Navegando por Autor "Kulasekara, Keerthi"
Agora exibindo 1 - 2 de 2
Resultados por página
Opções de Ordenação
Item Inactivation of neuronal function in the amygdaloid region reduces tail artery blood flow alerting responses in conscious rats.(2013) Mohammed, M.; Kulasekara, Keerthi; Menezes, Rodrigo Cunha Alvim de; Ootsuka, Youichirou; Blessing, William W.Few studies have investigated whether neuronal function in the amygdaloid complex is necessary for the occurrence of the cardiovascular response to natural (unconditioned) environmental threats. In the present investigation in conscious unrestrained Sprague–Dawley rats we inactivated neuronal function in the amygdaloid complex acutely (bilateral muscimol injections) or chronically (unilateral or bilateral ibotenic acid injections) and measured the effect on sudden falls in tail artery blood flow elicited by non-noxious salient stimuli (sympathetic cutaneous vasomotor alerting responses, SCVARs). After acute bilateral injection of vehicle (200 nl Ringer’s solution) the SCVAR index was 81± 2%, indicating that tail blood flow was reduced by 81% in response to the salient stimuli. After acute bilateral injection of muscimol (1 nmol in 200 nl of Ringer’s solution) into the amygdaloid complex the SCVAR index was 49± 5%, indicating that tail blood flow was reduced by 49% in response to the salient stimuli (p <0.01 versus vehicle, n= 7 rats for vehicle and 6 for muscimol). One week after unilateral ibotenic acid lesions, the SCVAR index was 68± 3%, significantly less than 90± 1%, the corresponding value after unilateral injection of vehicle (p < 0.01, n= 6 rats in each group). After bilateral ibotenic acid lesions the SCVAR index was 52± 4%, significantly less than 93± 1%, the corresponding value after bilateral injection of vehicle (p < 0.001, n= 6 rats in each group). Ibotenic acid caused extensive neuronal destruction of the whole amygdaloid complex, as well as lateral temporal lobe structures including the piriform cortex. Our results demonstrate that the amygdaloid complex plays an important role in mediating the tail artery vasoconstriction that occurs in rats in response to the animal’s perception of a salient stimulus, redirecting blood to areas of the body with more immediate metabolic requirements.Item SR59230A, a beta-3 adrenoceptor antagonist, inhibits ultradian brown adipose tissue thermogenesis and interrupts associated episodic brain and body heating.(2011) Ootsuka, Youichirou; Kulasekara, Keerthi; Menezes, Rodrigo Cunha Alvim de; Blessing, William W.SR59230A, a beta-3 adrenoceptor antagonist, inhibits ultradian brown adipose tissue thermogenesis and interrupts associated episodic brain and body heating. Am J Physiol Regul Integr Comp Physiol 301: R987–R994, 2011. First published August 3, 2011; doi:10.1152/ajpregu.00085.2011.—Brown adipose tissue (BAT) thermogenesis occurs episodically in an ultradian manner approximately every 80–100 min during the waking phase of the circadian cycle, together with highly correlated increases in brain and body temperatures, suggesting that BAT thermogenesis contributes to brain and body temperature increases. We investigated this in conscious Sprague-Dawley rats by determining whether inhibition of BAT thermogenesis via blockade of beta-3 adrenoceptors with SR59230A interrupts ultradian episodic increases in brain and body temperatures and whether SR59230A acts on BAT itself or via sympathetic neural control of BAT. Interscapular BAT (iBAT), brain, and body temperatures, tail artery blood flow, and heart rate were measured in unrestrained rats. SR59230A (1, 5, or 10 mg/kg ip), but not vehicle, decreased iBAT, body, and brain temperatures in a dose-dependent fashion (log-linear regression P 0.01, R2 0.3, 0.4, and 0.4, respectively, n 10). Ultradian increases in BAT, brain, and body temperature were interrupted by administration of SR59230A (10 mg/kg ip) compared with vehicle, resuming after 162 24 min (means SE, n 10). SR59230A (10 mg/kg ip) caused a transient bradycardia without any increase in tail artery blood flow. In anesthetized rats, SR59230A reduced cooling-induced increases in iBAT temperature without affecting cooling-induced increases in iBAT sympathetic nerve discharge. Inhibition of BAT thermogenesis by SR59230A, thus, reflects direct blockade of beta-3 adrenoceptors in BAT. Interruption of episodic ultradian increases in body and brain temperature by SR59230A suggests that BAT thermogenesis makes a substantial contribution to these increases.