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Titolo:
Animal model of neuropathic tachycardia syndrome
Autore:
Carson, RP; Appalsamy, M; Diedrich, A; Davis, TL; Robertson, D;
Indirizzi:
Vanderbilt Univ, Clin Res Ctr, Dept Pharmacol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Pharmacol, Nashville, TN 37232 USA Vanderbilt Univ, Dept Med, Nashville, TN USA Vanderbilt Univ Nashville TNUSA rbilt Univ, Dept Med, Nashville, TN USA Vanderbilt Univ, Dept Neurol, Nashville, TN USA Vanderbilt Univ NashvilleTN USA lt Univ, Dept Neurol, Nashville, TN USA
Titolo Testata:
HYPERTENSION
fascicolo: 6, volume: 37, anno: 2001,
pagine: 1357 - 1361
SICI:
0194-911X(200106)37:6<1357:AMONTS>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
IDIOPATHIC ORTHOSTATIC INTOLERANCE; ARTERIAL-PRESSURE LABILITY; RATS; SYMPATHECTOMY;
Keywords:
blood pressure; rats; sympathectomy; tachycardia; heart rate;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Robertson, D Vanderbilt Univ, Clin Res Ctr, Dept Pharmacol, AA3228 MCN, Nashville, TN 37232 USA Vanderbilt Univ AA3228 MCN Nashville TN USA 37232 N 37232 USA
Citazione:
R.P. Carson et al., "Animal model of neuropathic tachycardia syndrome", HYPERTENSIO, 37(6), 2001, pp. 1357-1361

Abstract

Clinically relevant autonomic dysfunction can result from either complete or partial loss of sympathetic outflow to effector organs. Reported animal models of autonomic neuropathy have aimed to achieve complete lesions of sympathetic nerves, but incomplete lesions might be more relevant to certain clinical entities. We hypothesized that loss of sympathetic innervation would result in a predicted decrease in arterial pressure and a compensatory increase in heart rate. Increased heart rate due to loss of sympathetic innervation is seemingly paradoxical, but it provides a mechanistic explanationfor clinical autonomic syndromes such as neuropathic postural tachycardia syndrome. Partially dysautonomic animals were generated by selectively lesioning postganglionic sympathetic neurons with 150 mg/kg 6-hydroxydopamine hydrobromide in male Sprague-Dawley rats. Blood pressure and heart rate weremonitored using radiotelemetry. Systolic blood pressure decreased within hours postlesion (Delta > 20 mm Hg). Within 4 days postlesion, heart rate rose and remained elevated above control levels. The severity of the lesion was determined functionally and pharmacologically by spectral analysis and responsiveness to tyramine. Low-frequency spectral power of systolic blood pressure was reduced postlesion and correlated with the diminished tyramine responsiveness (r=0.9572, P=0.0053). The tachycardia was abolished by treatment with the beta -antagonist propranolol, demonstrating that it was mediated by catecholamines acting on cardiac beta -receptors. Partial lesions ofthe autonomic nervous system have been hypothesized to underlie many disorders, including neuropathic postural tachycardia syndrome. This animal model may help us better understand the pathophysiology of autonomic dysfunction and lead to development of therapeutic interventions.

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Documento generato il 18/01/21 alle ore 16:32:59