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PubMed1988

Effects of the volatile anesthetic agents on sinus node function and atrioventricular conduction in dogs: a comparison with chloralose anesthesia.

The effects of equipotent concentrations (1.5 times minimum alveolar concentration) of the inhalational agents halothane, enflurane, and isoflurane on sinus node function, and atrioventricular (A-V) conduction and refractoriness were compared with chloralose anesthesia in 49 mongrel dogs. Sinus node function was assessed using corrected sinus node recovery time. Atrial-His and His-ventricular conduction times were measured at paced heart rates of 150, 180, and 200 beats/min, and A-V refractoriness was assessed by Wenckebach periodicity. There was no evidence that sinus node function was impaired by any of the inhalational agents. Enflurane anesthesia was associated with a significant prolongation of atrial-His conduction at paced heart rates of 180 and 200 beats/min when compared to chloralose anesthesia and the other two inhalational agents (P < .001). Atrioventricular refractoriness was impaired by enflurane (P < .001) and halothane (P < .05), but not isoflurane, when compared with chloralose anesthesia. Ventricular-His conduction was not altered by any of the agents. The authors conclude that enflurane is associated with a greater impairment of A-V conduction and refractoriness than halothane or isoflurane, and that these changes are related to the anesthetic agent and not the anesthetic state.

Anesthetics, Inhalation↗
PubMed2004

[Curarization for contributing symptomatic treatment of myoclonic jerks induced by chloralose poisoning].

Chloralose poisoning especially leads to consciousness failure and hyperexcitability with typical myoclonic jerks. In an observation of chloralose poisoning by ingestion of synthetic substance against moles, curarization by cistracurium besylate was proposed to contribute in the symptomatic treatment of myoclonus syndrome induced by chloralose poisoning and resistant to a large dose of diazepam.

Adult↗
PubMed2006

[Severe chloralose intoxication in a toddler].

UNLABELLED: We report a case of an accidental intoxication in a 20-month-old boy resulting from the ingestion of a rodenticide containing alpha-chloralose. CASE REPORT: Three hours after initial admission to the pediatric emergency department for wheezing bronchitis, this patient was readmitted with a clinical presentation of respiratory insufficiency, a Glasgow coma score of 9 alternating with agitation, areflexia and unilateral mydriasis. Parental interview revealed he had episodes of shaking in the afternoon. Chest x-ray showed thoracic distension. Blood investigations, electrocardiogram, cardiac echography, brain CT scan and CSF were normal. Electroencephalography registered slow delta waves 2-3 cycles/min and an aspect of degraded waves and spikes. The patient was transferred to the intensive care unit where he fully recovered within 48 hours. A second parental interview and clinical presentation confirmed an intoxication with a rodenticide containing alpha-chloralose. The late clinical orientation did not allow us to perform a urinanalysis. DISCUSSION: Clinical association of coma, spontaneous or triggered myoclonias and bronchial hypersecretion are indicative of chloralose intoxication. Presence of specific abnormalities on electroencephalogram and a positive Fujiwara-Ross reaction in an urine sample are additional elements for the diagnosis. The prognosis is usually good after early management which combines gastric lavage, activated charcoal, sedation with benzodiazepines, tracheal intubation and artificial ventilation if required. Severe clinical cases described in voluntary intoxications in adults and teenagers occur very rarely in toddlers.

Accidents↗
PubMed1978

Renal vascular response to haemorrhage in the rabbit after pentobarbitone, chloralose-urethane and ether anaesthesia.

1. Total renal blood flow and its cortical distribution were measured by the microsphere technique before and after haemorrhage in conscious rabbits, and after haemorrhage in rabbits anaesthetized with pentobarbitone, chloralose-urethane or ether. 2. The average blood loss necessary to achieve a fall in systolic blood pressure to about 65 mmHg was 101 ml in conscious rabbits and 38, 90 and 118 ml in weight-matched groups of rabbits anaesthetized with pentobarbitone, chloralose-urethane and ether respectively. 3. After haemorrhage in conscious rabbits total renal blood flow fell by 25%, this fall being confined to the superficial renal cortex. 4. In rabbits subject to haemorrhage under pentobarbitone anaesthesia renal blood flow fell by a further 23% when compared with the conscious bled rabbits. This reduction in blood flow was confined to the superficial cortex. 5. Haemorrhage in the rabbits subjected to chloralose-urethane anaesthesia caused no significant change in renal blood flow, as compared with conscious bled rabbits. 6. Haemorrhage under ether anaesthesia was associated with a further 33% fall in total renal blood flow, as compared with conscious bled rabbits. This was associated with a fall of 32% and 34% in superficial and deep cortical blood flow respectively. 7. Animals subjected to general anaesthesia may be particularly susceptible to the renal haemodynamic effects of haemorrhage.

Anesthesia, General↗
PubMedDate not supplied

Comparison of the cardiovascular actions of N,N-di-n-propyl dopamine and sodium nitroprusside in conscious and chloralose-anaesthetised dogs.

The cardiovascular actions of N,N-Di-n-propyldopamine (DPDA), a dopamine receptor agonist, and the directly acting vasodilator sodium nitroprusside have been compared in both conscious and chloralose-anaesthetised dogs. Bolus intravenous doses of DPDA (6.5-32 micrograms/kg) and sodium nitroprusside (3-10 micrograms/kg) induced dose-related falls in blood pressure associated with reflex tachycardia in both preparations. The dopamine receptor antagonist sulpiride (0.5 mg/kg) eliminated these effects of DPDA and its ability to reduce renal and femoral vascular resistances in the chloralose-anaesthetised dog, but did not influence the actions of sodium nitroprusside. Ganglion blockade (hexamethonium, 5-10 mg/kg alone or in a combination with atropine, 1 mg/kg) abolished the reflex tachycardia to both compounds and potentiated the depressor effects of sodium nitroprusside but either reduced or did not alter the hypotension produced by DPDA. The renal dilator response to DPDA was also reduced, while femoral vasodilation was abolished. This study illustrates that DPDA can reduce blood pressure in conscious and chloralose-anaesthetised dogs but that this effect is accompanied by reflex tachycardia. Inhibitory dopamine receptors on sympathetic nerves, and to a lesser extent postjunctional (vascular) dopamine receptors, are involved in these actions of DPDA.

Anesthesia↗
PubMed1990

Alpha-chloralose anesthesia inhibits the somato-sympathetic reflex response in cats more effectively than halothane.

The effect of halothane anesthesia (H; 0.8 Vol%) or alpha-chloralose anesthesia (AC; 60 mg/kg i.v.) on the somato-sympatho-adrenal reflex response evoked by supramaximal bilateral sciatic nerve stimulation, were examined in two groups of cats (H: n = 6; AC: n = 4). Blood samples were collected simultaneously from the adrenal vein and femoral artery at baseline (S1) and during bilateral sciatic nerve stimulation (S2) for the measurement of norepinephrine, epinephrine, neuropeptide Y, and Metenkephalin, while mean arterial blood pressure (MABP) and heart rate (HR) were recorded. There were no differences between groups at baseline. In halothane anesthetized cats, sciatic nerve stimulation caused significant increases in MABP (S1: 113 +/- 8 mm Hg, S2: 178 +/- 10 mm Hg; mean +/- SE), HR (S1: 223 +/- 15 bpm, S2: 278 +/- 22 bpm), and adrenal vein plasma levels of norepinephrine (S1: 3.1 +/- 0.98 ng/ml, S2: 19.53 +/- 11.5 ng/ml), epinephrine (S1: 15.5 +/- 4.76 ng/ml, S2: 67.31 +/- 14.9 ng/ml), neuropeptide Y (S1: 1.3 +/- 0.12 ng/ml, S2: 2.16 +/- 0.42 ng/ml), and Met-enkephalin (S1: 107 +/- 35.7 pg/ml, S2: 200 +/- 76.5 pg/ml). In contrast, sciatic nerve stimulation in alpha-chloralose anesthetized cats, caused a significant increase only in MABP during sciatic nerve stimulation (S1: 115 +/- 10 mm Hg, S2: 171 +/- 7 mm Hg), while HR and adrenal vein plasma levels of catecholamines, neuropeptide Y and Met-enkephalin remained unchanged from baseline. Adrenal vein epinephrine levels measured during stimulation in the alpha-chloralose group (S2: 6.17 +/- 0.86 ng/ml), were significantly lower as compared to values observed during halothane anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1977

The effects of pentobarbitone and chloralose anaesthesia on the vagal component of bronchoconstriction produced by histamine aerosol in the anaesthetized dog.

1 Total lung resistance (R(L)) and dynamic lung compliance (C(dyn)) were measured in dogs anaesthetized with pentobarbitone or chloralose and subjected to aerosols of histamine during 4 successive inspirations.2 Histamine caused concentration-dependent increases in R(L) and decreases in C(dyn). A significant vagal component was involved, but only when chloralose was employed and then only in the R(L) response.3 The resting values of R(L) and C(dyn) were similar regardless of which anaesthetic was used and remained essentially the same if the vagi were cooled.4 Electrical stimulation of the efferent vagi caused large increases in R(L) of dogs given chloralose and these effects were attenuated by the administration of pentobarbitone. Such stimulation was relatively ineffective in dogs given pentobarbitone alone.5In vitro, electrical field stimulation caused contractions of dog trachealis muscle. The responses were reduced by pentobarbitone in concentrations approximating to plasma levels in the anaesthetized dogs (1 to 5 x 10(-4) M), but the effects of exogenous acetylcholine were unaltered. The inhibition was dose-dependent, reversed by washing and unaltered by hexamethonium.6 The results suggest that pentobarbitone inhibits the vagal component of histamine-induced bronchoconstriction in the dog by an action on the efferent pathway. Furthermore, pentobarbitone acts either by blocking transmission along postganglionic parasympathetic nerves or by preventing the release of acetylcholine from the nerve endings in the lung.

Aerosols↗
PubMed1968

Circulatory effects of chloralose-urethane and sodium pentobarbitone anaesthesis in the rabbit.

1. The effects of chloralose-urethane and sodium pentobarbitone anaesthesia on heart rate, blood pressure and cardiac output were studied in normal rabbits, in animals given atropine and in animals without functioning autonomic effectors. The findings under anaesthesia were compared during spontaneous and artificial intermittent positive pressure respiration.2. The circulatory effects of chloralose-urethane and sodium pentobarbitone anaesthesia differed significantly for the first hour after induction of anaesthesia. During the subsequent 3 hr of maintained anaesthesia differences in the circulatory effects of the two anaesthetics were small.3. The direct local effects of these anaesthetics were assessed during the maintenance phase from the responses of animals without functioning autonomic effectors. With both anaesthetics there was peripheral vasodilatation and minimal effects on heart rate.4. The autonomic activity in the normal animal was assessed by comparing the changes in normal, atropinized and ;de-efferented' rabbits without functioning autonomic effectors. During chloralose-urethane anaesthesia there was reduction in cardiac vagal efferent activity and no change in cardiac sympatho-adrenal activity. With both anaesthetics there was an increase in peripheral sympatho-adrenal constrictor activity, tending to minimize the local vasodilator effects.

Anesthesia, Intravenous↗
PubMed1984

Ventricular fibrillation following canine coronary artery reperfusion: different outcomes with pentobarbital and alpha-chloralose.

We compared the incidence of ventricular fibrillation after release of a 20 min-proximal left anterior descending coronary artery ligation in dogs anesthetized with either pentobarbital (N = 26) or morphine sulfate plus alpha-chloralose (N = 26). Results were analyzed using the logistic risk regression model. In each group, outcome correlated with the amount of myocardium perfused by the ligated vessel (myocardium "at risk") as measured by postmortem coronary injection of monastral dyes. At any given myocardium at risk, animals anesthetized with alpha-chloralose were less likely to fibrillate after release than those anesthetized with pentobarbital (p less than 0.01). This difference in outcome can be described by the myocardium at risk at which half the animals are expected to fibrillate (MAR50). MAR50 was 20.9 g for the pentobarbital group and 30.7 g for the alpha-chloralose group. Myocardium at risk should be taken into account in intervention studies using this coronary reperfusion arrhythmia model. We chose the logistic risk regression model to correct for this variable because it allowed a good fit of the data and offered a concise standard format for expressing the results. Outcome in reperfusion studies may be influenced by the choice of anesthetic agent.

Anesthesia↗
PubMed1994

Crossed and uncrossed segmental synaptic effects on rectus abdominis motoneurons from cutaneous and cutaneous-muscle nerve in spinal cats and alpha-chloralose-anesthetized cats.

Segmental synaptic responses evoked by stimulation of the dorsal cutaneous and cutaneous-muscle (CD) nerve or the ventral cutaneous and cutaneous-muscle (CV) nerve were investigated with intracellular recording from rectus abdominis (RA) motoneurons in 49 spinal cats and 28 alpha-chloralose-anesthetized cats. No monosynaptic and few disynaptic connections existed in the circuit from the ipsilateral or contralateral CD or CV nerves to RA motoneurons in spinal cats. Polysynaptic EPSP responses equal to or over trisynaptic connections were dominant. In alpha-chloralose-anesthetized cats, RA motoneurons exhibited significantly more polysynaptic EPSP responses at lower stimulus intensities (1.5T and 2T) of ipsilateral CV nerve stimulation than at those of contralateral CV nerve stimulation. The result that there was no monosynaptic or disynaptic PSP in RA motoneurons produced by low-intensity stimulation of the ipsilateral CD or CV nerve containing the cutaneous-muscle nerves indicated that Ia afferents from the cutaneous-muscle did not connect mono- or di-synaptically to the RA motoneuron. RA motoneurons exhibited more polysynaptic IPSP responses in alpha-chloralose-anesthetized cats than in spinal cats. Segmental pathways from the CD or CV nerves to RA motoneurons might receive inhibitory descending inputs from the upper spinal cord or the brain, in contrast to those from the same nerves to obliquus externus abdominis motoneurons previously reported.

Anesthesia, General↗
PubMed1998

Cardiovascular responses to microinjection of trans-(+/-)-ACPD into the NTS were similar in conscious and chloralose-anesthetized rats.

The changes in mean arterial pressure (MAP) and heart rate (HR) in response to the activation of metabotropic receptors in the nucleus tractus solitarii (NTS) with trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylic acid (trans-(+/-)-ACPD) were evaluated in conscious and anesthetized Wistar, male rats weighing 240-260 g (N = 8). The responses obtained with trans-(+/-)-ACPD were compared with the responses to L-glutamate (1 nmol/100 nl), since in a previous study we showed that anesthesia converted a pressor response to L-glutamate microinjected into the NTS of conscious rats to a depressor response in the same rats under urethane or chloralose anesthesia. Microinjection of 3 doses of trans-(+/-)-ACPD (100, 500 and 1000 pmol/100 nl) produced a dose-dependent fall in MAP (range, -20 to -50 mmHg) and HR (range, -30 to -170 bpm) under both conscious and chloralose anesthesia conditions. These data indicate that the cardiovascular responses to the activation of metabotropic receptors by trans-(+/-)-ACPD are not affected by chloralose anesthesia while the cardiovascular responses to the activation of excitatory amino acid (EAA) receptors by L-glutamate are significantly altered.

Analysis of Variance↗
PubMed1989

Regional hemodynamic responses to nicotine in conscious and anesthetized dogs: comparative effects of pentobarbital and chloralose.

This study was conducted in 12 dogs to evaluate regional hemodynamic responses during intravenous infusion of nicotine (36 micrograms/kg/min) in the conscious state and compare them with those in the same dogs following either pentobarbital (n = 6) or chloralose anesthesia (n = 6). Values for regional blood flow were obtained with 15-microns radioactive microspheres and used to calculate regional vascular conductance. In the conscious state, nicotine increased aortic pressure (+70%) and caused hyperventilation that reduced arterial PCO2 (-44%). These systemic effects were associated with decreases in vascular conductance in the renal cortex (-48%), pancreas (-81%), duodenum (-58%), and cerebral cortex (-55%), whereas no significant change in vascular conductance was evident in spleen, liver, or myocardium. Pentobarbital anesthesia blunted the increases in aortic pressure and respiratory activity and the reductions in vascular conductance in the renal cortex, pancreas, duodenum, and cerebral cortex during nicotine infusion. In contrast, chloralose anesthesia accentuated the increase in aortic pressure and the decrease in vascular conductance in the renal cortex during nicotine infusion, while it converted no change in vascular conductance in the spleen into a decrease and no change in vascular conductance in the myocardium into an increase. Chloralose anesthesia blunted nicotine-induced hyperventilation. These findings demonstrate that general anesthetic agents may have markedly different effects on cardiovascular reflex pathways. They emphasize the importance of considering the particular characteristics of the anesthetic agent used in interpreting results from studies of cardiovascular pharmacology and physiology in anesthetized animals.

Animals↗
PubMed1991

[The cat has not always done it. A case of alpha-chloralose poisoning in wild birds].

Neglected hens caused annoyance at a graveyard. Following veterinary advice, the authorities used alpha-chloralose-dressed feed in an attempt to sedate the animals, thus facilitating transport to a more suited place. However, the feed was also consumed by other birds. Moreover, the dosage alpha-chloralose appeared to be too high. Hence the resulting mortality struck both the hens and the wild birds. Obviously, alpha-chloralose should not be used for these applications.

Animals↗
PubMed1978

Alterations in blood sugar, serum insulin and circulating free fatty acid responses to glucose load produced in dogs by chloralose anaesthesia.

The effects of chloralose anaesthesia on the BS, serum IRI and circulating FEA responses to glucose in dogs, in the course of glucose tolerance tests were studied. Chloralose induced a moderate glucose intolerance, and abolished both, the insulin response to hyperglycaemia in these animals and the lipolytic response at the end of the test. These effects indicate that chloralose anaesthesia is definitely improper for metabolic studied in experimental biology.

Anesthesia↗
PubMed1998

Effects of halothane and urethane-chloralose anaesthesia on the pressor and cerebrovascular responses to 7-NITROINDAZOLE, an inhibitor of nitric oxide synthase.

We examined the effect of 7-nitroindazole (7NI), a reportedly relatively specific inhibitor of the neuronal isoform of nitric oxide synthase (nNOS), on mean arterial blood pressure and on cerebral blood flow in rats under three different types of anaesthesia: urethane-chloralose, halothane, or urethane preceded by induction of anaesthesia with halothane. In rats under urethane-chloralose anaesthesia, 7NI induced an increase in mean systemic arterial blood pressure. In contrast, halothane used for induction and maintenance of anaesthesia eliminated the 7NI-induced systemic pressor effect, while halothane used only for induction of anaesthesia greatly attenuated the 7NI-induced systemic pressor effect. Cerebral blood flow, as measured by Laser Doppler flowmetry, decreased significantly to 85-72% of baseline within 5-10 min after i.p. 7NI injection regardless of the type of anaesthesia. Blockade of the systemic pressor effect of 7NI by halothane but not of the reduction in cerebral blood flow produced by 7NI is consistent with prior evidence that: (1) the cerebral vasculature and the peripheral vasculature differ in the isoforms of NOS involved in maintaining vascular tone, with nNOS more important in the former and endothelial NOS (eNOS) in the latter; and (2) halothane interferes with eNOS-mediated vascular tone but not nNOS-mediated control of cerebral blood flow. The fact that 7NI yields a pressor effect that can be attenuated by halothane, as also true for isoform-non-selective NOS inhibitors, raises the possibility that 7NI may to some extent inhibit endothelial NO formation. (c) 1998 The Italian Pharmacological Society.

Anesthetics, General↗
PubMedDate not supplied

Vagal afferents inhibit the antidiuresis and antinatriuresis secondary to bilateral carotid occlusion in the chloralose-anesthetized dog.

It has been reported that bilateral carotid occlusion (BCO) does not alter renal excretory function in conscious dogs on a high-salt diet with intact vagi provided renal perfusion pressure (RPP) is held constant. In contrast, low carotid sinus pressures in chloralose-anesthetized dogs with severed vagi elicit significant reductions in renal excretory function which were mediated by renal sympathetic nerves. The purpose of the present study was to investigate the influence of BCO on renal function in chloralose-anesthetized, volume expanded dogs with and without intact cervical vagi and with RPP held constant. A total of 10 dogs, volume expanded with hypotonic saline, were prepared to measure systemic arterial pressure (SAP), carotid sinus pressure (CSP), RPP, and urine flow. With the cervical vagi intact, BCO elicited an increase in SAP from 132 +/- 4 mm Hg to 172 +/- 5 mm Hg (p less than 0.01). This was associated with significant and paradoxical increases in urine flow (+35%), sodium excretion (+63%), osmolar clearance (+32%), and free water clearance (+33%). These changes were also accompanied by small but significant increases in ERBF (+11%) and GFR (+12%). Bilateral cervical vagotomy alone (Vx) increased SAP (129 +/- 6 mm Hg to 146 +/- 5 mm Hg, p less than 0.05). Urine flow and free water clearance were decreased but sodium excretion and osmolar clearance were increased. No change in ERBF or GFR was measured. BCO after Vx elicited a greater increase in SAP as compared to BCO alone (194.5 +/- 6.2 mm Hg) which was accompanied by significant decreases in urine flow (-60%), sodium excretion (-55%), osmolar clearance (-43%), ERBF (-13%), and GFR (-19%). Therefore, the results of this study demonstrate that the contrasting influences of BCO on renal function reported previously in conscious and anesthetized animal models may be due to the presence or absence of the inhibitory influences of afferent fibers contained in the cervical vagi, probably cardiac in origin.

Anesthesia, Intravenous↗
PubMed1997

Effects of halothane, alpha-chloralose, and pCO2 on injury volume and CSF beta-endorphin levels in focal cerebral ischemia.

Anesthetic agent, arterial pCO2 level, and opioid peptides have all been implicated in the pathophysiology of experimental stroke models. The effects of halothane, alpha-chloralose, and differing concentrations of arterial pCO2 on injury volume and CSF beta-endorphin levels were studied in a feline model of experimental focal cerebral ischemia. The type of anesthetic agent used had no effect on injury volume following 6 h of focal cerebral ischemia. Over a 6-h period, beta-endorphin levels significantly increased from 10.1 +/- 5.0 fmol/mL at zero time to 14.4 +/- 7.2 fmol/mL at 6 h under halothane anesthesia (p < 0.05), whereas they did not significantly change (10.1 +/- 6.7 to 7.8 +/- 4.7 fmol/mL) under alpha-chloralose anesthesia. In contrast, hypercapnia had no effect on beta-endorphin levels, but significantly increased injury volume from 30.6 +/- 5.7% of the ipsilateral hemisphere under normocapnic conditions to 37.1 +/- 5.9% under hypercapnic conditions (p < 0.05). These results suggest that hypercapnia increases injury volume in a feline model of focal cerebral ischemia, and pCO2 should be controlled in experimental focal cerebral ischemia models.

Anesthetics, Inhalation↗
PubMed1988

Effect of indomethacin on modest pressure natriuresis in chloralose-anesthetized, non-laparotomized dogs.

To determine if indomethacin (indo) would attenuate the effects of changed renal perfusion pressure on sodium excretion as reported by others, we performed clearance studies in chloralose-anesthetized dogs without the major stress of laparotomy. Mean renal arterial pressure was varied by a balloon-tipped catheter indwelling the aorta suprarenally. With pressure decreases to mean values above 85 mm Hg during isotonic saline infusion, sodium output decreased only by 10.7 +/- 2.4% per 10 mm Hg pressure decrease without indo pre-treatment but decreased by 22.0 +/- 3.8% per 10 mm Hg pressure decrease with indo pre-treatment. The greater, rather than lesser, pressure effect on excretory function after indo in these experiments with chloralose anesthesia suggest that renal prostaglandin (PG) activity does not mediate normally pressure natriuresis. Instead, the data suggest that, in the absence of major stress, the renal pressure effects on excretory function may become more sensitive after indo. In addition, we postulate that the normal acute pressure natriuresis may be modest and may average no more than 20% change for each 10 mm Hg change in mean pressure above 90 mm Hg when stress is minimal and when vasoactive preglomerular autoregulation is nearly perfect. This is a phenomenon which keeps intrarenal tissue pressure and urine output relatively constant with arterial pressure elevations.

Anesthesia↗