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  • Title: Role of the nucleus parabrachialis in cardiovascular regulation in cat.
    Author: Mraovitch S, Kumada M, Reis DJ.
    Journal: Brain Res; 1982 Jan 28; 232(1):57-75. PubMed ID: 7055711.
    Abstract:
    Electrical stimulation of the nucleus parabrachialis (NPB) and surrounding areas of the dorsolateral pons in anesthetized immobilized cats elicits a rise of arterial pressure (AP) and tachycardia: the parabrachial pressor response (PBPR). The most excitable sites were concentrated within the intermediate one-third of the NPB in its medial and lateral subdivisions. The magnitude of pressor responses and their stimulus sensitivity were substantially greater in NPB than in adjacent areas of the dorsal pons including nucleus locus coeruleus and brachium conjunctivum, suggesting that cardiovascular responses heretofore attributed to locus coeruleus may have been due to excitation of the NPB. The PBPR persisted after chronic cerebellectomy, acute transection of the brain stem at the lower midbrain, or acute bilateral lesions of the nucleus tractus solitarii (NTS), the latter abolishing baroreceptor reflexes. Thus the PBPR cannot be attributed to antidromic or orthodromic stimulation or from NTS. Change in blood flow and regional vascular resistances during the PBPR were measured by electromagnetic flow meters placed on the thoracic aorta, superior mesenteric, renal and femoral arteries. When elicited with stimuli 5 times threshold, the PBPR was associated with an 80% increase in AP, 14+ increase in heart rate, 25% increase in cardiac output, and a 42% increase in total peripheral resistance. There was a differentiated vasoconstriction in the order of superior mesenteric greater than renal greater than femoral arteries. The baroreflex elicited by electrical stimulation of the carotid sinus nerve was reduced during stimulation of the NPB. The tachycardia was abolished by bilateral vagotomy, combined with beta-adrenergic blockade. Such treatment attenuated but did not abolish the hypertension which was only eliminated by subsequent alpha-adrenergic blockade. Thus the hypertension caused by stimulation of NPB is a result both of an increase of total peripheral resistance and of cardiac output. The cardiovascular pattern of the PBPR differ from other responses elicited from the dorsal pons, including the defense response, and the response to cerebral ischemia. We conclude that a powerful cardiovascular response pattern is organized within intrinsic neurons of the NPB. This nucleus may play an important role in organization of cardiovascular control by brain.
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