Fulminating arterial hypertension with pulmonary edema from release of adrenomedullary catecholamines after lesions of the anterior hypothalamus in the rat.

Abstract

Bilateral electrolytic lesions of the anterior hypothalamus in unrestrained rats resulted in the development, within 2 hours, of arterial hypertension, tachycardia, hyperthermia, and increased locomotor activity, often leading to pulmonary edema and death. Similar lesions in paralyzed, artificially ventilated rats produced comparable changes in arterial blood pressure and body temperature with a similar time course. The arterial hypertension was a consequence of an increase in total peripheral resistance to 15% of control with a reduction in cardiac output to 49% of control. Arterial hypertension, elevated peripheral resistance, and diminished cardiac output were reversed toward normal by alpha-receptor blockade with phentolamine (1 mg/kg, iv). Bilateral adrenalectomy, adrenal demedullation, or adrenal denervation performed prior to lesion placement prevented the development of arterial hypertension and pulmonary edema as well as the changes in peripheral resistance, cardiac output, and body temperature. We conclude that arterial hypertension following lesions of the anterior hypothalamus is due to a neurally mediated increase in peripheral resistance initiated by the release of adrenal medullary catecholamines and that pulmonary edema is due to myocardial failure secondary to the ensuing ventricular overload. Structures originating in or passing through the anterior hypothalamus may exert selective control over the adrenal medulla independent of vasomotor neurons.• In 1954, Maire and Patton (1) demonstrated that bilateral electrolytic lesions of the anterior hypothalamus (AH) result in the development of a syndrome of hyperactivity, hyperthermia, and fatal pulmonary edema in the rat. Although cardiovascular measurements were not made, Maire and Patton attributed the pulmonary edema to a neurogenically mediated shift of blood from the capacitance vessels into the pulmonary circulation (2). More recently, Doba and Reis (3, 4) have observed that fulminating pulmonary edema can also be produced in the rat by bilateral lesions of the nucleus tractus solitarii (NTS), a brainstem nucleus in the medulla oblongata serving as a site of termination of arterial baroreceptors. In this instance, the pulmonary edema is due to the rapid development of neurogenic arterial hypertension with a marked increase in total peripheral resistance leading to a reduction in cardiac output and myocardial failure. Thus, the possibility exists that the pulmonary edema observed by Maire and This work was supported by Grant NS 03346 from NINDS and Grant NGR-33-010-179 from NASA and by the Harris Foundation.Received September 11, 1974. Accepted for publication May 13, 1975. Patton (1,2) after lesion of the AH was secondary to the development of arterial hypertension.In the present study, we investigated the hemodynamic changes following placement of lesions in the AH in the rat. Such lesions produced pulmonary edema as a consequence of arterial hypertension, and the hypertension was due to a neurally mediated release of adrenomedull...

Hemodynamic parameters and neurogenic pulmonary edema following spinal cord injury: an experimental model

“…They observed that a rterial hypertension, elevated peripheral re s i s t a nce, and diminished cardiac output were reversed t o n o rmal by alpha-receptor blockade with phentolamine. Also, these authors demonstrated that bilateral adre n a l e c t o m y, adrenal demedullation or a d renal denervation perf o rmed prior to lesion inducement prevented the development of art e r i a l h y p e rtension and pulmonary edema, as well as the changes in peripheral resistance, cardiac output, and body temperature 7 . Glazer and Ross obs e rved noradre n e rgic (NE) bulb-spinal innerv a t i o n to midthoracic sympathetic preganglionic nuclei in the rat thoracic cord by immunocytochemical l ocalization of dopamine-beta-hydroxylase, a specific NE antigen 8 .…”

Early Embolization for Ruptured Aneurysm in Acute Stage of Subarachnoid Hemorrhage with Neurogenic Pulmonary Edema

“…The mechanism by which NPE occurs is unclear. Several experimental investigations suggest that a sudden increase in intracranial pressure or hypo- thalamic lesions may elicit massive sympathetic discharges, with redistribution of blood to the pulmonary circulation resulting in high pulmonary capillary pressure and increased permeability 6,7 . Therefore, it is beneficial that treatment of NPE be used to control intracranial pressure and reduce subarachnoid hemorrahge by early placement of continuous lumbar spinal drainage.…”

Brain and Vascular Monoamine Oxidase Activity in the Deoxycorticosterone‐salt Hypertensive Rat

“…Many workers have reported on the importance of the central nervous system in the development or maintenance of various forms of experimental hypertension, such as renal hypertension (Chalmers, Dollery, Lewis & Reid, 1974), deoxycorticosterone (DOCA)-salt hypertension (Finch, Haeusler & Thoenen, 1972), and hypertension induced by lesions of the anterior hypothalamus in the rat (Nathan & Reis, 1975). It has also been suggested (de Champlain, Mueller & Axelrod, 1969; Reid, Zivin & Kopin, 1975) that DOCA-salt hypertension causes increased peripheral adrenergic activity through a central component.…”