Juliana Hott de Fúcio Lizardo

Introdução: A cirurgia bariátrica é uma opção eficaz de tratamento amplamente utilizada para graus avançados de obesidade. É essencial conhecer o perfil e características clínicas dos pacientes e identificar fatores associados a complicações pós-operatórias. Objetivos: Descrever o perfil dos pacientes submetidos à cirurgia bariátrica em um Hospital Escola no Município de Vitória-ES/Brasil, caracterizar a amostra, descrever as principais complicações no período pós-operatório e os fatores associados a elas. Métodos: Estudo descritivo transversal, com indivíduos submetidos à cirurgia bariátrica. Dados sociodemográficos e clínicos relacionados ao pré e pós-cirúrgico foram coletados dos prontuários físicos. Resultados e conclusão: Foram analisados 181 prontuários de pacientes submetidos à cirurgia bariátrica entre janeiro de 2014 a janeiro de 2016. Houve predomínio do sexo feminino (91,2%), pardos (53,6%), com uma média de idade de 42,4±10,7 anos. A comorbidade prevalente foi a hipertensão arterial sistêmica (67,4%) seguida de gastrite (66,3%). A via de acesso aberta (não laparoscópica) e a presença de maior número de comorbidades pré-operatórias apresentou uma associação positiva com a incidência de complicações no pós-operatório. Não foram encontradas associações entre via de acesso e as variáveis: tempo de internação e frequência de uso de cateter de O2 no pós-operatório. A realização de fisioterapia pré-operatória e o valor do IMC não apresentaram associação com: número de complicações respiratórias e não respiratórias, tempo de internação e uso de cateter O2. A identificação de fatores associados com a maior incidência de complicações pós-operatórias é de suma importância para a busca de estratégias que minimizem o risco de pacientes cirúrgicos.

Purpose The purpose of this study was to investigate if the anterolateral ligament of the knee (ALL) is present in the human fetus and describe its topography along with other structures of the region. Methods Forty human fetuses knee joints, at mean age 34 weeks (± 2.57 weeks), fixed in 10% formalin, were submitted to cross-sectional dissection and mesoscopic analysis. Results The ALL was not identified, although the usual topography of the region was identified in all specimens: skin, subcutaneous tissue, iliotibial tract (ITT), fibular collateral ligament, popliteal muscle tendon, lateral meniscus, patellar ligament, infrapatellar fat pad, lateral patellar retinaculum, knee joint capsule, lateral inferior genicular vessels, and the biceps femoris tendon. The ITT reveals anterior (n = 12) and lateral thickening (n = 17) in some specimens. This thickening was found in both knees of the same subject in 6/20 specimens. Conclusion The anterolateral ligament of the knee is not a congenital or solid structure. Our results suggest that the ALL may be a deep layer of the ITT or part of the knee joint capsule, or its identification is evaluator dependent.

Objective: To verify the incidence and characterize morphologically the anterolateral ligament of the knee (ALL) in cadaveric samples of the collection of the Laboratory of Anatomy of the Department of Morphology of the Universidade Federal do Espírito Santo. Methods: Dissections and cross sections were performed for mesoscopic analysis of the anterolateral region of 15 knees preserved in 4% formalin solution in order to identify the ALL. Results: After dissection of the skin and subcutaneous tissue of the knee anterolateral region, it was possible to identify the iliotibial tract (ITT), the patellar ligament and the femoral biceps tendon. The ITT was removed from the Gerdy tubercle and the following structures were visualized: knee joint capsule, fibular collateral ligament and popliteal tendon. However, the ALL was not identified in any of the samples. Conclusions: The ALL could not be identified in any of the specimens studied, either through dissection or mesoscopic analysis. Level of Evidence III, Diagnosis Studies - Investigation of an Exam for Diagnosis.

Physical exercise is an important tool for the improvement of endothelial function. To assess the effects of acute dynamic resistance exercise on the endothelial function of spontaneously hypertensive rats (SHR). Ten minutes after exercise, the aorta was removed to evaluate the expression of endothelial nitric oxide synthase (eNOS), phosphorylated endothelial nitric oxide synthase (p-eNOS1177) and inducible nitric oxide synthase (iNOS) and to generate concentration-response curves to acetylcholine (ACh) and to phenylephrine (PHE). The PHE protocol was also performed with damaged endothelium and before and after NG-nitro-L-arginine methyl ester (L-NAME) and indomethacin administration. The maximal response (Emax) and the sensitivity (EC50) to these drugs were evaluated. ACh-induced relaxation increased in the aortic rings of exercised (Ex) rats (Emax= -80 ± 4.6%, p < 0.05) when compared to those of controls (Ct) (Emax = -50 ± 6.8%). The Emax to PHE was decreased following exercise conditions (95 ± 7.9%, p < 0.05) when compared to control conditions (120 ± 4.2%). This response was abolished after L-NAME administration or endothelial damage. In the presence of indomethacin, the aortic rings' reactivity to PHE was decreased in both groups (EC50= Ex -5.9 ± 0.14 vs. Ct -6.6 ± 0.33 log µM, p < 0.05 / Emax = Ex 9.5 ± 2.9 vs. Ct 17 ± 6.2%, p < 0.05). Exercise did not alter the expression of eNOS and iNOS, but increased the level of p-eNOS. A single resistance exercise session improves endothelial function in hypertensive rats. This response seems to be mediated by increased NO production through eNOS activation.

Resistance training evokes myocardial adaptation; however, the effects of a single resistance exercise session on cardiac performance are poorly understood or investigated. This study aimed to investigate the effects of a single resistance exercise session on the myocardial contractility of spontaneously hypertensive rats (SHRs). Male 3-month-old SHRs were divided into two groups: control (Ct) and exercise (Ex). Control animals were submitted to sham exercise. Blood pressure was measured in conscious rats before the exercise session to confirm the presence of arterial hypertension. Ten minutes after the exercise session, the animals were anesthetized and killed, and the hearts were removed. Cardiac contractility was evaluated in the whole heart by the Langendorff technique and by isometric contractions of isolated left ventricular papillary muscles. SERCA2a, phospholamban (PLB), and phosphorylated PLB expression were investigated by Western blot. Exercise increased force development of isolated papillary muscles (Ex=1.0±0.1 g/mg vs Ct=0.63±0.2 g/mg, Pvs Ct=1.7±0.2%, P<0.05). Papillary muscles of exercised animals developed greater force under increasing isoproterenol concentrations (P<0.05). In the isolated heart, exercise increased left ventricular isovolumetric systolic pressure (LVISP; Δ +39 mmHg; P<0.05) from baseline conditions. Hearts from the exercised rats presented a greater response to increasing diastolic pressure. Positive inotropic intervention to calcium and isoproterenol resulted in greater LVISP in exercised animals (P<0.05). The results demonstrated that a single resistance exercise session improved myocardial contractility in SHRs.

Http://dx.doi.org/10.5007/1980-0037.2009v11n4p373 Postexercise hypotension plays an important role in the non-pharmacological treat-ment of hypertension and is characterized by a decrease in blood pressure after a single exercise bout in relation to pre-exercise levels. This study investigated the effects of exercise intensity and creatine monohydrate supplementation on postexercise hypotension, as well as the possible role of blood lactate in this response. Ten normotensive subjects underwent resistance exercise sessions before (BC) and after (AC) creatine supplementation: 1) muscle endurance (ME) consisting of 30 repetitions at 30% of one-repetition maximum; 2) hypertrophy (HP) consisting of 8 repetitions at 75% of one-repetition maximum. Blood pressure was measured before and after the exercise bout. Blood lactate was measured after the exercise bout. The HP and ME sessions promoted a decrease in systolic blood pressure (∆ -19 ± 1.0 mmHg; ∆ -15 ± 0.9 mmHg, respectively, P< 0.05), which was attenuated after creatine supplementation (∆ -7.1 ± 1.0 mmHg; ∆ -11 ± 1.0 mmHg, respectively, P 0.05). In conclusion, resistance exercise intensity did not influence postexercise hypotension. Creatine supplementation attenuated the decrease in blood pressure after resistance exercise. The results suggest the involvement of blood lactate in post-resistance exercise hypotension.

The aim of the present study was to assess the effects of acute dynamic resistance exercise on resting blood pressure (BP) and on endothelial function of vascular bed of spontaneously hypertensive rats. Hemodynamic measurements were performed before and after acute dynamic resistance exercise in conscious animals. After exercise, the tail artery was cannulated for mean perfusion pressure with constant flow measurement and for performing concentration–response curves to acetylcholine (ACh) and sodium nitroprusside (SNP) and dose–response curves to phenylephrine (PHE). PHE protocol was also repeated with damaged endothelium and after L-NAME and indomethacin perfusion on the tail. The maximal response (E _max) and sensitivity (pD₂) were evaluated to these drugs. Exercise reduced resting systolic and diastolic BP (Δ −79 ± 1.8; −23 ± 2.3 mmHg, respectively; P < 0.05). ACh-induced relaxation increased in the exercise group (pD₂ = 9.8 ± 0.06, P < 0.05) when compared with control rats (pD₂ = 8.7 ± 0.1). The E _max to PHE with intact endothelium decreased following exercise condition (439 ± 18 mmHg, P < 0.05) when compared with control rats (276 ± 22 mmHg). This response was abolished after L-NAME and indomethacin administration. After damage of the endothelium, PHE responses were not significantly different between the groups; however, E _max and pD₂ increased when compared with responses obtained with intact endothelium. The results demonstrated that acute dynamic resistance exercise decreased resting BP and reactivity to PHE and increased endothelium-dependent relaxation. Nitric oxide and vasodilators prostanoids appear to be involved in post-exercise endothelial and pressor responses.

Chronic lead exposure induces hypertension in humans and animals, affecting endothelial function. However, studies concerning acute cardiovascular effects are lacking. We investigated the effects of acute administration of a high concentration of lead acetate (100 µΜ) on the pressor response to phenylephrine (PHE) in the tail vascular bed of male Wistar rats. Animals were anesthetized with sodium pentobarbital and heparinized. The tail artery was dissected and cannulated for drug infusion and mean perfusion pressure measurements. Endothelium and vascular smooth muscle relaxation were tested with acetylcholine (5 µg/100 µL) and sodium nitroprusside (0.1 µg/100 µL), respectively, in arteries precontracted with 0.1 µM PHE. Concentration-response curves to PHE (0.001-300 µg/100 µL) were constructed before and after perfusion for 1 h with 100 µΜ lead acetate. In the presence of endothelium (E+), lead acetate increased maximal response (Emax) (control: 364.4 ± 36, Pb2+: 480.0 ± 27 mmHg; P < 0.05) and the sensitivity (pD2; control: 1.98 ± 0.07, 2.38 ± 0.14 log mM) to PHE. In the absence of endothelium (E-) lead had no effect but increased baseline perfusion pressure (E+: 79.5 ± 2.4, E-: 118 ± 2.2 mmHg; P < 0.05). To investigate the underlying mechanisms, this protocol was repeated after treatment with 100 µM L-NAME, 10 µM indomethacin and 1 µM tempol in the presence of lead. Lead actions on Emax and pD2 were abolished in the presence of indomethacin, and partially abolished with L-NAME and tempol. Results suggest that acute lead administration affects the endothelium, releasing cyclooxygenase-derived vasoconstrictors and involving reactive oxygen species