Comportamento da pressão intra-ocular segundo os efeitos cardiorrespiratórios e hemodinâmicos induzidos pela anestesia com desflurano, em cães submetidos à hipovolemia experimental

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Architecture of the caudal vena cava wall of the dog at the level of the liver caudate lobe

The vascular segment of the caudal vena cava of the dog at the level of the caudate lobe was shown to be intimately related to hepatic tissue through the hepatic capsule and parenchyma. The tunica adventitia of the caudal vena cava was formed mainly by smooth muscle cells with collagen and elastic fibers arranged in bundles. The thin tunica media of the vein was also formed by smooth muscle cells, collagen and elastic fibers arranged in bundles. The tunica intima presented an elastic sub-endothelial network. The hepatic segment of the caudal vena cava showed a myoconnective architecture and propulsive characteristics in terms of its hemodynamic pattern.

Haemodynamic effects of hypothalamic disconnection in anaesthetized rats

The aim of the present study was to analyse the haemodynamic effects induced by the hypothalamic disconnection (HD) caudal or rostral to the paraventricular nucleus of the hypothalamus (PVN). Mean arterial pressure (MAP), hindlimb, renal and mesenteric blood flow and vascular conductance (HVC, RVC and MVC, respectively) were measured in urethane (1.2 g/kg, i.v.) anesthetized rats for 60 min after disconnection. HD caudal to the PVN was performed with a double-edged microknife of bayonet shape (R=1 mm, H=2 mm) stereotaxically placed, lowered 2.8 mm caudal to the bregma along the midline. The cut was achieved by rotating the microknife 90° right and 90° left. HD rostral to the PVN was performed with the knife placed 0.8 mm caudal to the bregma. Thirty minutes after the hypothalamic disconnection caudal (HD-C), a decrease in MAP was observed (-14±3 mm Hg), reaching a 60-min decrease of 30±3 mm Hg. Hindlimb conductance increased 10 min after HD (156±14%) and remained elevated throughout the experimental period. On the contrary, we observed a transitory renal vasoconstriction (82±9%, ≤20 min) and a late mesenteric vasodilation, starting at 30 min (108±4%) and reaching 138±6% at 60 min. In rats with HD rostral to the PVN, we only observed minor changes in the cardiovascular parameters. In the MAP, there was a slight decrease 60 min after the hypothalamic disconnection rostral (HD-R) (-9±4 mm Hg). There were no significant changes in HVC. RVC and MVC were increased 60 min after the HD-R (116±12% and 124±11%, respectively). These results suggest that vasodilation in the hindlimb and in the mesenteric bed could contribute to the observed decrease in MAP in HD caudal to PVN rats. © 2002 Elsevier Science B.V. All rights reserved.

Central nitric oxide modulates hindquarter vasodilation elicited by AMPA receptor stimulation in the NTS of conscious rats

Microinjection of S-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) in the nucleus of the solitary tract (NTS) of conscious rats causes hypertension, bradycardia, and vasoconstriction in the renal, mesenteric, and hindquarter vascular beds. In the hindquarter, the initial vasoconstriction is followed by vasodilation with AMPA doses >5 pmol/100 nl. To test the hypothesis that this vasodilation is caused by activation of a nitroxidergic pathway in the NTS, we examined the effect of pretreatment with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10 nmol/100 nl, microinjected into the NTS) on changes in mean arterial pressure, heart rate, and regional vascular conductance (VC) induced by microinjection of AMPA (10 pmol/100 nl in the NTS) in conscious rats. AMPA increased hindquarter VC by 18 ± 4%, but after pretreatment with L-NAME, AMPA reduced hindquarter VC by 16 ± 7% and 17 ± 9% (5 and 15 min after pretreatment, P < 0.05 compared with before pretreatment). Pretreatment with L-NAME reduced AMPA-induced bradycardia from 122 ± 40 to 92 ± 32 beats/min but did not alter the hypertension induced by AMPA (35 ± 5 mmHg before pretreatment, 43 ± 6 mmHg after pretreatment). Control injections with D-NAME did not affect resting values or the response to AMPA. The present study shows that stimulation of AMPA receptors in the NTS activates both vasodilatatory and vasoconstrictor mechanisms and that the vasodilatatory mechanism depends on production of nitric oxide in the NTS. Copyright © 2006 the American Physiological Society.