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Abstract Background: Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. Methods: Rabbits were randomly divided into 4 groups. Group Control (n = 7); no intervention performed. Group Catheter (n = 7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n = 7); rabbits were given 4 mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n = 7); rabbits were given 1 µg/kg dexmedetomidine into the central artery of the ear. After 72 h, the ears were amputated and histologically investigated. Results: There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p < 0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. Conclusion: Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.

Resumo Justificativa: A injeção intra-arterial de medicamentos pode causar isquemia aguda e grave e resultar em morbidade e mortalidade. Não há informações na literatura que avaliem os efeitos endoteliais arteriais de sugamadex e dexmedetomidina. A hipótese de nosso estudo foi que dexmedetomidina e sugamadex causariam alterações histológicas na estrutura endotelial arterial quando administrados por via intra-arterial. Método: Os coelhos foram randomicamente divididos em quatro grupos: grupo controle (n = 7), sem intervenção; grupo cateter (n = 7), uma cânula foi inserida na artéria central da orelha e medicamentos não foram administrados; grupo sugamadex (n = 7), receberam 4 mg/kg de sugamadex na artéria central da orelha; grupo dexmedetomidina (n = 7), receberam 1 µg/kg de dexmedetomidina na artéria central da orelha. Após 72 horas, as orelhas foram amputadas e histologicamente examinadas. Resultados: Não houve diferença significativa entre os grupos controle e cateter referente aos escores histológicos. Os escores do dano causado ao endotélio e à membrana e fibra elásticas, da hipertrofia do músculo liso e do aumento do tecido conjuntivo foram significativamente maiores nos grupos dexmedetomidina e sugamadex do que nos grupos controle e cateter (p < 0,05). Não houve diferença significativa entre os grupos dexmedetomidina e sugamadex nos escores histológicos. Conclusão: A administração de sugamadex e dexmedetomidina a coelhos por via intra-arterial causou danos arteriais histológicos. Para entender as alterações histológicas causadas por sugamadex e dexmedetomidina com mais clareza, estudos experimentais adicionais são necessários.

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BACKGROUND: Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. METHODS: Rabbits were randomly divided into 4 groups. Group Control (n=7); no intervention performed. Group Catheter (n=7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n=7); rabbits were given 4mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n=7); rabbits were given 1µg/kg dexmedetomidine into the central artery of the ear. After 72h, the ears were amputated and histologically investigated. RESULTS: There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p<0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. CONCLUSION: Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.

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O exercício aeróbio promove efeitos benéficos na prevenção e tratamento de doenças como hipertensão arterial, aterosclerose, insuficiência venosa e doença arterial periférica. Os receptores β-adrenérgicos estão presentes em várias células. No sistema cardiovascular, promovem inotropismo e cronotropismo positivo cardíaco e relaxamento vascular. Embora os efeitos do exercício tenham sido investigados em receptores cardíacos, estudos focados nos vasos são escassos e controversos. Esta revisão abordará os efeitos do exercício físico sobre os receptores β-adrenérgicos vasculares em modelos animais e humanos e os mecanismos celulares envolvidos na resposta relaxante. Em geral, os estudos mostram resultantes conflitantes, onde observam diminuição, aumento ou nenhum efeito do exercício físico sobre a resposta relaxante. Assim, os efeitos do exercício na sensibilidade β-adrenérgica vascular merecem maior atenção, e os resultados mostram que a área de fisiopatologia vascular é um campo aberto para a descoberta de novos compostos e avanços na prática clínica.

Aerobic exercise promotes beneficial effects on the prevention and treatment of diseases such as arterial hypertension, atherosclerosis, venous insufficiency, and peripheral arterial disease. β-adrenergic receptors are present in a variety of cells. In the cardiovascular system, β-adrenergic receptors promote positive inotropic and chronotropic response and vasorelaxation. Although the effect of exercise training has been largely studied in the cardiac tissue, studies focused on the vascular tissue are rare and controversial. This review examines the data from studies using animal and human models to determine the effect of physical exercise on the relaxing response mediated by β-adrenergic receptors as well as the cellular mechanisms involved in this response. Studies have shown reduction, increase, or no effect of physical exercise on the relaxing response mediated by β-adrenergic receptors. Thus, the effects of exercise on the vascular β-adrenergic sensitivity should be more deeply investigated. Furthermore, the physiopathology of the vascular system is an open field for the discovery of new compounds and advances in the clinical practice.

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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 subendothelial network. The hepatic segment of the caudal vena cava showed a myoconnective architecture and propulsive characteristics in terms of its hemodynamic pattern.

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Age-related anatomical changes in the human renal veins and their valves were studied. The principal changes were: 1. The muscle fiber bundles were noted to progressively atrophy as a function of age, while conservely the elastic fiber bundles hypertrophied. 2. The valves of the renal veins were observed to become gradually thicker with age as a result of the increased number of collagen fiber bundles.

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Chronic hypobaric hypoxia induces a mild degree of pulmonary arterial hypertension with structural alterations in the peripheral portions of the pulmonary arterial tree of the native Andean highlanders. On the other hand, animals indigenous to high altitude do not show these changes and are adapted to hypobaric hypoxia. The small pulmonary arteries of seven native Himalayan highlanders were examined at autopsy and found to be thin-walled with no medial hypertrophy of the muscular pulmonary arteries or muscularization of the arterioles. These findings suggest that the Himalayan highlanders may be adapted to hypobaric hypoxia.

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Using mesoscopic techniques, the authors observed that fibrous muscular bundles were distributed in three layers, from the external to the intima, in the cava-hepatic venous transition zone; these bundles start with a helical course, and bend progressively towards their outlet. Regarding the collagen component, two kinds of fibre bundles were observed: 1) as longitudinal strips, two for each vein that join in an arched form close to the outlet; 2) bundles running in the same direction as muscular bundles. The elastic tissue appears as a component of the myoelastic tendons or as independent bundles. The latter follow the direction of the muscular fibres, but show a decreasing amount when they approach the transition zone. At this point, however, the myoelastic tendons grow thicker.

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The spatial arrangement of the muscular, elastic and collagenous fibers was examined in 20 splenic veins of adult humans. Histologic and panorganographic sections were stained by the following methods: azan, resorcinfuchsin (Weigert), Verhoeff-van Gieson's stain and Masson's trichrome. Unstained sections were examined under polarized light. The results show that the muscular and collagenous fibers of the splenic vein exhibit an elongated spiral arrangement with no polarization. The elastic fibers form a threedimensional network disposed predominantly in a longitudinal direction. Hemodynamics are discussed based on the spatial structure of the muscular, elastic and collagenous elements of the vein wall and its relationship with the circulatory functions of the spleen.

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The arrangement of muscle, collagenous and elastic fibers in the inferior mesenteric vein was studied in 36 necropsy specimens, using micro- and mesoscopic methods. The muscle fiber bundles are disposed in helicoidal trajectories. The collagenous and elastic fibers also form networks, the latter presenting longitudinal meshes and the former, different angles of intersection, in the vein wall. Functional considerations are made based on these results.

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The authors observed the microscopic anatomy of both left and right testicular veins, of young and old subjects, as well as the structure of the ostial and parietal venous valves. They verified that the testicular veins walls are of a conjunctive muscular nature, showing at the discharge level, besides the ostial valves, the presence of a functional dispositive that modulates the blood flow into the inferior cava and left renal veins. The authors present a functional interpretation of the architectonic structure of the tissue components from these propelling veins. It is also discussed the causes that lead to the appearance of varices.

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Estuda-se o músculo grácil em 38 cadáveres a fresco. O estudo abrange: anatomia, compreendendo situaçäo, forma, origem e inserçäo, açäo e variaçöes; inervaçäo, vascularizaçäo e território vascular. Os resultados säo comparados aos da literatura. Säo ressaltados os aspectos práticos da pesquisa

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