Central Monaminergic Neuronal Effects on Minimum Alveolar Concentrations (MAC) of Halothane and Cyclopropane in Rats

Mueller, Robert A.; Smith, Rebecca; Spruill, W A; Breese, G. R.

doi:10.1097/00000542-197502000-00006

Cited by 32 publications

(14 citation statements)

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“…Therefore, we tested dopamine ß-hydroxylase ( Dbh ) null mice, which are devoid of norepinephrine and epinephrine, and compared them with Dbh heterozygous sibling controls shown previously to have normal catecholamine levels [26]. As predicted from previous studies [23], [24], [25], Dbh null mice exhibit hypersensitivity to induction by isoflurane. However, their most striking phenotype is a dramatic increase in neural inertia, due to a profoundly altered threshold for emergence (Figure 5A).…”

Section: Resultsmentioning

confidence: 93%

“…Based upon pharmacologic and lesion studies that impair adrenergic signaling and modulate supra-hypnotic anesthetic endpoints [23], [24], [25], we considered the adrenergic system as a candidate that might affect neural inertia. Therefore, we tested dopamine ß-hydroxylase ( Dbh ) null mice, which are devoid of norepinephrine and epinephrine, and compared them with Dbh heterozygous sibling controls shown previously to have normal catecholamine levels [26].…”

Section: Resultsmentioning

confidence: 99%

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A Conserved Behavioral State Barrier Impedes Transitions between Anesthetic-Induced Unconsciousness and Wakefulness: Evidence for Neural Inertia

et al. 2010

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One major unanswered question in neuroscience is how the brain transitions between conscious and unconscious states. General anesthetics offer a controllable means to study these transitions. Induction of anesthesia is commonly attributed to drug-induced global modulation of neuronal function, while emergence from anesthesia has been thought to occur passively, paralleling elimination of the anesthetic from its sites in the central nervous system (CNS). If this were true, then CNS anesthetic concentrations on induction and emergence would be indistinguishable. By generating anesthetic dose-response data in both insects and mammals, we demonstrate that the forward and reverse paths through which anesthetic-induced unconsciousness arises and dissipates are not identical. Instead they exhibit hysteresis that is not fully explained by pharmacokinetics as previously thought. Single gene mutations that affect sleep-wake states are shown to collapse or widen anesthetic hysteresis without obvious confounding effects on volatile anesthetic uptake, distribution, or metabolism. We propose a fundamental and biologically conserved concept of neural inertia, a tendency of the CNS to resist behavioral state transitions between conscious and unconscious states. We demonstrate that such a barrier separates wakeful and anesthetized states for multiple anesthetics in both flies and mice, and argue that it contributes to the hysteresis observed when the brain transitions between conscious and unconscious states.

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Section: Resultsmentioning

confidence: 93%

Section: Resultsmentioning

confidence: 99%

A Conserved Behavioral State Barrier Impedes Transitions between Anesthetic-Induced Unconsciousness and Wakefulness: Evidence for Neural Inertia

et al. 2010

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“…In order to understand causality, one approach has been to alter central monoamine content pharmacologically or surgically, followed by an assessment of the effect on anesthetic potency. In general, drugs that produce global depletion of monoamines cause a decrease in the anesthetic requirement of halothane (18,19). Specifically, Mueller et al (18) found that the decrease in halothane MAC (10-2770) was small compared to extensive depletion of central monoamines (50-86%) after drug treatment.…”

Section: Discussionmentioning

confidence: 99%

“…In general, drugs that produce global depletion of monoamines cause a decrease in the anesthetic requirement of halothane (18,19). Specifically, Mueller et al (18) found that the decrease in halothane MAC (10-2770) was small compared to extensive depletion of central monoamines (50-86%) after drug treatment. Roizen et al (20) effected more pronounced decreases in halothane MAC (31-35%) by specific brain lesions of the locus ceruleus, nucleus raphe dorsalis, and ventral bundle.…”

Section: Discussionmentioning

confidence: 99%

Analgetic Contribution of Sufentanil during Halothane Anesthesia

Althaus

Miller

Moscicki

et al. 1985

Anesthesia & Analgesia

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DiFAZIO CA. Analgetic contribution of sufentanil during halothane anesthesia: a mechanism involving serotonin. Anesth Analg 1985;64:857-63.Catecholamine and serotonin concentrations in the cord, medulla, and hypothalamus were measured in rats after saline, after sufentanil sufficient to reduce the minimum alveolar concentration (MAC) of halothane by 30% or less, or after sufentanil sufficient to reduce the MAC of halothane by 80% or more. In the cord, high doses of sufentanil resulted in a 13.4% reduction (P < 0.05) in serotonin concentration compared to saline control and a 17.4% reduction ( P < 0.05) in serotonin concentration compared to low dosages of sufentanil. A 12.8% reduction ( P < 0.05) in medullary serotonin also was observed with high sufentanil compared to low sufentanil. Epinephrine decreased significantly in the hypothalamus at the high sufentanil dose. No other significant differences were found in catecholamine content. The experimental results support the hypothesis that sufentanit may contribute to an analgetic component of general anesthesia by modulating nociception via the release of 5-HT.Sufentanil is a substituted derivative of fentanyl that is more potent and less toxic than fentanyl or morphine (1). Recently sufentanil was shown to reduce the minimum alveolar concentration (MAC) of halothane by more than 90% in rats ( 2 ) .Evidence suggests that central monoamines may play an important role in the analgetic control of anesthesia, although this has not been clearly elucidated. Yaksh and Tyce showed that microinjections of morphine into the periaqueductal gray (PAG) evoked the release of serotonin from the spinal cord (3). These injections resulted in analgesia that could be reduced by inhibition of 5-HT terminals in the spinal cord (4). Wang showed that the direct intrathecal administration of serotonin resulted in antinociception (5) and mimicked the analgetic effect of morphine injected into the PAG, as reported by Yaksh and Tyce. When the PAG was electrically stimulated in human patients, Newfield et al. (6) found that halothane MAC was reduced by 73%. Ahtee showed that chronic morphine administration decreased 5-HT in rat brains (7).These findings suggest that the ability of narcotics to contribute to an analgetic component of general anesthesia may be related to modulation of nociception by the narcotic activation of 5-HT release in central nervous system tissues. To test this possibility further, we have measured concentrations of monoamines in nervous tissue in three groups of rats. One group, receiving only halothane anesthesia at 1 MAC, was designated as the control. The other two groups were designated as the low-dose and the high-dose sufentanil groups. The proposed mechanism of halothane MAC reduction by narcotics would be supported if our data showed a relationship between increased dosages of sufentanil and decreased levels of 5-HT in central nervous system tissue. MethodsHalothane MAC and reductions in halothane MAC were established as reported previously (2). Briefly, 19 S...

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“…6 In animals, the use of vasopressors did not affect minimum alveolar concentration (MAC) of halothane for immobility, 7 whereas sympathoexcitation, a physiological consequence of baroreceptor unloading, increased MAC for cyclopropane and halothane. 8,9 On the other hand, reduction of the mean arterial pressure to 50 mmHg reduced MAC by approximately 20%, possibly due to decreased cerebral perfusion. 10 Anesthetics generally suppress baroreceptor function in clinically relevant concentrations.…”

Section: Méthode : La Méthode De L'escalier De Dixon a éTé Utilisée Pmentioning

confidence: 99%

Sitting position does not alter minimum alveolar concentration for desflurane

Lin

Lee

et al. 2007

Can J Anesth/J Can Anesth

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Purpose: Hypotension is a common complication of the sitting position during anesthesia, and is often counteracted by decreasing anesthetic depth, thereby exposing patients to the risk of being inadequately anesthetized. Baroreceptor unloading and the consequent sympathoexcitation, as during head up tilt, decreases pain threshold and arouses the central nervous system (CNS), whereas hypotension exerts a direct CNS depressant effect. We estimated the minimal alveolar concentration (MAC) of desflurane for immobility in patients undergoing surgery in the sitting position, in comparison to MAC desflurane for patients having a similar type of surgery in the supine position. Methods:The Dixon up-and-down method was used to evaluate the MAC for desflurane in patients undergoing cervical spine laminoplasty (n = 24) or discectomy (n = 24) in the sitting and supine positions, respectively. Logistic regression with co-variate adjustment was employed to examine if the two positions (sitting and supine) have different or share the same concentration vs response relationship for immobility. Monte Carlo simulation was used to calculate 95% confidence intervals (CI) for the MAC in each position, and to estimate the difference in MAC (delta MAC) between the sitting and supine positions. Results:Modeling both sitting [6.54% (6.50-6.66, 95% CI)] and supine [6.70 (6.55-6.81)] patients as having different MAC concentrations did not significantly improve our simplified model, which treats the two patient groups as one [6.61 (6.52-6.70), delta -2 log likelihood = 2.735, P = 0.098]. Mean delta MAC (95% CI) was -0.14 (-0.30, 0.03). Conclusion:The sitting position does not change desflurane anesthetic requirements for immobility. [6,54 % (6,66, 95 % IC)] et ceux en décubitus dorsal [6,70 (6,55-6,81)] présentent des concentrations MAC différentes, n'a pas amélioré de façon significative notre modèle simplifié, lequel considère les deux groupes de patients en tant qu'un seul groupe [6,61 (6,52-6,70), delta -2 logarithme du rapport de vraisemblance = 2,735, P = 0,098]. 30, 0,03). REPORTS OF ORIGINAL INVESTIGATIONS 523CAN J ANESTH 54: 7 www.cja-jca

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Central Monaminergic Neuronal Effects on Minimum Alveolar Concentrations (MAC) of Halothane and Cyclopropane in Rats

Cited by 32 publications

References 0 publications

A Conserved Behavioral State Barrier Impedes Transitions between Anesthetic-Induced Unconsciousness and Wakefulness: Evidence for Neural Inertia

A Conserved Behavioral State Barrier Impedes Transitions between Anesthetic-Induced Unconsciousness and Wakefulness: Evidence for Neural Inertia

Analgetic Contribution of Sufentanil during Halothane Anesthesia

Sitting position does not alter minimum alveolar concentration for desflurane

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