Pineal function in burns: melatonin is not a marker for general sympathetic activity

Vaughan, George M.; Taylor, Thomas J.; Lasko, James; Coggins, Sandy H

doi:10.1016/0022-4731(84)90627-7

Cited by 13 publications

(17 citation statements)

References 12 publications

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“…However, neither burned rats or hamsters (pineal melatonin content) nor burned humans (serum concentration) had elevated daytime melatonin. Thus, the sympathetic pathway to the pineal does not share in the general sympathetic activation following burn injury, 134 which conforms with previous evidence that melatonin is not an index of general sympathetic tone. 132 Further, in burned humans the nocturnal surge of serum melatonin, though still evident, is blunted 134 ( Fig.…”

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confidence: 73%

Neuroendocrine and Sympathoadrenal Response to Thermal Trauma

Vaughan¹

1990

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The previous chapters have described many alterations in secreted hormones and metabolic processes that occur for weeks to months after major burn injury. Interpretation of these alterations can be bewildering; however, many of the findings can be simplified and/or unified to a certain extent if they are viewed as part of an overall alteration in central nervous system (CNS) function characterized by modified control settings. The Neuroendocrine Reflex ArcEarly work with acute surgical trauma provided the conceptual framework of the neuroendocrine reflex arc. 12 In this framework, a signal from an injured area is transmitted by an afferent limb to the brain, which integrates the formation and orchestrates a neural and hormonal output as the efferent limb.Hume and Egdahl 3 studied dogs anesthetized with ether or Nembutal and with a catheter in an adrenal vein. Upon application of a scald burn, the corticosteroid (CS) secretion rate rose promptly within minutes. This response was blocked by prior section of the medulla oblongata, the spinal cord, or the peripheral nerve innervating the area of the lesion. Subcutaneous injection of ACTH in the denervated burned area provoked a CS response, indicating that if a burn toxin were present and capable of stimulating this acute response humorally, it would likely have been detected. Thus, the acute CS response to a burn did not result from pain per se, which was blocked by the anesthesia, nor from systemic absorption of a humoral toxin from the burned area, but from afferent neural information signaling the presence of an injury. In some experiments, crude measurements of circulating ACTH indicated that the CS response was associated with a surge in endogenous ACTH release. Lesions of the anterior hypothalamus blocked the CS and ACTH responses to operative trauma. These and the cord section experiments indicated that the adrenocortical response was via brain control of ACTH secretion, not via innervation of the adrenals. Nevertheless, activation of the adrenal medullae through the neural route was indicated by observation of elevated catecholamine (CA) secretion rates in the adrenal vein after injury.

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confidence: 73%

Neuroendocrine and Sympathoadrenal Response to Thermal Trauma

Vaughan¹

1990

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“…The in transducer. Science 184, 1341-1348. vivo values (Vaughan et al, 1985) were obtained Bowers C. W. and Zigmond R. E. (1980) Electrical without nocturnal exposure of the animals to light, stimulation of the cervical sympathetic trunks mimics Other recent experiments (Vaughan et al, 1986) have the effects of darkness on the activity of serotonin: endings in the pineal gland protect against acute stress--known. However, a contributory role for a nyctoinduced increase in N-acetyltransferase (EC 2.3.1.5.)…”

Section: Resultsmentioning

confidence: 99%

“…In production acutely to near-daytime levels (Rollag et al, these experiments, isoproterenol (ISO) was com-1980). Pineals were incubated individually as described monly used as the beta-agonist because its action is (Vaughan et al, 1986) in I ml Minimal Essential Medium not influenced by the nerve ending uptake mechanism containing 10% fetal calf serum at pH 7.4 and 37°C under (Parfitt and Klein, 1976). In contrast to the studies in an atmosphere of 95% 02 and 5% C0 2 , without or with rats, injection of ISO into Syrian hamsters (with isoproterenol (ISO) at one of several tenfold different conrat, ijecionof SO nt Syianhamter (wth centrations ranging from 10-I to 10-$ M for pineals taken intact or denervated pineals) during the day did not cnations0rag from 0-9 to 10-'M for those taken at a. at 2000 hr or from 10-'t 0Mfrtoetkna increase pineal melatonin cdntent (Lipton et at., 0230 hr.…”

Section: Introductionmentioning

confidence: 99%

“…For graphic purposes, best fit tay/nighe betarener actpionealth endogsenusity-t curves were drawn from a three-parameter exponential tta ne o abe tregression of the MEL data against ISO concentration, pathetic neurotransmitter sensitivity to a betawhich allows a sigmoid plot with respect to log concenagonist could be demonstrated at night when the tration, and data were analyzed by t-tests with the Bonsympathetic nerves to the pineal ordinarily mediate ferroni correction for multiplicity of comparisons, analyses the nocturnal surge of me? ýtonin synthesis (Bowers of covariance, and in one case a two-way analysis of and Zigmond, 1980;Vaughan and Reiter, 1986). The variance (Dixon, 1983).…”

Section: Introductionmentioning

confidence: 99%

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Nyctohemeral rhythm in melatonin response to isoproterenol in vitro: Comparison of rats and Syrian hamsters

Vaughan

Pruitt

Mason

1987

Comparative Biochemistry and Physiology Part C: Comparative Pha

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“…The nocturnal pineal melatonin rise in this species is prevented by beta-blockade [Lipton et al, 1981] and SCGX [Panke et al, 1979;Vaughan and Reiter, 19851. In the light of such findings, the nocturnal appearance of a pineal melatonin response to NE and protection from humoral-route activation by a neuronal uptake system in Syrian hamsters (a) indicate that NE is likely the pineal neurotransmitter responsible for the nocturnal melatonin surge, (b) explain previous negative results with NE, and (c) provide possible mechanisms to eliminate noise in the 24-h rhythmic melatonin signal by preventing untimely rises in melatonin synthesis due to general sympathetic stimuli. Indeed, such partitioning of sympathetic function for independent and specific control of the pineal may help explain the observed lack of evidence for augmented melatonin production after general sympathetic stimuli in Syrian hamsters and humans [see Vaughan, 1984;Gupta et al, 1983;Champney et al, 1985;Vaughan et al, 1985]. Pineal neuronal uptake might afford protection against the humoral limb of a general sympathetic response.…”

Section: Hw-ister Melatonin Response To Norepinephrine 247mentioning

confidence: 99%

Rhythmic Melatonin Response of the Syrian Hamster Pineal Gland to Norepinephrine In Vitro and In Vivo

Vaughan

Lasko

Coggins

et al. 1986

Journal of Pineal Research

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Norepinephrine (NE, 10−6 M) stimulated melatonin accumulation in the incubation medium of rat (but not Syrian hamster) pineals taken at the end of the light phase. However, NE elevated melatonin accumulation in the medium of pineals taken after 20 min of light exposure of animals of either species at 6 h into the 10‐h dark phase. A dose response to 10−7−10−5 M NE was observed in both the medium and pineals upon incubation of pineals taken from rats at 4 h into the light phase and from hamsters after 20 min light exposure at 6 h into the dark phase. Approximately 95% of the melatonin present was in the medium. The incubation time was 4 h in all cases. Subcutaneous injection of 1 μg/g NE (either at the end of the light phase or after 30 min of light at 6 h into the dark phase) did not stimulate in vivo Syrian hamster pineal melatonin content determined 1 or 2 h after injection, whether the hamsters were placed in light or darkness after the injection. However, after 30 min of light beginning at 6 h into dark, injection of 5 μg/g desipramine (DMI, a blocker of catecholamine uptake into nerve endings) allowed a dramatic hamster pineal melatonin response to additional injection of 1 μg/g NE, observed at 1 and 2 h in light after injection. A small effect of DMI alone was seen. DMI also potentiated the effect of NE (each 10−6 M) on melatonin accumulation in the medium of incubated hamster pineals taken after a short light exposure at night. No significant stimulatory effect of NE and/ or DMI was seen in vivo or in vitro near the middle of the light phase. Measurement of melatonin in the incubation medium is a useful method for studying pineal function. The Syrian hamster pineal has rhythm of sensitivity to NE (sensitivity evident at night) and even at night is protected by neuronal uptake from circulating NE‐induced stimulation of melatonin production. NE appears to be the neurotransmitter for stimulation of pineal melatonin production in the Syrian hamster. The sensitivity rhythm and uptake protection might provide specificity of control of the nightly melatonin signal by reducing the chance of a melatonin response during the day or a response to circulating catecholamines from general sympathetic stimuli.

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Pineal function in burns: melatonin is not a marker for general sympathetic activity

Cited by 13 publications

References 12 publications

Neuroendocrine and Sympathoadrenal Response to Thermal Trauma

Neuroendocrine and Sympathoadrenal Response to Thermal Trauma

Nyctohemeral rhythm in melatonin response to isoproterenol in vitro: Comparison of rats and Syrian hamsters

Rhythmic Melatonin Response of the Syrian Hamster Pineal Gland to Norepinephrine In Vitro and In Vivo

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