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H Laborit

Publications and source records attributed to H Laborit.

At least 37 records · Page 2Linked to original sources

On the mechanism of activation of the hypothalamo--pituitary--adrenal reaction to changes in the environment (the 'alarm reaction').

The amount of circulating noradrenaline increases considerably in parallel with an improvement in cardiovascular haemodynamics in adrenalectomized rabbits after intravenously injected hydrocortisone. In view of this finding, that as well as a constant regulation with negative retroaction of the corticotrophic-releasing factor--adrenocorticotrophic hormone (ACTH)--cortisol system, there exists an externally controlled servomechanism from nervous system activity related to the environment. Hydrocortisone favours passive avoidance, extinction and facilitates the activity of the cholinergic inhibiting system; ACTH facilitates active avoidance and catecholaminergic activation. It has already been demonstrated that stimulation of the inhibiting system or inhibition of the activating system released noradrenaline from the peripheral nerves of an adrenalectomized animal. It therefore seems that the early release of ACTH after aggression is capable of favouring locomotor activity in 'flight or fight'. If the latter is effective, there is a return to the previous behavioural and endocrine balance. On the other hand, if 'flight or fight' should be ineffective, there arises a vicious circle with positive retroaction, because secondary secretion of glucocorticoids will maintain inhibition and considerable activity in the noradrenergic system. The significance of the alarm reaction and the secondary release of the mineralocorticoids are discussed as well as the central mechanism of allegedly psychosomatic, illness. Aggression, as well as the lesion it induces, causes a reaction from the organism subjected to aggression. This is a non-specific reaction to which Selye (1936) has drawn attention. This reaction sets the central nervous system in action, which activates the vegetative nervous system and the endocrine system through the hypothalamus and the pituitary gland. In the vegetative system and the vasomotor changes related to it, the alarm syndrome has to be understood as a way to induce flight or fight, which allows the organism to move away from the aggressor. When this behaviour is impossible or ineffective the vasomotor reaction is threatened and it is depressed or inhibited (Laborit, 1952). Resuscitation techniques involving central or peripheral inhibitors, such as lytic cocktails, neuroplegy or neuroleptanalgesia, derive from this concept. The neuro--endocrine significance of the alarm reaction is still not understood and resuscitation techniques are quite empirical in relation to it.

Acetylcholine

[The mechanism of releasing and bio-behavioral significance of the hypothalamo-hypophyso-adrenal gland reaction to the environment (alarm reaction)].

Laboratory experimentation has demonstrated the large increase in the rate of circulating norepinephrin (N.E.), in a parallel with an improvement in cardiovascular dynamism of suprarenalectomized rabbits under the action of injection IV of hydrocortisone. As from this ascertainment, the author attempts to make a synthesis of known experimental facts demonstrating that next to a regulation in constancy (with negative retroaction) of the C.R.F. leads to A.C.T.H. leads to cortisol system, there exists a servomechanism (control external to the system) as from the activity of the nervous systems as compared with environment. Hydrocortisone favouring passive avoidance, and extinction facilitating the activity of the cholinergic inhibiting system of action (I.S.A.). A.C.T.H. facilitates active avoidance and the catecholaminergic activating system of action (A.S.A.). Now, it has already been demonstrated in the same laboratory that stimulation of I.S.A. or inhibition of the A.S.A. freed N.E. from the peripherous nerves of a adrenalectomized animal. It, therefore, seems that the early freeing of A.C.T.H. following aggression is capable of favouring locomotive activity (flight or fight). Should the latter be efficient, there is a return to the prior behavioural and endocrinal balance. On the other hand, should they be inefficient, there arises a vicious circle (regulation with tendency, positive retroaction) because secondary secretion of glucocorticoids will maintain inhibition of action and the secondary freing of the mineralocorticoids are discussed as well as the central mechanism of illness so called "psychosomatic".

Adrenal Glands

The action of arachidonic acid on the locomotive activity of mice.

The intraperitoneal administration of methyl or sodium arachidonate (100 and 200 mg-kg causes, in mice, a significant decline in locomotive activity 30 min later, and is able to oppose completely the antagonistic action of D-amphetamine (2.5 and 5 mg-kg). This effect seems to be related to increased synthesis of prostaglandins, for it disappears partially after pretreatment with acetylsalicylic acid, which alone has no effect on the spontaneous activity of mice. Oleic acid, an unsaturated fatty acid not involved in prostaglandin synthesis does not give significant results in the same conditions.

Amphetamine

The action of arachidonic acid on experimental hypertension in the rat.

Keeping in mind the vasodilator action of prostaglandins, the control that they exercise over the vascular supply of kidneys and the sympathetic activity, research was conducted in order to establish the effect of arachidonic acid, the precursor of PGE2, on experimental hypertension in the rat. The experimental hypertension was induced by unilateral nephrectomy, followed by the administration of DOCA and the elevated sodium diet. The treatment was short in one group, long in the other, and both groups were compared to a control hypertensive group which received no treatment at all. Arachidonic acid worsened the experimental hypertension by 37% in the long treatment, and by 25% in the short treatment. The administration of lysine-acetylsalicylate diminished this hypertension. A non-saturated acid, oleic acid, which is not involved in prostaglandin synthesis, has no action. The authors would like to emphasize that in one of the previous experiments, L-tyrosine, the precursor of catecholamines, diminished the experimental hypertension in the rat, and also that L-DOPA and IMAO (MAOI) have comparable effects. It seems, therefore, that the depression of the central catecholaminergic activity, which is supposed to be the action of arachidonic acid via an increase in the PGE2 synthesis, appears to increase hypertension. It is noteworthy that the medial forebrain bundle (MFB) is catecholaminergic and that the periventricular system (PVS) is cholinergic. Thus hypertension may represent the peripheral vascular response to anguish which results from the activation of PVS and from the depression of MFB.

Administration, Oral