Fulminating Arterial Hypertension with Pulmonary Edema from Release of Adrenomedullary Catecholamines after Lesions of the Anterior Hypothalamus in the Rat

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.

[1]  D. Reis,et al.  Hypoxemia, atelectasis, and the elevation of arterial pressure and heart rate in paralyzed artificially ventilated rat. , 1975, Life sciences.

[2]  J. Colombo,et al.  Local changes in multiple unit activity induced by electrochemical means in preoptic and hypothalamic areas in the female rat. , 1974, Brain research.

[3]  D. Reis,et al.  Role of Central and Peripheral Adrenergic Mechanisms in Neurogenic Hypertension Produced by Brainstem Lesions in Rat , 1974, Circulation research.

[4]  D. Reis,et al.  Acute Fulminating Neurogenic Hypertension Produced by Brainstem Lesions in the Rat , 1973, Circulation research.

[5]  D. Cocchi,et al.  Drug control of hyperglycemia and inhibition of insulin secretion due to centrally administered 2-deoxy-D-glucose. , 1973, The American journal of physiology.

[6]  D. Cocchi,et al.  A central site for the hyperglycemic action of 2-deoxy-d-glucose in mouse and rat. , 1971, Life sciences. Pt. 1: Physiology and pharmacology.

[7]  A. Luisada Pulmonary edema in man and animals , 1970 .

[8]  J. Uther,et al.  Bulbar and Suprabulbar Control of the Cardiovascular Autonomic Effects during Arterial Hypoxia in the Rabbit , 1970, Circulation research.

[9]  F. Plum,et al.  Buffering capacity of cerebrospinal fluid in acute respiratory acidosis in dogs. , 1969, The American journal of physiology.

[10]  O. E. Millhouse A Golgi study of the desending medial forebrain bundle. , 1969, Brain research.

[11]  D. Reis,et al.  Termination and secondary projections of carotid sinus nerve in the cat brain stem. , 1969, The American journal of physiology.

[12]  H. Ursin,et al.  Obesity produced by iron and tissue destruction in the ventromedial hypothalamus , 1969 .

[13]  H. Ikeda Adrenal medullary secretion in response to insulin hypoglycemia in dogs with transection of the spinal cord. , 1968, The Tohoku journal of experimental medicine.

[14]  B. Rabin,et al.  Behavioral comparison of the effectiveness of irritative and non-irritative lesions in producing hypothalamic hyperphagia , 1968 .

[15]  P. Korner The effect of section of the carotid sinus and aortic nerves on the cardiac output of the rabbit. , 1965, The Journal of physiology.

[16]  R. W. Reynolds AN IRRITATIVE HYPOTHESIS CONCERNING THE HYPOTHALAMIC REGULATION OF FOOD INTAKE. , 1965, Psychological review.

[17]  H. L. Borison,et al.  Central mechanisms in pulmonary oedema of nervous origin in guinea‐pigs , 1959, The Journal of physiology.

[18]  P. Lindgren,et al.  The release of catechols from the adrenal medulla on activation of the sympathetic vasodilator nerves to the skeletal muscles in the cat by hypothalamic stimulation. , 1958, Acta physiologica Scandinavica.

[19]  H. D. Patton,et al.  Role of the splanchnic nerve and the adrenal medulla in the genesis of preoptic pulmonary edema. , 1956, The American journal of physiology.

[20]  H. D. Patton,et al.  Neural structures involved in the genesis of preoptic pulmonary edema, gastric erosions and behavior changes. , 1956, The American journal of physiology.

[21]  H. D. Patton,et al.  Hyperactivity and pulmonary edema from rostral hypothalamic lesions in rats. , 1954, The American journal of physiology.

[22]  M. Vogt,et al.  The concentration of adrenaline in the peripheral blood during insulin hypoglycaemia. , 1954, British journal of pharmacology and chemotherapy.

[23]  U. V. von Euler,et al.  Selective Activation of Noradrenaline and Adrenaline Producing Cells in the Cat's Adrenal Gland by Hypothalamic Stimulation , 1954, Circulation research.

[24]  E. Gellhorn,et al.  Nature of sympathetico-adrenal discharge under conditions of excitation of central autonomic structures. , 1953, The American journal of physiology.

[25]  George W. Snedecor,et al.  Statistical methods applied to experiments in agriculture and biology. , 1946 .

[26]  U. Trendelenburg,et al.  Degeneration activity after parasympathetic or sympathetic denervation. , 1972, Ergebnisse der Physiologie, biologischen Chemie und experimentellen Pharmakologie.

[27]  N. Kirshner,et al.  Effect of stimulation on the levels of tyrosine hydroxylase, dopamine beta-hydroxylase, and catecholamines in intact and denervated rat adrenal glands. , 1971, Molecular pharmacology.

[28]  H. Dunér The effect of insulin hypoglycemia on the secretion of adrenaline and noradrenaline from the suprarenal of cat. , 1954, Acta physiologica Scandinavica.