; Brain; Brain Chemistry; Female; Fetal Hypoxia; Fetus; Glycine; Glycine Agents; Guinea Pigs; Hypoxia; Pregnancy; Receptors, N-Methyl-D-Aspartate; Strychnine; Synaptosomes; Tritium

This study investigated the effects of hypoxia and glucose on motor functions of spinal cord, monitoring ventral root motor-evoked potential in the in vitro cervical cord preparations.. To study ischemia-induced changes in ventral root motor-evoked potential of spinal cord.. Previous studies demonstrated ischemic changes caused by local circulatory impairment might be a major pathophysiologic basis of neuron damage in cord compression.. Ventral root motor-evoked potential elicited by stimulation of ventrolateral funiculus was recorded from the ventral root in the isolated spinal cord preparations obtained from a newborn rat. The preparations were exposed to artificial cerebrospinal fluid equilibrated with severe or mild hypoxia for 90 minutes. Inhibitory and excitatory neurotransmitter antagonists were added to artificial cerebrospinal fluid to investigate synaptic transmission. The artificial cerebrospinal fluids containing various concentrations of glucose were used to study the glucose's effects.. Ventral root motor-evoked potential consisted of the early and late components, which were excitatory transsynaptic potentials. The amplitudes were increased in the early phase of severe hypoxia and declined in the prolonged exposure. In mild hypoxia, there was a sustained increase of the amplitudes. The application of inhibitory neurotransmitter antagonists abolished the augmentation of the amplitudes in the early phase of severe hypoxia. Hypoxia without glucose accelerated hypoxic change.. Inhibitory synaptic transmission was depressed preferentially in the early phase of severe hypoxia or in mild hypoxia. Excitatory and inhibitory transmissions were suppressed in prolonged severe hypoxia. Glucose deficiency aggravated hypoxic inhibition of synaptic transmissions.

Topics: Animals; Animals, Newborn; Evoked Potentials, Motor; Glucose; Hypoxia; In Vitro Techniques; Neck; Picrotoxin; Rats; Rats, Wistar; Spinal Cord; Spinal Nerve Roots; Strychnine; Synaptic Transmission

Hypoxic and convulsive resistances have daily rhythms, the pattern of which depends on the year season. Latent period of occurrence of epileptic seizures and time of life at the "height" of 11,000 m above the sea level undergo similar changes in autumn and spring. In winter minimal similarity between daily dynamics of each of these resistances and analogous ones in other seasons is observed, but rhythms of tolerance to hypoxia are maximally synchronized with the rhythms of convulsive resistance. In autumn hypoxic and convulsive resistances are minimal. Maximums of these indices are observed in different seasons: for tolerance to hypoxia it is summer, for convulsive resistance--spring.

Topics: Animals; Atmosphere Exposure Chambers; Circadian Rhythm; Disease Susceptibility; Hypoxia; Male; Rats; Reaction Time; Seasons; Seizures; Strychnine; Time Factors

Topics: Acidosis; Adult; Critical Care; Female; Humans; Hypoxia; Pregnancy; Pregnancy Complications; Strychnine; Suicide, Attempted

In decerebrate, paralyzed and vagotomized cats, we recorded activities of hypoglossal and phrenic nerves and of the mylohyoid branch of the trigeminal nerve. At normocapnia, a respiratory-modulated trigeminal discharge could be discerned in most cats. This discharge was characterized by a diminution of activity during neural inspiration and a peak in expiration. In hypercapnia or hypoxia, peak activity increased and its time of occurrence moved to late inspiration. Augmentations of peak trigeminal, hypoglossal and phrenic activities were proportional. Peak trigeminal and hypoglossal activities increased more than phrenic following administrations of protriptyline, strychnine and, in some cats, cyanide or doxapram. Peak trigeminal activity fell more than phrenic after diazepam. Pentobarbital or halothane reduced peak hypoglossal, but not trigeminal, activity more than phrenic. However, after these anesthetics, trigeminal activity became restricted to the inspiratory-expiratory junction. We conclude that trigeminal and hypoglossal activities are more dependent upon processes within the reticular formation than is the bulbospinal-phrenic system. Central and peripheral chemoreceptor influences are distributed equivalently upon trigeminal, hypoglossal and phrenic motoneurons.

Topics: Animals; Cats; Chemoreceptor Cells; Decerebrate State; Diazepam; Doxapram; Electromyography; Electrophysiology; Female; Halothane; Hypercapnia; Hypoglossal Nerve; Hypoxia; Male; Pentobarbital; Phrenic Nerve; Protriptyline; Respiration; Strychnine; Trigeminal Nerve

Topics: Animals; Bicuculline; Cats; Electric Stimulation; Eye Movements; Gallamine Triethiodide; Hypoxia; Methoxamine; Ophthalmoplegia; Strychnine; Sympathectomy; Sympathetic Nervous System; Urethane

Topics: Adenosine Diphosphate; Animals; Blood Pressure; Cats; Cerebral Cortex; Fluorometry; Hypoxia; Mitochondria; NAD; NADP; Norepinephrine; Oxidation-Reduction; Oxidative Phosphorylation; Oxygen Consumption; Pentylenetetrazole; Polarography; Seizures; Strychnine; Time Factors

Topics: Amphetamine; Analgesics; Animals; Anticonvulsants; Barbiturates; Depression, Chemical; Electroshock; Ethyl Ethers; Female; Hypoxia; Injections, Intraperitoneal; Locomotion; Male; Mice; Orientation; Oxygen Consumption; Pentylenetetrazole; Rats; Stimulation, Chemical; Strychnine; Tissue Extracts; Tranquilizing Agents

Topics: Adult; Ascorbic Acid; Barbiturates; Caffeine; Female; Humans; Hypoxia; Male; Middle Aged; Oxygen Consumption; Respiratory Insufficiency; Strychnine; Thiamine; Vascular Resistance

Topics: Acceleration; Body Temperature Regulation; Electric Stimulation; Hypothermia; Hypoxia; Mice; Rats; Research; Strychnine; Toxicology

Topics: Animals; Brain; Carbon Dioxide; Dogs; Epinephrine; Ergotamine; Humans; Hypoxia; Phenobarbital; Strychnine

Topics: Action Potentials; Anticonvulsants; Asphyxia; Atropine; Brain; Hypoxia; Nervous System Physiological Phenomena; Strychnine

Topics: Animals; Caffeine; Cerebral Cortex; Hypoxia; Nervous System Physiological Phenomena; Rats; Strychnine; Torso