Hyperglycemic response to hemorrhage is modulated by baroreceptors unloading but not by peripheral chemoreceptors activation Simonton Andrade Silveira, Andre ´a Siqueira Haibara, Ca ˆndido Celso Coimbra * Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, ICB-UFMG, 6627 Av. Antonio Carlos, 31270-901 Belo Horizonte, Brazil Received 20 April 2005; received in revised form 21 July 2005; accepted 25 August 2005 Abstract The aim of this study was to assess the relative participation of carotid baro- and chemoreceptors on plasma glucose and lactate level in response to hemorrhagic hypotension. We also evaluated the effects of selective activation of carotid chemoreceptors. One week before the experiments, male Wistar rats (250 –300 g) were submitted to bilateral total carotid denervation (BCD-group), or to bilateral ligature of the carotid body artery (ChD-group). During the same surgical procedure, a chronic jugular catheter for blood sampling and hemorrhage (1.2 mL/100 g/2 min) and polyethylene cannula was inserted into the left femoral artery for cardiovascular monitoring. One group submitted to fictitious surgery was used as a surgical control (Sham-group). Carotid chemoreceptors were selectively activated by sodium cyanide (NaCN, 40 Ag/0.1 mL i.v.) in the Sham and ChD group. The results showed that hyperglycemic response to hemorrhage in the BCD-group was reduced whereas in the ChD-group there was no significant change in this parameter compared to the Sham group (8.6 T 0.5 mM, Sham-hemorrhaged, n = 8; 7.2 T 0.3 mM, BCD-hemorrhaged, n =8 and 9.4 T 0.6 mM, ChD, n =8, p < 0.05). Increased plasma lactate levels following hemorrhage were observed in all the three experimental groups throughout the experimental period and there were no differences between the groups. Chemoreceptor stimulation by NaCN also produced hyperglycemia, as well as an increase in blood pressure and bradycardia but did not affect plasma lactate concentration. Ligature of the carotid body artery annulled the cardiovascular responses induced by NaCN, but did not change the hyperglycemic response to hypoxia. In conclusion, our data indicate that carotid chemoreceptors do not play any major role in overall metabolic response to hypoxia or hemorrhagic hypotension. Furthermore, the results suggest that carotid baroreceptors unloading play a predominant role as main source of afferent impulses leading to the hyperglycemic response to hemorrhage. In addition our data shows that the metabolic response and cardiovascular adjustment to hypoxia can be dissociated by ligature of the carotid body artery. D 2005 Elsevier B.V. All rights reserved. Keywords: Hemorrhage; Plasma glucose; Lactate; Carotid receptor 1. Introduction Hemorrhage is a powerful stimulus that induces an increase in plasma glucose and lactate (Yamaguchi, 1992; Machado et al., 1995a,b; Silveira et al., 2003), as also seen under many other stressful conditions (Yamaguchi, 1992; Lima et al., 1998; Reis et al., 1998). Hemorrhagic hypo- tension induces cardiovascular adjustments that are trig- gered by a change in the pressure load at arterial baroreceptors located at the aortic arch and the carotid sinuses. However, these two pressure-sensitive sites are not equivalent in their ability to protect arterial blood pressure during hypotensive challenges and hypovolemia (Abdel- Rhaman, 1992; Blombery and Korner, 1979; Barazanji and Cornish, 1987; Stauss, 2002). As in the case of arterial blood pressure, the relative contribution of carotid sinus and aortic baroreceptors to the metabolic adjustments made in response to hemorrhage hypotension appear to be different. Our previous studies showing that carotid receptor (baro- and chemoreceptors) denervation markedly reduced the 1566-0702/$ - see front matter D 2005 Elsevier B.V. All rights reserved. doi:10.1016/j.autneu.2005.08.007 * Corresponding author. Tel.: +55 31 3499 2936; fax: +55 31 3499 2924. E-mail address: coimbrac@icb.ufmg.br (C.C. Coimbra). Autonomic Neuroscience: Basic and Clinical 123 (2005) 36 – 43 www.elsevier.com/locate/autneu