[Research on chloralose. III. The constitution of A and B chloralose].
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Chloralose↗
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[Danger for birds of prey through the use of chloralose in seagull control. Detection of chloralose poisoning in 2 buzzards].
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Animals↗
[Metabolism of chloralose. I. Colorimetric determination of free and glucuroconjugated chloralose in urines].
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Chloralose↗
Influence of chloralose on brain regional glucose utilization.
Choralose, a widely used anesthetic in neurophysiology, produces a unique pattern of anesthesia characterized by both an excitant (myoclonic jerks and startle response) and depressant (sedation and anesthesia) action. We investigated the influence of chloralose on the rate of regional brain glucose metabolism to determine if chloralose produces anesthesia by hyperexciting certain brain regions. That is, does chloralose act as an 'epileptoid anesthetic'. Rats were anesthetized with either 60 or 120 mg/kg chloralose and regional brain glucose utilization rates quantitated by the 2-deoxyglucose method. In chloralose-anesthesized rats, glucose consumption rates decreased in the frontal and auditory cortex, reticular nucleus of thalamus, superior colliculus, medial geniculate body, midbrain reticular formation and hippocampus. Rates of glucose use were not decreased in the lateral lemniscus and a zone in the vicinity of the oculomotor nucleus, medial longitudinal fasciculus and surrounding reticular formation. Since chloralose did not induce any discernible focal points of high activity, chloralose appears not to be an epileptogen. Rather, chloralose appears to act as a general depressant except in certain gray areas of the midbrain and lower brain stem. Retained and possibly increased functional activity in the vicinity of the oculomotor nucleus and medial longitudinal fasciculus may represent active reflex pathways involved in mediating the paradoxical startle response and myoclonic activity observed in chloralose-anesthetized animals.
Analysis of Variance↗
Effect of beta-adrenergic receptor antagonism on chloralose-induced hemodynamic changes in newborn lambs.
alpha-Chloralose is an anesthetic commonly used in cardiovascular research. Using a chronically instrumented neonatal lamb model, we previously determined that chloralose has important effects on basal hemodynamics and arterial oxygen tension as compared with those of paired conscious control lambs. We wished to determine whether beta-adrenergic receptor stimulation accounted for chloralose-induced hemodynamic effects and to investigate the influence of chloralose and beta-adrenergic receptor antagonism on oxygen metabolism. In paired studies, five lambs were given chloralose intravenously (30 mg/kg i.v.) after propranolol (1 mg/kg i.v.) or saline control. The group pretreated with propranolol had reduced heart rate (HR 206 +/- 12 vs. 244 +/- 10 beats/min, p = 0.04) and cardiac output (CO 253 +/- 29 vs. 302 +/- 40 ml/min/kg, p = 0.005) 30 min after chloralose as compared with control; pretreatment with propranolol also attenuated the systemic hypertensive response to chloralose (77 +/- 8 vs. 89 +/- 5 mm Hg, p = 0.055). No difference in the response of stroke volume (SV), atrial or pulmonary arterial pressures, or pulmonary and systemic vascular resistances (PVR, SVR) were observed between treatment groups. No differences between propranolol and saline treatment groups were observed in arterial and mixed venous oxygen contents, arteriovenous (A-V) oxygen difference, oxygen extraction, or oxygen consumption; a reduction in oxygen delivery observed after propranolol as compared with saline was not altered by chloralose. We conclude that tachycardia and increase in CO induced by chloralose in lambs probably are mediated by beta-adrenergic receptor stimulation, which may be direct or indirect.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic beta-Antagonists↗
Enhancement of gamma-aminobutyric acidA receptor activity by alpha-chloralose.
alpha-Chloralose is widely used as an anesthetic in the laboratory due to its minimal effects on autonomic and cardiovascular systems, yet little is known about its mechanism of action. We examined the effects of alpha-chloralose on gamma-aminobutyric acid type A (GABAA) receptor activity because recent studies have shown that several classes of general anesthetics modulate the function of this receptor. GABAA receptor activity was assayed by measuring the GABA-induced current in Xenopus oocytes expressed with human GABAA receptor alpha-1, beta-1 and gamma-2L subunits. alpha-Chloralose produced a concentration-dependent potentiation of the GABA-induced current with an EC50 value of 49 microM and a maximal effect of 239% of control. Membrane current was not affected by alpha-chloralose in the absence of GABA. alpha-Chloralose (100 microM) increased the affinity for GABA 5-fold and produced a small (17%) increase in the efficacy of GABA. Measurement of the reversal potentials for the alpha-chloralose response suggested that the effect is mediated through increased Cl- conductance. Studies of alpha-chloralose interactions with other allosteric modulators determined that alpha-chloralose binds to a site on the GABAA receptor complex distinct from the benzodiazepine, neurosteroid and barbiturate sites. Chloral hydrate, trichloroethanol and urethane also augmented GABA-induced currents. alpha-Chloralose had no effect on the hydroxytryptamine-induced currents in oocytes expressed with the 5-hydroxytryptamine3 receptor. These data extend the number of classes of anesthetics that allosterically modulate GABAA receptor activity and indicate that GABAA receptors may be a common site of action for diverse classes of general anesthetics.
Anesthetics, Intravenous↗
1H NMR spectroscopy and GC-MS analysis of alpha-chloralose. Application to two poisoning cases.
Alpha-chloralose, a compound widely used as a rodenticide and in the control of bird pests, is readily available. Two cases of intentional poisoning are reported. Both patients became comatose and presented hypersialorrhea and myoclonal crises in the legs. They were discharged from hospital after several days. As clinical signs of alpha-chloralose poisoning lack specificity, anamnesis might be difficult, particularly in the case of delayed diagnosis. Toxicological analysis is therefore critical, and this article reports the investigation of serum and urine samples by gas chromatography-mass spectrometry (GC-MS) in the electron-impact mode, and by 1H nuclear magnetic resonance (1H NMR) spectroscopy. Non-hydrolyzed urinary samples and those hydrolyzed by beta-glucuronidase were taken into consideration. After acetylation, GC-MS analysis was based on characteristic mass-to-charge ratio values of 272 for alpha-chloralose and 206 for beta-hydroxyethyltheophylline, which was used as internal standard. Characterization of alpha-chloralose species by 1H NMR spectroscopy was performed taking two parameters into account: chemical shift and coupling-constant values. Without any pretreatment, 1H NMR spectroscopy revealed the presence of free (5.50 and 6.15 ppm) and conjugated forms of alpha-chloralose by characteristic resonances of H1 and chloral-type protons, respectively. Quantitative analysis was performed by relative integration of peak areas. Serum alpha-chloralose showed concentrations below the quantitation limit of both methods. In urine samples, the free chemical species rapidly decreased. GC-MS analysis revealed the predominence of conjugation after a beta-glucuronidase hydrolysis step. 1H NMR analysis directly showed that on admission of the first patient, average urinary concentrations were 1.73 mmol/L (535 mg/L) for the free form and 13.72 and 6.25 mmol/L for the two conjugated forms. A later enzymatic treatment confirmed the total concentration of alpha-chloralose chemical species. Analysis of alpha-chloralose in urine by either GC-MS or 1H NMR spectroscopy methods proved to be comparable.
Adult↗
The effect of polyethylene glycol-200 on metabolic acidosis induced by chloralose anaesthesia.
Chloralose may be used in a 10% solution as an anaesthetic in dogs. The solubility of chloralose was found to be much higher in polyethylene glycol-200 (PEG-200) than in either warm (body temperature) or cold saline (0.9% NaCl). The intravenous (i.v.) administration of chloralose in warm saline solution induced acidosis as a result of the increase in the level of metabolic acids. The acidity generated by chloralose in almost neutral saline was probably the result of increase in the base deficit in the animal. The infusion of PEG-200 (almost neutral) significantly reduced the base deficit without disturbing the PaO2 or PaCO2 in the arterial blood. The base deficit value was significantly lower after administration of chloralose solution in PEG-200 (almost neutral) than after administration in saline. The use of PEG-200 as a solvent for chloralose was advantageous in two ways. Firstly, it prevented the production of acids in anaesthetic solution and neutralized the blood metabolic acids generated by chloralose administration in saline. Secondly, the solubility of chloralose (10% w/v solution) in PEG-200 was very much higher than in warm or cold saline.
Acidosis↗
Alpha-chloralose opens the chloride channel of frog isolated sensory neurons.
The effect of alpha-chloralose on the sensory neurons isolated enzymatically and mechanically from frog dorsal root ganglia was studied using a suction-pipette technique. The threshold concentration of alpha-chloralose was around 3 x 10(-5) M and the current produced by alpha-chloralose saturated at the concentration of 3 x 10(-3) M or more. The dose-response curve for alpha-chloralose provided a Ka value of 6 x 10(-4) M and a Hill coefficient of 1.8. The reversal potential of the response elicited by alpha-chloralose was close to the equilibrium potential for Cl- (ECl), indicating that the current was carried through Cl- channels. The current-voltage relationship indicated that there was little voltage dependence in the alpha-chloralose-induced response. The analysis of the variance of the alpha-chloralose-induced Cl- current fluctuations showed two types of the receptor-ionophore complexes with different channel conductances.
Animals↗
Is alpha-chloralose plus halothane induction a suitable anesthetic regimen for cerebrovascular research?
The aim of this study was to determine whether alpha-chloralose, when associated with an initial period of halothane, is a suitable anesthetic regimen for cerebrovascular studies. For this purpose, rats anesthetized with alpha-chloralose plus halothane induction were first subjected to noxious stimuli, and the behavior, EEG and systemic variables were recorded. During a second step, cortical blood flow was measured with laser-Doppler flowmetry and the time-course of the cerebrovascular reactivity to hypercapnia were measured in artificially ventilated rats anesthetized with either alpha-chloralose (40 mg.kg-1, s.c.) plus halothane induction (1.5% given during the first 45-60 min) or halothane alone (1.5%). Finally, an experimental paradigm was developed that allowed the comparison of the hypercapnic reactivity, both in awake and anesthetized conditions in the same animal. Our results show that the association of alpha-chloralose with halothane leads to stable cardiovascular parameters and immobility of ventilated rats, placed in ear bars without curare, for 3 h without any sign of discomfort. Based on EEG criteria, we found that halothane induction lengthens the duration of alpha-chloralose anesthesia (253 +/- 19 vs. 200 +/- 15 min, P < 0.01). Under alpha-chloralose alone or in association with halothane induction, the vascular reactivity to hypercapnia was considerably impaired (-85% compared to the awake state, P < 0.01), but this impairment was transient, since a control reactivity was restored 150-190 min after induction of anesthesia. Under halothane alone, the vascular reactivity remained reduced throughout the experiment. These results provide evidence that alpha-chloralose plus halothane induction is a suitable anesthetic regimen which displays a temporal window of normal cerebrovascular reactivity.
Anesthesia↗
Muscle atonia can be induced by carbachol injections into the nucleus pontis oralis in cats anesthetized with alpha-chloralose.
Cholinergic excitation of structures in the pontine reticular formation appears to be a key step in the generation of active sleep. For example, muscle atonia which occurs as a result of the postsynaptic inhibition of motoneurons during active sleep is also present after carbachol, a cholinergic agonist, is injected into the nucleus pontis oralis. In the present study, in order to obtain information regarding the mechanisms that generate atonia during active sleep and to provide a paradigm for studying atonia in anesthetized cats, we determined whether cholinergically induced atonia could be generated in an animal that was anesthetized with alpha-chloralose. Cats which were initially anesthetized with alpha-chloralose (40 mg/kg, I.V.) exhibited spikes in the EEG, hippocampus and lateral geniculate nuclei. Muscle atonia occurred after carbachol (200 mM) was injected by microiontophoresis (300-500 nA) into the nucleus pontis oralis; the spikes in the EEG, hippocampus and lateral geniculate nuclei were still present. We believe that the atonia induced by carbachol in alpha-chloralose-anesthetized cats is mediated by the same mechanisms that operate during active sleep in the unanesthetized animal for the following reasons. First, in the same cats when they were not anesthetized with alpha-chloralose, carbachol injections in the identical brainstem sites induced active sleep with its accompanying pattern of muscle atonia. Second, after carbachol was injected into the same sites in alpha-chloralose-anesthetized cats, intracellular recordings from lumbar motoneurons revealed that inhibitory postsynaptic potentials were bombarding motoneurons; these inhibitory potentials were similar to those which are present during naturally occurring active sleep. In addition, stimulation of the nucleus reticularis gigantocellularis (NRGc) was found to induce large amplitude depolarizing potentials in lumbar motoneurons in alpha-chloralose-anesthetized cats prior to the administration of carbachol, whereas after its administration, accompanying muscle atonia there were large amplitude hyperpolarizing potentials and a reduction in the amplitude of depolarizing potentials. We therefore conclude that the cholinergically induced processes that initiate and maintain muscle atonia are not blocked by the actions of alpha-chloralose.
Animals↗
Comparative study of the effects of nitric oxide synthase and cyclo-oxygenase inhibition on duodenal functions in rats anaesthetized with inactin, urethane or alpha-chloralose.
This study was undertaken to investigate the effects of a cyclo-oxygenase and a nitric oxide synthase (NOS) inhibitor on duodenal mucosal alkaline secretion (DMAS), motility and mucosal permeability in inactin-, urethane- and alpha-chloralose anaesthetized rats. Proximal duodenum was perfused with a 150 mM NaCl solution and DMAS was determined by back titration. Mucosal permeability was assessed by measuring blood to lumen clearance of 51Cr-EDTA and duodenal motility by measuring intraluminal pressure. Mean arterial blood pressure and mucosal permeability were significantly lower in urethane- than in inactin- or alpha-chloralose anaesthetized rats (urethane: 90 +/- 2 mm Hg and 0.15 +/- 0.02 mL min-1 100 g-1; inactin: 112 +/- 5 mm Hg and 0.62 +/- 0.15 mL min-1 100 g-1; alpha-chloralose: 111 +/- 4 mm Hg and 0.61 +/- 0.06 mL min-1 100 g-1, respectively). Basal (pre-drug) DMAS was significantly lower in urethane rats (6.2 +/- 1.0 mumol cm-1 h-1) than in alpha-chloralose (9.3 +/- 1.2 mumol cm-1 h-1), but not different from that in inactin-anaesthetized rats (7.5 +/- 0.8 mumol cm-1 h-1). No or very few spontaneous duodenal contractions occurred under the control (pre-drug) conditions in any group. All animals responded to the cyclo-oxygenase inhibitor indomethacin or the NOS inhibitor N-nitro-L-arginine-methyl-ester (L-NAME) with induction of duodenal motility and an increase in DMAS. The effect of indomethacin or L-NAME on mucosal permeability was similar in all anaesthetic groups except that L-NAME induced a transient increase in the inactin and alpha-chloralose groups but a sustained increase in urethane-anaesthetized animals. It is concluded that inactin- and alpha-chloralose anaesthetized rats do not differ regarding the studied basal values. Urethane-anaesthetized animals differed from rats given the other two anaesthetics in that basal mucosal permeability and mean arterial blood pressure were lower. Endogenous prostaglandins and NO contribute to the postoperative ileus and the low rate of DMAS also in urethane- and alpha-chloralose.
Anesthesia, General↗
The electrophysiological effects of alpha-chloralose anesthesia in the intact dog: (1) alone and (2) in combination with verapamil.
The electrophysiological effects of alpha-chloralose anesthesia were determined in 13 chronically instrumented dogs and compared to baseline electrophysiological parameters in the conscious state. Alpha-chloralose anesthesia (75 mg/kg of a 4% solution in polyethylene glycol (PEG) delayed conduction and prolonged refractoriness of the AV node: (1) the P-R interval increased from 108 +/- 14 msec (mean +/- SD) in the conscious state to 125 +/- 23 msec (P less than 0.02); (2) the A-H from 98 +/- 12 msec to 108 +/- 16 msec (P less than 0.04); (3) the AV nodal effective refractory period from 136 +/- 16 to 153 +/- 29 msec (P = .05) and the AV nodal functional refractory period from 232 +/- 58 to 247 +/- 46 msec (P = 0.07); and (4) the AV block cycle length from 228 +/- 54 msec to 248 +/- 43 msec (P less than 0.04). Chloralose anesthesia also increased the ventricular refractory period from 139 +/- 13 msec to 161 +/- 22 msec (P less than .03) and the QTc interval from 273 +/- 22 to 306 +/- 32 msec (P less than 0.0002). To determine whether these effects on AV nodal conduction would influence experimental results, responses to verapamil were studied in the conscious state and during chloralose anesthesia. During chloralose anesthesia, (1) no relationship was detected between the sinus cycle length and verapamil concentrations; (2) a greater increment in AV conduction time was seen for a given verapamil concentration; and (3) AV block occurred at verapamil concentrations associated with 1:1 conduction in the conscious state. We conclude that chloralose anesthesia has significant electrophysiological effects and that these effects must be taken into consideration during the interpretation of experiments performed in animals during chloralose anesthesia.
Anesthesia, General↗
alpha-Chloralose alters autonomic reflex function of the lower urinary tract.
The effects of alpha-chloralose on the micturition reflex were evaluated using an efficiently voiding decerebrate cat model. At laparotomy cannulas were introduced into the urethra and/or bladder for measurement of urethral perfusion pressure and/or bladder pressure during bladder filling and voiding. After establishment of efficient voiding in the anesthetic-free decerebrate cat, chloralose, 50 mg/kg iv, was administered. Parameters assessed before and after anesthetic included bladder pressure at peak of contraction (voiding pressure), intravesical pressure at onset of bladder contraction (threshold pressure), contraction amplitude, duration of bladder contraction, bladder volume at onset of bladder contraction (volume threshold), and residual bladder volume after voiding (postvoid residual). In addition to these parameters, preparations with intact bladder-urethra and with divided bladder-urethra were used to assess effects of chloralose on voiding efficiency and coordination between bladder and urethra, respectively. Chloralose significantly reduced voiding pressure, contraction amplitude, and voiding efficiency. Neither vehicle for the chloralose nor sympathetic denervation of the lower urinary tract affected these reductions. Chloralose had no effect on direct contraction of the bladder and urethra produced by intra-arterial acetylcholine (25-100 micrograms). Chloralose converted the synergic bladder and urethral responses during voiding to dyssynergic responses. Neuromuscular blockade with gallamine, 10 mg/kg iv, improved voiding efficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
Chloralose alters both basal hemodynamics and cardiovascular responses to alveolar hypoxia in chronically instrumented, spontaneously breathing lambs.
We studied the effects of chloralose anesthesia on the basal hemodynamic state and on the cardiovascular response to alveolar hypoxia in chronically instrumented, spontaneously breathing lambs, compared with responses to the saline vehicle. Chloralose significantly increased heart rate (23%), mean systemic arterial pressure (11%), systemic vascular resistance (21%), mean pulmonary arterial pressure (23%), and pulmonary vascular resistance (46%) (n = 30, p less than 0.05, ANOVA). These changes were unrelated to baseline tone of the circulation, cardiac output, mean left atrial pressure, or physiologically important changes in arterial blood gas tensions. In addition, chloralose-treated lambs had increased heart rate, systemic vascular resistance, and pulmonary vascular resistance compared to controls during alveolar hypoxia (13-15% FiO2). Importantly, chloralose-treated lambs did not increase their cardiac output during alveolar hypoxia as did control lambs. During hypoxia, systemic vascular resistance remained elevated in chloralose-treated lambs, but declined in control lambs. Chloralose has been recommended as an ideal anesthetic agent for cardiovascular experimentation. Our data suggest that chloralose-induced alterations in basal hemodynamics and in cardiovascular responses to alveolar hypoxia represent an uncontrolled variable in acute experimental studies. Complex cardiovascular alterations caused by anesthesia should be considered in experimental design.
Animals↗
Influence of alpha-chloralose on reflex control of the cardiovascular system in lambs.
Alpha-chloralose is an anesthetic agent sometimes used for experiments in fetal and neonatal cardiovascular physiology. However, its effect on baseline cardiovascular variables and reflex control of the circulatory system has not been determined in young animals. We, therefore, investigated the effect of chloralose on blood pressure, heart rate and baroreflex activity in 12 lambs. Each lamb was anesthetized and a single-lumen catheter was placed in the inferior vena cava and a double-lumen balloon-tipped catheter was placed in the descending aorta. Following recovery from surgery for at least 48 h, blood pressure and heart rate were measured during quiet wakefulness and 30 min following the administration of polyethylene glycol-400 or alpha-chloralose (30, 60 or 90 mg/kg of body weight). Baroreflex activity was assessed by reflex slowing of the heart during an acute increase in blood pressure, produced by inflating the balloon in the descending aorta. Administration of polyethylene glycol-400 alone did not significantly affect blood pressure, heart rate or baroreflex activity. However, alpha-chloralose significantly decreased baroreflex activity in all the doses tested, compared to control responses obtained following the administration of polyethylene glycol-400 alone. Baseline blood pressure and heart rate were increased by 30 and 60 mg/kg of alpha-chloralose, whereas, 90 mg/kg decreased the blood pressure and did not change heart rate. We conclude that alpha-chloralose significantly alters baseline cardiovascular variables as well as reflex circulatory control in lambs. These effects should be taken into consideration when evaluating studies done during alpha-chloralose anesthesia.
Animals↗
Arrhythmias, haemodynamic changes and extent of myocardial damage during coronary ligation in rabbits anaesthetized with halothane, alpha chloralose or pentobarbitone.
We investigated the incidence of ventricular arrhythmias, extent of myocardial infarction and alteration in haemodynamic parameters during 30 minutes of coronary arterial occlusion in rabbits anaesthetized with halothane, alpha chloralose and pentobarbitone. Ventricular tachycardia and fibrillation occurred in 10 of 15 given halothane and in 11 of 15 animals given alpha chloralose while of 15 animals given pentobarbitone, 5 developed tachycardia and 8 had fibrillation. Following ligation, blood pressure promptly fell in each group to 71-76% of control values at 1 minute and remained low throughout the occlusion period. This was most marked in the group receiving halothane which had significantly lower pressures at 30 minutes than those anaesthetized with alpha chloralose or pentobarbitone (P less than 0.01 in each case). Those receiving halothane also recovered less on reperfusion. Heart rate remained stable with pentobarbitone anaesthesia during coronary occlusion and reperfusion, but promptly declined in the first minute of occlusion in the groups given halothane and alpha-chloralose and then remained low throughout occlusion, especially in the group given alpha-chloralose (P less than 0.001 vs pentobarbitone and P less than 0.01 vs halothane). The extent of myocardial damage was measured from nitroblue tetrazolium-stained sections and expressed as a percentage of the zone at risk, which was obtained in five hearts following 90 minutes coronary ligation. Values were 44.0% with pentobarbitone, 54.0% with alpha chloralose (P less than 0.01 vs pentobarbitone) and 62.1% with halothane (P less than 0.001 vs pentobarbitone). Thus, the choice of anaesthetic employed during experimental myocardial ischaemia may have significant effects on the incidence of ventricular tachycardia, haemodynamic changes and extent of necrosis observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of Variance↗
Rabbit carotid sinus reflex under pentobarbital, urethan, and chloralose anesthesia.
To determine the effects of different anesthesias on the performance of the arterial baro-reflex, the open-loop characteristic of the carotid sinus reflex was analyzed in 24 rabbits under anesthesia with pentobarbital (30 mg/kg), urethan (800 mg/kg), alpha-chloralose (80 mg/kg), or a mixture of alpha-chloralose (40 mg/kg) and urethan (0.4 g/kg). For each rabbit and anesthesia, mean systemic arterial pressure and heart rate were measured as carotid sinus pressure was changed in 10-mmHg steps between 40 and 150 mmHg. This set of measurements was repeated four times at 1-h intervals. A logistic function curve was fitted to the carotid sinus pressure-arterial pressure relationship. The parameters of this curve were then analyzed to delineate the specific effects of the anesthesias on the relationship. The main finding was that the response range and the slope parameters under alpha-chloralose anesthesia were significantly smaller than those obtained under the other anesthesias. Propylene glycol, used as the solvent for chloralose, did not affect the reflex control of arterial pressure or heart rate. The reflex under chloralose-urethan anesthesia showed characteristics similar to those under urethan anesthesia. We conclude that although alpha-chloralose has traditionally been used in the dog to obtain strong reflex responses, it weakens the reflex control of arterial pressure in the rabbit.
Anesthesia, General↗