The Adrenal Medullary Response to Graded Hemorrhage in Awake Dogs

The cardiovascular effects of tetrahydroaminoacridine (tacrine; THA) were investigated in haemorrhaged rats. Intracerebroventricular (i.c.v.) injection of THA (10, 25 and 50 µg) restored blood pressure in a dose- and time-dependent manner. Atropine (10 µg, i.c.v.), a muscarinic receptor antagonist, attenuated the pressor response to THA (25 µg, i.c.v.), while mecamylamine (50 µg, i.c.v.), a nicotinic receptor antagonist, caused only a slight blockade in the pressor effect of THA. Simultaneous pretreatment with atropine and mecamylamine almost abolished the blood pressure effect of i.c.v. THA (25 µg). Haemorrhage increased plasma levels of adrenaline, noradrenaline, vasopressin and plasma renin activity. THA (25 µg, i.c.v.) administration caused additional increases in vasopressin and adrenaline levels but not of renin activity and noradrenaline levels. The reversal of hypotension by THA was greatly attenuated by administration of either prazosin, an α₁-adrenoceptor antagonist (0.5 mg/kg, i.v.) or by the vasopressin V₁ receptor antagonist [β-mercapto-β,β-cyclopenta-methylenepropionyl¹, O-Me-Tyr²-Arg⁸]-vasopressin (10 µg/kg, i.v.). Pretreatment of rats with both prazosin and the vasopressin antagonist simultaneously completely inhibited the pressor response. Intravenous administration of THA (1, 1.5 and 3 mg/kg) also reversed hypotension in rats. Atropine (10 µg, i.c.v.) greatly attenuated the pressor response to THA (1.5 mg/kg, i.v.), while mecamylamine (50 µg, i.c.v.) failed to change the pressor effect of THA. In anaesthetised haemorrhaged rats, THA (1.5 mg/kg, i.v.) increased blood pressure and survival time of the animals. These results show that centrally and peripherally injected THA reverses haemorrhagic hypotension and increases survival time in rats. Activation of central muscarinic and nicotinic receptors is involved in the pressor response to i.c.v. THA. The pressor effect of i.v. THA is solely mediated by central muscarinic receptors. Moreover, the increase in plasma adrenaline and vasopressin levels appears to be involved in the pressor effect of THA.

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“…These findings are similar to those of previous reports [23][24][25][26]. The pressor response to i.c.v.…”

Section: Discussionsupporting

confidence: 93%

Reversal of Haemorrhagic Shock in Rats by Tetrahydroaminoacridine

Savci¹,

Çavun²,

Gurun³

et al. 2001

Pharmacology

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“…Adrenal venous catecholamines were determined from 100 pi of plasma after alumina extraction by high performance liquid chromatography with electrochemical detection as described pre viously [13]. The intraassay and interassay coefficients of variation for a cat plasma pool having 3.81 ng/ml norepinephrine were 2.7 and 6.7%, respectively; having 24.22 ng/ml epinephrine were 5.1 and 6.6%, respectively, and having 0.71 ng/ml dopamine were 5.8 and 8.9%, respectively.…”

Section: Catecholamine Determinationsmentioning

confidence: 99%

Adrenal Secretion of Epinephrine after Stimulation of Trigeminal Nucleus caudalis Depends on Stimulus Pattern

Bereiter

Engeland²,

Gann

1987

Neuroendocrinology

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Adrenal catecholamine secretion after stimulation of trigeminal nucleus caudalis (Vc) was compared to that evoked from more ventrolateral brain stem areas (VLM) by sampling adrenal venous blood in anesthetized cats. The effect of stimulus pattern on catecholamine secretion was assessed by presenting an equal number (300 pulses over 15 s) of electrical stimuli (75 µA, 0.2 ms) as a continuous pattern and as a burst pattern pulse train at each electrode site. Epinephrine secretion increased promptly by 1 min after burst pattern stimulation of Vc, whereas continuous pattern stimuli had no consistent effect. Burst pattern stimulation of VLM sites caused a small decrease in epinephrine secretion, whereas continuous pattern stimuli had no significant effect. Adrenal norepinephrine increased equally after Vc or VLM stimulation regardless of stimulus pattern. The adrenal catecholamine secretory responses could not be explained by the transient evoked changes in adrenal venous plasma flow or arterial pressure. The data indicate that stimulation of Vc evokes a pattern-dependent increase in epinephrine secretion, whereas the increase in norepinephrine secretion is equal after burst or continuous pattern stimuli. Further, adrenal activation by brief neural stimuli cannot be assessed adequately in the cat by measuring epinephrine secretion alone, since stimulation of many ventrolateral brain stem sites caused a significant increase in norepinephrine secretion with no corresponding increase in epinephrine secretion.

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“…Hemorrhage is a potent stimulus of the hypothalamo-pituitaryadrenal (HPA) axis (for reviews see I, 2). Acute blood loss triggers an adrenocorticotropin (ACTH) release (3)(4)(5) which is sensitive to dexamethasone (DEX) (6) according to the well-known negative feedback regulation of the HPA by glucocorticoids for a great variety of stress stimuli (for review see 7). The neuroanatomical connections between the peripheral cardiovascular receptors and the hypothalamic paraventricular nucleus (PVN), that contains the corticotropin-releasing factor (CRF) neurons controlling the ACTH release from the anterior pituitary (for reviews see 8,9), are fairly well documented.…”

mentioning

confidence: 99%

Hemorrhage‐Induced Activations of Adrenocorticotropin Release and Catecholamine Metabolism in the Ventrolateral Medulla are Differently Affected by Glucocorticoid Feedback

Ponec

Lachuer

Suaud-Chagny

et al. 1992

J Neuroendocrinology

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We have compared the effects of increasing doses of dexamethasone on the hemorrhage-induced stimulation of the corticotropic axis and the metabolism of the catecholamines of the A1 group in the ventrolateral medulla. Adrenocorticotropin was measured in sequential samples of plasma while the metabolism of the catecholamines was recorded by in vivo electrochemistry in urethane-anesthetized rats. Combined intracerebroventricular injection of specific adrenergic blockers (α(1) -antagonist, prazosin and ß-antagonist, propranolol) prevented the stimulation of the adrenocorticotropin release by hemorrhage. Pretreatment with dexamethasone (1 mg/kg sc) fully blocked the hemorrhage-induced adrenocorticotropin release but did not affect the concomitant stimulation of the catecholamine metabolism in A1 cells. The latter was partially decreased only with the highest dose (10 mg/kg sc). While a central catecholaminergic input appears to be necessary for the hemorrhage-induced stimulation of the corticotropic axis, it does not seem to play a significant role in the feedback regulation by glucocorticoids.

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The Adrenal Medullary Response to Graded Hemorrhage in Awake Dogs

Cited by 36 publications

References 18 publications

Reversal of Haemorrhagic Shock in Rats by Tetrahydroaminoacridine

Reversal of Haemorrhagic Shock in Rats by Tetrahydroaminoacridine

Adrenal Secretion of Epinephrine after Stimulation of Trigeminal Nucleus caudalis Depends on Stimulus Pattern

Hemorrhage‐Induced Activations of Adrenocorticotropin Release and Catecholamine Metabolism in the Ventrolateral Medulla are Differently Affected by Glucocorticoid Feedback

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