Effects of hemorrhage and naloxone on adrenal release of methionine-enkephalin and catecholamines in halothane anesthetized dogs

Gaumann, Dorothee M.; Yaksh, Tony L.; Dousa, M. K.; Tyce, Gertrude M.; Lucas, Darlene L.; Hench, Victoria S.

doi:10.1016/0165-1838(87)90089-0

Cited by 6 publications

(2 citation statements)

References 33 publications

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“…Free plasma catecholamines in the alumina eluate were further purified on small columns of Amberlite CG50 (Dousa and Tyce, 1988). The coefficient of variation of this assay procedure has been shown by us to be 5.3% for norepinephrine, 10% for epinephrine, and 7.4% for dopamine (Gaumann et al, 1987). The recoveries of 2 ng of internal standards added to 1 ml of plasma varied between 81 and 88%.…”

Section: Catecholamines Precursors and Metabolitesmentioning

confidence: 99%

Catecholamine Release and Excretion in Rats with Immunologically Induced Preganglionic Sympathectomy

Brimijoin

Hammond

Khraibi

et al. 1994

Journal of Neurochemistry

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Plasma and urinary catecholamines were quantified to assess global sympathoadrenal function in rats with preganglionic lesions caused by antibodies to acetylcholinesterase (AChE). Rats were given intravenous injections of normal mouse IgG or murine monoclonal anti-acetylcholinesterase IgG (1.5 mg). Five or 16 days afterward, basal blood samples were taken through indwelling arterial cannulae. A few hours later, the rats were immobilized for 10 min in padded restrainers, and another blood sample was drawn. HPLC determinations showed low basal levels of norepinephrine and epinephrine (<0.2 ng/ml in all rat plasma samples). In control rats, immobilization stress increased levels of plasma catecholamines up to 35-fold. In rats tested 5 days after injection of antibody, the norepinephrine response was much smaller (15% of control), and the epinephrine response was nearly abolished (5% of control). There was some recovery at 16 days after antibody treatment, but stress-induced catecholamine release was still markedly impaired. Reduced stress-induced release was not accompanied by major changes in tissue epinephrine or norepinephrine (heart, spleen, adrenal glands, and brain), although adrenal dopamine content dropped by 60%. Urinary excretion was studied in parallel experiments to gain insight into the effects of AChE antibodies on basal syrnpathoadrenal activity. Epinephrine, norepinephrine, dopamine, and selected metabolites were quantified in 24-h urine samples collected at frequent intervals for 30 days after antibody injection. No statistically significant changes were detected in the urinary output of doparnine, 3-methoxytyramine, normetanephrine, or 3methoxy-4-hydroxyphenylglycol. On the other hand, epinephrine and norepinephrine output increased sharply at the time of antibody injection and then fell significantly below control levels. Norepinephrine output returned to normal after 2 weeks, but epinephrine output remained depressed. These results are consistent with previous evidence of widespread and persistent antibody-mediated damage to the preganglionic sympathetic system.

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Section: Catecholamines Precursors and Metabolitesmentioning

confidence: 99%

Catecholamine Release and Excretion in Rats with Immunologically Induced Preganglionic Sympathectomy

Brimijoin

Hammond

Khraibi

et al. 1994

Journal of Neurochemistry

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“…1986 ), etc. The factors of the second type comprise the platelet activating factor and antihypertensive renomedullary lipid (medullipin, Muirhead 1990), some opioid peptides ( Gaumann et al . 1987 ), recently discovered adrenomedullin ( Kitamura et al .…”

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Evidence for an antihypertensive factor from the adrenal medulla of SHR modulating neurogenic vasoconstriction

Nesterova

Chuiko

Sokolova

et al. 1999

Acta Physiologica Scandinavica

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The aim of this study is to investigate some vasoactive properties of the blood of spontaneously hypertensive rats (SHR). Isolated segments of rat tail arteries obtained from normotensive rats (Wistar-Kyoto (WKY) and Wistar) were perfused with blood from conscious donor rats (WKY, Wistar or SHR). Alterations of the neurogenic constrictor responses (NCR) of the isolated segments evoked by electrical stimulation were studied. The amplitude of NCR of the isolated arteries was studied during perfusion with blood according to the perfusion scheme WKY1(1)-SHR1(2)-WKY1(3) and WKY1(1)-WKY2(2)-WKY1(3). The release of 3H-noradrenaline ([3H]-NA) from vascular sympathetic fibres was measured. The influence of adrenal demedullation on NCR was estimated. We have shown that NCR of isolated arteries decreased by 28.3 +/- 7.9% (P < 0.05 vs. WKY1(1)) during perfusion with blood from SHR (scheme WKY1(1)-SHR1(2)-WKY1(3)). In these experiments, release of [3H]-NA from sympathetic fibres of the artery segments decreased by 39.9 +/- 9.6% during the perfusion with blood from SHR vs. WKY1(1) (P < 0.05). Adrenal demedullation prevented the decrease of NCR during perfusion of the arteries with blood from SHR. In conclusion, the blood of SHR has some antihypertensive factor(s), which causes decrease of NCR in the tail artery from normotensive rats. This decline is accompanied by the decrease of release in [3H]-NA from the transmural sympathetic fibres and is abolished after adrenal demedullation of blood donor rats.

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Endogenous Opioid Peptides, Glucocorticoids, and Shock: Specificity, Site, and Mechanism of Action

Giersbergen¹,

Berg²,

Eijgelshoven³

et al. 1991

Central Neural Mechanisms in Cardiovascular Regulation

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Effects of hemorrhage and naloxone on adrenal release of methionine-enkephalin and catecholamines in halothane anesthetized dogs

Cited by 6 publications

References 33 publications

Catecholamine Release and Excretion in Rats with Immunologically Induced Preganglionic Sympathectomy

Catecholamine Release and Excretion in Rats with Immunologically Induced Preganglionic Sympathectomy

Evidence for an antihypertensive factor from the adrenal medulla of SHR modulating neurogenic vasoconstriction

Endogenous Opioid Peptides, Glucocorticoids, and Shock: Specificity, Site, and Mechanism of Action

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