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Introduction: This systematic review aims to summarize the existing evidence relating to preoperative anemia and clinical outcomes in peripheral vascular surgery patients. Methods: The following databases were searched—PubMed, COCHRANE, LILACS, and Science Research—from 1 January 2010 up to 8 May 2020, with the last search performed on 1 January 2021. An additional manual search for potential primary studies was conducted on major journals (e.g., Anesthesiology, the British Journal of Anesthesia and the European Journal of Anaesthesiology) and reference lists of included studies. Google Scholar was also checked for additional eligible studies. Reviewers independently screened potentially eligible articles and extracted data from included studies on populations, interventions, comparisons, and outcomes. This review was registered at PROSPERO as CRD 180954. Results: In total, 6 observational studies with a combined total of 87,327 participants were analyzed. Data collected in this review suggest that preoperative anemia, especially when hemoglobin is p < 0.0001), limb amputation (OR: 5.2; 95% CI 3.1–8.6, p < 0.0001), and death (p < 0.0031). Conclusions: These data suggest an association between preoperative anemia, blood transfusion requirements, and other adverse clinical outcomes among patients subjected to peripheral vascular interventions. However, further investigations, particularly randomized controlled trials, are warranted to better understand the association between preoperative anemia and patients’ prognosis.

Echinodorus grandiflorus is a semiaquatic plant native to Brazil and belongs to the Alismataceae family. Infusion preparations of the leaves of this plant are often used due to its diuretic, blood pressure lowering, and anti-inflammatory properties. Our aim was to investigate the effects of chronic treatment with the crude hydroalcoholic extract of E. grandiflorus on central and peripheral microvascular changes induced in a model of hypertension and diabetes. The hemodynamic and microvascular effects of E. grandiflorus extract (50, 100, or 200 mg/kg/day for 28 days) or the isolated major diterpene from E. grandiflorus (3 to 10 mg/kg i. v.) were evaluated in spontaneously hypertensive rats using tail plethysmography and intravital fluorescence videomicroscopy, respectively, and were compared to vehicle-treated normotensive Wistar-Kyoto rats. We also investigated the protective effects of chronic treatment with E. grandiflorus (100 mg/kg/day) in brain capillary density and leukocyte-endothelium interactions on the brain vessels of DM-spontaneously (DM: diabetes mellitus) hypertensive rats. Chronically treating spontaneously hypertensive rats with increasing doses of crude hydroalcoholic E. grandiflorus extract resulted in significant dose-dependent reductions in systolic blood pressure and an anti-inflammatory effect on the brain microcirculation of DM-spontaneously hypertensive rat animals. Using laser speckle contrast imaging, we observed that intravenous administration of the major isolated clerodane diterpene metabolite (1 – 10 mg/kg) increased microvascular blood flow by 25% in spontaneously hypertensive rat skeletal muscle. The results of this study show that E. grandiflorus extracts can be useful in the prevention and reduction of microcirculatory damage in arterial hypertension and other diseases that involve microvascular dysfunction.

We report the clinical case of a patient with coronavirus disease 2019 (COVID-19) who had recently undergone neurosurgery and presented with dilated nonreactive pupils during continuous rocuronium infusion, which was reversible with the suspension of the drug. Both the neurosurgical procedure and possible disruption of the blood-brain barrier due to COVID-19 infection may have led to the action of rocuronium in the central nervous system (CNS). Thus, clinicians must remember that neuromuscular blocking agents (NMBAs) can cause dilated nonreactive pupils in patients with COVID-19.

The objective of this study was to investigate the role of the sympathetic nervous system (SNS) on hemodynamic, metabolic and microvascular alterations in a rat model of high-fat diet (HFD)-induced metabolic syndrome with salt supplementation. In total, forty adult male Wistar rats were fed normal chow (n=10) or a HFD (n=30) for 20 weeks. Thereafter, the HFD group received the centrally acting sympatho-modulatory drugs clonidine (0.1 mg/kg) or rilmenidine (1 mg/kg) or vehicle (n=10/group) orally by gavage. Functional capillary density (FCD) was evaluated using intravital video microscopy, and the structural capillary density (SCD) was evaluated using histochemical analysis. The pharmacological modulation of the SNS induced concomitant reductions in SBP, HR and plasma catecholamine levels. These effects were accompanied by a reversal of functional and structural capillary rarefaction in the skeletal muscle in both treated groups and an increase in SCD in the left ventricle only in the rilmenidine group. Improvement of the lipid profile and of glucose intolerance was also obtained only with rilmenidine treatment. Modulation of sympathetic overactivity results in the reversal of microvascular rarefaction in the skeletal muscle and left ventricle and improves metabolic parameters in an experimental model of metabolic syndrome in rats. This article is protected by copyright. All rights reserved.

Objective: We investigated the acute effects of SIM on cerebral microvascular rarefaction and dysfunction in SHRs. Methods: Male WKY and SHRs were divided into 4 groups of 8 animals each: WKY-CTL and SHR-CTL, treated with 0.9% saline; and WKY+SIM and SHR+SIM, treated with SIM (30 mg/kg/d) for 3 days by gavage. Cerebral FCD was assessed by intravital fluorescence videomicroscopy. mCBF before and after administration within the cranial window of angiotensin II (1 μmol L−1) was investigated using laser speckle contrast imaging. Results: Cerebral FCD was reduced in SHR-CTL compared to WKY-CTL (P < .05). SIM increased cerebral FCD in SHRs compared to SHR-CTL (P < .05). The mCBF was reduced in SHR-CTL compared to WKY-CTL (P < .05), and SIM increased mCBF compared with SHR-CTL (P < .05). Angiotensin II elicited a reduction of mCBF in SHR-CTL and increased mCBF in WKY-CTL (SHR-CTL -13.53 ± 2% vs WKY-CTL +13.74 ± 4%; P < .001), which was attenuated in SHRs treated with SIM (SHR+SIM -6.7 ± 1% vs SHR-CTL -13.53 ± 2%; P < .01). Conclusions: The antihypertensive effect of SIM is associated with an improvement in cerebral microvascular perfusion and capillary density that may help to prevent hypertension-induced cerebrovascular damage independent of cholesterol-lowering.

Objective The pathophysiology underlying hyperthyroidism-induced left ventricle (LV) dysfunction and hypertrophy directly involves the heart and indirectly involves the neuroendocrine systems. The effects of hyperthyroidism on the microcirculation are still controversial in experimental models. We investigated the effects of hyperthyroidism on the cardiac function and microcirculation of an experimental rat model. Methods Male Wistar rats (170–250 g) were divided into two groups: the euthyroid group (n = 10), which was treated with 0.9% saline solution, and the hyperthyroid group (n = 10), which was treated with l-thyroxine (600 μg/kg/day, i.p.) during 14 days. An echocardiographic study was performed to evaluate the alterations in cardiac function, structure and geometry. The structural capillary density and the expression of angiotensin II AT1 receptor in the LV were analyzed using histochemistry and immunohistochemistry, respectively. Results Hyperthyroidism was found to induce profound cardiovascular alterations, such as systolic hypertension, tachycardia, LV dysfunction, cardiac hypertrophy, and myocardial fibrosis. This study demonstrates the existence of structural capillary rarefaction and the down-regulation of the cardiac angiotensin II AT1 receptor in the myocardium of hyperthyroid rats in comparison with euthyroid rats. Conclusions Microvascular rarefaction may be involved in the pathophysiology of hyperthyroidism-induced cardiovascular alterations.

Objective To investigate microvascular alterations in an experimental model of metabolic syndrome induced by a high-fat diet (HFD) associated with salt supplementation (0.5% NaCl). Design and Methods Wistar Kyoto rats were fed standard chow (control group, CONT) or HFD for 20 weeks. The functional capillary density (FCD) was assessed using intravital fluorescence videomicroscopy. Results The HFD group presented a higher systolic blood pressure, plasma glucose and insulin levels, total and LDL-cholesterol levels, triglycerides, and visceral and epididymal fat when compared with the CONT group. When compared with the CONT group, the HFD group showed a lower FCD in the skeletal muscle (P 0.05). The HFD group also had a lower capillary-to-fiber ratio in the skeletal muscle (P < 0.01). The capillary volume density-to-fiber volume density ratio in the left ventricle of the HFD was also reduced (P < 0.01). Finally, rats fed with HFD showed ventricular hypertrophy and increased cardiomyocyte diameter (P < 0.01). Conclusions The long-term administration of a HFD associated with salt supplementation to rats generates an experimental model of metabolic syndrome characterized by central body fat deposition, insulin resistance, glucose intolerance, hypertriglyceridemia, hypercholesterolemia, arterial hypertension, cardiac remodeling, and rarefaction of the microcirculation in the heart and skeletal muscle.

We examined the functional and structural microcirculatory alterations in the brain, skeletal muscle and myocardium of non-diabetic spontaneously hypertensive rats (SHR) and diabetic SHR (D-SHR), as well as the effects of long-term treatment with the angiotensin AT1-receptor antagonist olmesartan and the angiotensin-converting enzyme inhibitor enalapril. Diabetes was experimentally induced by a combination of a high-fat diet with a single low dose of streptozotocin (35 mg/kg, intraperitoneal injection). D-SHR were orally administered with olmesartan (5 mg/kg/day), enalapril (10 mg/kg/day) or vehicle for 28 days, and compared with vehicle-treated non-diabetic SHR or normotensive non-diabetic Wistar-Kyoto rats. The cerebral and skeletal muscle functional capillary density of pentobarbital-anesthetized rats was assessed using intravital fluorescence videomicroscopy. Chronic treatment with olmesartan or enalapril significantly lowered blood pressure and reversed brain functional capillary rarefaction. Brain oxidative stress was reduced to non-diabetic control levels in animals treated with olmesartan or enalapril. Histochemical analysis of the structural capillary density showed that both olmesartan and enalapril increased the capillary-to-fiber ratio in skeletal muscle and the capillary-to-fiber volume density in the left ventricle. Olmesartan and enalapril also prevented collagen deposition and the increase in cardiomyocyte diameter in the left ventricle. Our results suggest that the association between hypertension and diabetes results in microvascular alterations in the brain, skeletal muscle and myocardium that can be prevented by chronic blockade of the renin-angiotensin system.

Background Metabolic syndrome (MetS) is associated with an increased risk of cerebrovascular diseases, including cerebral ischemia. Microvascular dysfunction is an important feature underlying the pathophysiology of cerebrovascular diseases. In this study, we aimed to investigate the impacts of ischemia and reperfusion (IR) injury on the cerebral microvascular function of rats with high-fat diet-induced MetS. Results We examined Wistar rats fed a high-fat diet (HFD) or normal diet (CTL) for 20 weeks underwent 30 min of bilateral carotid artery occlusion followed by 1 h of reperfusion (IR) or sham surgery. Microvascular blood flow was evaluated on the parietal cortex surface through a cranial window by laser speckle contrast imaging, functional capillary density, endothelial function and endothelial–leukocyte interactions by intravital videomicroscopy. Lipid peroxidation was assessed by TBARs analysis, the expression of oxidative enzymes and inflammatory markers in the brain tissue was analyzed by real-time PCR. The cerebral IR in MetS animals induced a functional capillary rarefaction (HFD IR 117 ± 17 vs. CTL IR 224 ± 35 capillary/mm2; p

— Aim: To compare the amount of cardioprotection induced by a single exercise session with those achieved after an 8-week aerobic exercise training following ischemia reperfusion injury in rats. Methods: Twenty-five male Wistar rats (250-300g) were assigned into a group submitted to physical training (TR; n=12) or a single maximal exercise session (EXE; n=13). Following sedentarism or physical training (8 weeks, 5 sessions/wk, 1h/session at 70% of maximal speed) both groups performed a maximal exercise test. Then, groups were submitted to ischemia reperfusion injury (30 min/1h) through an isolated heart protocol, in which left ventricle developed pressure was measured. Results: The TR group presented greater maximal oxygen consumption compared to the EXE group (77.25±20.41 vs 41.32±25.86 ml/Kg/min; P=0.003). Regarding left ventricle developed pressure, no differences were detected between groups at baseline (TR: 89.78±24.40 vs EXE: 81.37±31.84 mmHg; P=0.48). However, after reperfusion, the TR group presented superior intraventricular pressure than EXE group (37.94±18.34 vs 21.59±13.67 mmHg; P=0.03). Conclusion: Eight-week aerobic training induced greater cardioprotection against ischemia reperfusion injury in rats compared to a single exercise session, due to an increased cardiac function. This suggests that exercise-induced cardioprotection is a multifactorial process that may involve different mediators according to the exercise duration.

The antihypertensive action of a crude ethanolic extract (EEEG) from leaves of Echinodorus grandiflorus (Alismataceae) was investigated in spontaneously hypertensive rats. The intraperitoneal injection of increasing doses of EEEG (300-1000 mg/kg) elicited dose-dependent reductions in mean arterial pressure (MAP) that were paralleled by reductions of cardiac output and systemic vascular resistance, reaching the maximum of 23 +/- 5%, 13 +/- 3% and 18 +/- 4%, respectively (n = 5, P < 0.05). Comparable reductions of MAP were obtained upon i.v. administration of EEEG (3-100 mg/kg), reaching the maximum decrease of 51 +/- 6% (n = 7; P < 0.001). The blockade of nitric oxide synthesis significantly reduced the hypotension induced by i.v. administration of EEEG. Moreover, the pre-treatment of the animals with a selective antagonist of cholinergic muscarinic receptors or of platelet-activating factor (PAF) receptors partially blunted the cardiovascular effects of EEEG. The i.v. pre-treatment with the selective B(2) bradykinin receptor antagonist HOE 140 or with indomethacin, an inhibitor of the enzyme cyclooxygenase, did not prevent the hypotensive effects induced by EEEG. Finally, the chronic oral treatment with EEEG presented a significant antihypertensive effect that was comparable to that of reference antihypertensive drugs currently used to treat arterial hypertension. It is concluded that EEEG elicits significant acute antihypertensive effects through the release of nitric oxide and the stimulation of cholinergic muscarinic and PAF receptors. Moreover, our results suggest that EEEG may be appropriate to chronic oral treatment of arterial hypertension.

JUSTIFICATIVA E OBJETIVOS: As propriedades medicinais da Cannabis sativa tem sido relatadas por muitos seculos para o tratamento de diversos disturbios e, mais recentemente, para o tratamento da dor. O objetivo deste estudo foi revisar os principais avancos na farmacologia do sistema endocanabinoide e no potencial uso terapeutico de alguns compostos canabinoides no tratamento de diversas formas de dor. CONTEUDO: Foi realizada uma busca nos bancos de dados Pubmed, Scielo e Lilacs, identificando-se estudos e revisoes da literatura sobre a farmacologia e o uso terapeutico de substâncias canabinoides em dor. Nessa busca foram utilizadas as seguintes palavras-chaves: Cannabis sativa, tetra-hidrocanabinol, canabidiol, sativex®, cannador®, canabinoides, endocanabinoide, dor e dor neuropatica. Os canabinoides sinteticos e os extratos de Cannabis sativa apresentaram efeito analgesico em diversos ensaios clinicos, sugerindo um potencial papel no tratamento da dor, em particular naquela de origem neuropatica. Os canabinoides sinteticos e os extratos de Cannabis sativatambem apresentaram efeitos ansioliticos quando usados como adjuvantes no tratamento da dor no câncer, na artrite reumatoide e na esclerose multipla. Porem, efeitos adversos significativos, como euforia, depressao e sedacao limitam o uso clinico desses agentes canabinoides. CONCLUSAO: Um melhor conhecimento sobre a farmacologia do sistema endocanabinoide, juntamente com os resultados dos estudos envolvendo o tratamento da dor com substâncias de natureza canabinoide, podem ser de grande valor para o desenvolvimento de farmacos que permitam um avanco significativo na terapeutica de pacientes portadores de sindromes dolorosas, em particular nos casos de dificil controle. Porem, mais estudos sao necessarios para confirmar esses resultados e determinar a seguranca desses compostos.

The ability of continuous aerobic exercise training (AET) to increase baroreflex control and cardiac function in heart failure (HF) has been well described, but the comparison between continuous and interval AET on these functions is inconclusive.To compare the effects of continuous and interval AET on cardiac function and baroreflex sensitivity (BrS) in an experimental model of HF.Rats were divided into the following groups: continuous training (HF-CT), intense interval training (HF-IIT), moderate interval training (HF-MIT), sedentary group (HF-SED), and sham sedentary (SHAM-SED). Animals underwent surgery to induce HF by ligation of the interventricular coronary artery. Six weeks after surgery, AET was started (8weeks, 3sessions/week). Echocardiography studies to assess cardiac function were performed before and after AET. At the end of the training protocols, the BrS index was assessed by stepwise intravenous infusions of sodium nitroprusside and phenylephrine.All methods of exercise prevented the HF-induced increase in left ventricular diameter in diastole observed in the HF-SED rats (0.88±0.09 vs. 1.03±0.09cm; P0.05), but only the HF-CT (28.5±6.3 vs. 39.2±12.7%; P0.05) and HF-MIT (31.0±8.5 vs. 42.0±10.3%; P0.05) groups exhibited an increase in ejection fraction. Nevertheless, the HF-CT group was the only group that showed a tachycardia reflex higher than that of the HF-SED group (0.87±0.34 vs. 0.20±0.05bpm/mmHg; P0.05) and similar to that of the SHAM-SED group (1.04±0.11bpm/mmHg).These results suggest that continuous and moderate interval training induced similar improvements in cardiac function but that only continuous training induced higher BrS in HF rats.

Background We investigated the involvement of central and peripheral opioid receptors (OR) in the cardioprotective effects of fentanyl (FENT) in a model of myocardial ischemia/reperfusion injury associated with pharmacologically induced sympathetic overactivity in anesthetized rabbits. Methods Central sympathetic stimulation was achieved through intracerebroventricular injection of l-glutamate in animals submitted to 35 min of coronary occlusion followed by 120 min of reperfusion. Rabbits received naloxone HCl intracerebroventricularly or naloxone methiodide IV, a quaternary compound that does not cross the blood-brain barrier, 5 min before FENT treatment (5 or 50 microg/kg, IV). Results Infarct area was reduced only by FENT 50 (from 51% +/- 2% to 24% +/- 2%). This protective effect was abolished by peripheral (42% +/- 4%), but not central, OR blockade (32% +/- 3%). The number of premature ventricular complexes during the ischemic period (54 +/- 3) was reduced by FENT 50 (19 +/- 7), an effect blunted by central (40 +/- 3) but not peripheral (18 +/- 7) blockade of OR. During reperfusion, the number of premature ventricular complexes (134 +/- 50) was reduced to 9 +/- 5 by FENT 50 and was prevented by central (42 +/- 4) as well as peripheral (20 +/- 11) OR blockade. The mortality rate (50%) and incidence of ventricular tachycardia (55%) were completely abolished by FENT 50. Conclusions We conclude that fentanyl's effects for limiting myocardial ischemic injury are mediated via peripheral ORs while opioid's antiarrhythmic actions are mediated via central OR agonism.

Background:Acute myocardial infarction is the leading cause of morbidity and mortality worldwide. Furthermore, research has shown that exercise, in addition to reducing cardiovascular risk factors, can also protect the heart against injury due to ischemia and reperfusion through a direct effect on the myocardium. However, the specific mechanism involved in exerciseinduced cardiac preconditioning is still under debate.Objective:To perform a systematic review of the studies that have addressed the mechanisms by which aerobic exercise promotes direct cardioprotection against ischemia and reperfusion injury.Methods:A search was conducted using MEDLINE, Literatura Latino-Americana e do Caribe de Informação em Ciências da Saúde, and Scientific Electronic Library Online databases. Data were extracted in a standardized manner by two independent researchers, who were responsible for assessing the methodological quality of the studies.Results:The search retrieved 78 studies; after evaluating the abstracts, 30 studies were excluded. The manuscripts of the remaining 48 studies were completely read and, of these, 20 were excluded. Finally, 28 studies were included in this systematic review.Conclusion:On the basis of the selected studies, the following are potentially involved in the cardioprotective response to exercise: increased heat shock protein production, nitric oxide pathway involvement, increased cardiac antioxidant capacity, improvement in ATP-dependent potassium channel function, and opioid system activation. Despite all the previous investigations, further research is still necessary to obtain more consistent conclusions. Fundamento:O infarto agudo do miocárdio é a principal causa de mortalidade e de morbidade na população mundial. Por outro lado, pesquisas já demonstraram que o exercício físico, além de reduzir os fatores de risco cardiovascular, também é capaz de promover cardioproteção contra lesões por isquemia e reperfusão, por meio de um efeito direto no miocárdio. No entanto, o mecanismo específico envolvido no pré-condicionamento cardíaco induzido pelo exercício ainda é alvo de discussão.Objetivo:Realizar uma revisão sistemática acerca dos estudos que se debruçaram sobre os mecanismos pelos quais o exercício físico aeróbio promove cardioproteção direta contra lesões por isquemia e reperfusão.Métodos:Foi realizada uma pesquisa nas seguintes bases de dados: MEDLINE, LILACS e SciELO. Os dados foram extraídos de forma padronizada, por dois investigadores independentes, responsáveis pela avaliação da qualidade metodológica dos manuscritos.Resultados:A busca inicial resultou em 78 estudos, dos quais, após revisão dos resumos, 30 foram excluídos. Os 48 manuscritos restantes foram lidos na íntegra e, destes, 20 foram excluídos, restando 28 estudos incluídos nesta revisão sistemática.Conclusão:Com base nos estudos selecionados, os seguintes mecanismos estão potencialmente envolvidos na resposta cardioprotetora do exercício: aumento na produção de proteínas de choque térmico; envolvimento da via do óxido nítrico; aumento na capacidade antioxidativa cardíaca; melhora na função dos canais de potássio dependentes de ATP; e ativação do sistema de opióides. Apesar de todo o investimento já realizado, ainda é necessário mais investimento em trabalhos futuros, para obtenção de conclusão mais consistente.

Obesity and metabolic syndrome are related to systemic functional microvascular alterations, including a significant reduction in microvessel density. The aim of this study was to investigate the effects of exercise training on functional capillary density in the skeletal muscle and skin of obese rats with metabolic syndrome.We used male Wistar-Kyoto rats that had been fed a standard commercial diet (CON) or high-fat diet (HFD) for 32 weeks. Animals receiving the HFD were randomly divided into sedentary (HFD+SED) and training groups (HFD+TR) at the 20(th) week. After 12 weeks of aerobic treadmill training, the maximal oxygen uptake (VO2max); hemodynamic, biochemical, and anthropometric parameters; and functional capillary density were assessed. In addition, a maximal exercise test was performed.Exercise training increased the VO2max (69 ± 3 mL/kg per min) and exercise tolerance (30 ± 1 min) compared with the HFD+SED (41 ± 6 mL/kg per min, P0.05 and 16 ± 1 min, P0.001) and with the CON (52 ± 7 mL/kg per min and 18 ± 1 min, P0.05) groups. The HFD+TR group also showed reduced retroperitoneal fat (0.03 ± 0.00 vs. 0.05 ± 0.00 gram/gram, P0.001), epididymal fat (0.01 ± 0.00 vs. 0.02 ± 0.00 gram/gram, P0.001), and systolic blood pressure (127 ± 2 vs. 150 ± 2 mmHg, P0.001). The HFD+TR group also demonstrated improved glucose tolerance, as evaluated by an intraperitoneal glucose tolerance test, fasting plasma glucose levels (5.0 ± 0.1 vs. 6.4 ± 0.2 mmol/L, P0.001) and fasting plasma insulin levels (26.5 ± 2.3 vs. 38.9 ± 3.7 μIU/mL, P0.05). Glucose tolerance did not differ between HFD+TR and CON groups. Exercise training also increased the number of spontaneously perfused capillaries in the skeletal muscle (252 ± 9 vs. 207 ± 9 capillaries/mm(2)) of the training group compared with that in the sedentary animals (260 ± 15 capillaries/mm(2)).These results demonstrate that exercise training reverses capillary rarefaction in our experimental model of metabolic syndrome and obesity.

Objectives To evaluate the effectiveness of single-point laser Doppler perfusion monitoring (LDPM) in the assessment of microvascular reactivity in the skin during cardiopulmonary bypass (CPB). Design Cross-sectional observational study. Setting Government-affiliated teaching hospital. Participants Twenty male patients aged 60±2 years who underwent coronary artery bypass grafting under CPB. Interventions The authors assessed the endothelium-dependent vasodilation of the skin microcirculation at the forehead and forearm using LDPM coupled with thermal hyperemia. This measurement was performed before and after the induction of anesthesia, during and after CPB, and 24 h after the end of the surgical procedure. Results The basal values of microvascular flow before the induction of anesthesia were significantly higher in the skin of the forehead compared with that of the forearm. There were no significant alterations in microvascular reactivity throughout the recording periods for both recording sites, as assessed by the vasodilation range expressed as cutaneous vascular conductance (arbitrary perfusion units/mean arterial pressure). Conclusions Using LDPM, the authors showed that the microcirculatory bed of the skin of the forehead, which is readily accessible during cardiac surgery, is a suitable model for the study of microvascular reactivity and tissue perfusion in cardiovascular surgical procedures using CPB. This technique could, thus, be suitable for evaluating the effects of drugs or technical procedures on tissue perfusion during cardiac surgery under cardiopulmonary bypass.

Background: Aerobic interval exercise training has greater benefits on cardiovascular function as compared with aerobic continuous exercise training. Objective: The present study aimed at analyzing the effects of both exercise modalities on acute and subacute hemodynamic responses of healthy rats. Methods: Thirty male rats were randomly assigned into three groups as follows: continuous exercise (CE, n = 10); interval exercise (IE, n = 10); and control (C, n = 10). Both IE and CE groups performed a 30-minute exercise session. The IE group session consisted of three successive 4-minute periods at 60% of maximal velocity (Max Vel), with 4-minute recovery intervals at 40% of Max Vel. The CE group ran continuously at 50% of Max Vel. Heart rate (HR), blood pressure(BP), and rate pressure product (RPP) were measured before, during and after the exercise session. Results: The CE and IE groups showed an increase in systolic BP and RPP during exercise as compared with the baseline values. After the end of exercise, the CE group showed a lower response of systolic BP and RPP as compared with the baseline values, while the IE group showed lower systolic BP and mean BP values. However, only the IE group had a lower response of HR and RPP during recovery. Conclusion: In healthy rats, one interval exercise session, as compared with continuous exercise, induced similar hemodynamic responses during exercise. However, during recovery, the interval exercise caused greater reductions in cardiac workload than the continuous exercise.

BACKGROUND Propofol is an intravenous anesthetic that is widely used to anesthetize patients during neurosurgical procedures. Although propofol is considered to be an essential component of contemporary management of acute brain injury in the operating room and in critical care settings, propofol-induced hypotension (PIH) remains a frequent and undesirable side effect. After 3 decades of clinical use, multiple proposed causes of PIH, and conflicting experimental results, the mechanism of PIH is still a puzzle for neuroscience and anesthesiology. This study evaluated the role of opioid receptors in PIH. METHODS Pentobarbital-anesthetized rats were subjected to systemic or central pretreatment with naloxone followed by intravenous or central administration of propofol. RESULTS In the absence of pretreatment with naloxone, intravenous (7.5 mg/kg) and intracistenal propofol (10 µg) injection induced 45% and 35% reductions in the mean arterial pressure, respectively (P

BACKGROUND: The use of vasoactive drugs to restore arterial blood pressure in patients with septic shock remains a cornerstone of intensive care medicine. However, vasopressors can accentuate the hypoperfusion of the gut during septic shock, allowing bacterial translocation and endotoxemia. In this study, we compared the effects of different vasoactive drugs on intestinal microcirculation and tissue oxygenation, independent of the effects of fluid therapy, in a rat model of endotoxemic shock. METHODS: Pentobarbital-anesthetized Wistar Kyoto rats were submitted to endotoxemic shock induced by Escherichia coli lipopolysaccharide (2 mg/kg IV). Arterial blood pressure was normalized by a continuous infusion of different vasoactive drugs, including epinephrine, norepinephrine, phenylephrine, dopamine, dobutamine, or a combination of dobutamine and norepinephrine. The functional capillary density (FCD) of the muscular layer of the small intestine was evaluated by intravital video-microscopy. Mesenteric venous blood gases and lactate concentrations were also analyzed. RESULTS: FCD decreased by approximately 25% to 60% after the IV infusion of epinephrine, norepinephrine, and phenylephrine. Administration of dopamine, dobutamine, and the combination of dobutamine and norepinephrine did not induce significant alterations in gut FCD. In addition, the mesenteric venous lactate concentration increased in the presence of phenylephrine and showed a tendency to increase after the administration of epinephrine and norepinephrine, whereas there was no observable increase after the administration of dopamine, dobutamine, and the combination of dobutamine with norepinephrine. CONCLUSION: This study confirms dissociation of the systemic hemodynamic and microvascular alterations in an experimental model of septic shock. Moreover, the results indicate that the use of dopamine, dobutamine, and dobutamine in combination with norepinephrine yields a protective effect on the microcirculation of the intestinal muscular layer in endotoxemic rats.

We investigated the vascular effects of a crude aqueous extract (AEEG) of Echinodorus grandiflorus (Alismataceae) using the in vitro experimental models of the rabbit isolated aorta and perfused kidney. Echinodorus grandiflorus, a native semi-aquatic plant widely distributed in Brazil, has been extensively used in Brazilian folk medicine for the treatment of high blood pressure and inflammatory diseases. The bolus injection of AEEG (0.1-10 mg) into the rabbit renal circulation pre-contracted with norepinephrine induced marked and dose-dependent vasodilator responses (maximum of 37+/-4%; n=6; P

An 84-year-old man presenting with triple-vessel coronary artery disease and unstable angina pectoris associated with mitral valve stenosis was scheduled for coronary artery bypass graft surgery and mitral valve replacement. His medical history was significant for chronic pulmonary obstructive disease and moderate left ventricular dysfunction, thus warranting the use of a PAC for the accurate monitoring of hemodynamic parameters. Although transesophageal echocardiography has been widely used during cardiac surgery, the use of a PAC is still an alternative when TEE is not available in the operating room. The patient was premedicated with a combination of midazolam, 5 mg, and fentanyl, 50 g, intravenously, 30 minutes before surgery. PAC insertion was performed by using a modified Seldinger technique. The right internal jugular vein was punctured with a 22-G seeker needle at the angle formed by the bellies of the sternocleidomastoid muscle near the level of the cricoid cartilage. The vessel was cannulated with an 18-G straight introducer needle to a depth of 2 to 3 cm. Dark, nonpulsatile venous blood was obtained by aspiration during needle placement. A J-tip wire guide was inserted through the needle without difficulty, and an 8.5F introducer sheath of the PAC was placed over a dilator, which was introduced to its full length. Once again dark, nonpulsatile venous blood was easily aspirated from the sheath. A 7.5F PAC (model 831F75, Baxter Edwards, Irvine, CA) was inserted via the introducer into the right internal jugular vein. The balloon had been previously checked for proper inflation over the end of the catheter. After the insertion of 25 cm of the PAC with the balloon inflated, a significant resistance to pass the catheter into the RV was experienced. After several attempts that took about 5 minutes and without taking any additional measures, the catheter was successfully introduced into the right ventricle and then into the pulmonary artery, as assessed by the corresponding pressure waves. The final position of the catheter was at about 50 cm of insertion. There were no significant alterations in hemodynamic parameters or in electrocardiographic tracings during the wire guide or PAC insertion. General anesthesia was induced by using a combination of fentanyl, 300 g, and etomidate, 10 mg; pancuronium, 6 mg, was used for neuromuscular blockade. Anesthesia was maintained with isoflurane, 1.5% to 2% in oxygen. The chest was opened with a median sternotomy incision. After opening the pericardium, the presence of blood within the pericardial sac led to the identification of a perforation in the right atrium. It was an elliptically-shaped perforation with about 1 mm of diameter in the inferior portion of the atrial lateral wall, about 2 to 3 cm from the superior vena cava junction. The perforation was then sutured, and the patient underwent coronary artery bypass graft surgery without presenting further complications. Recovery was uneventful, and the patient was discharged 10 days after surgery with no residual complications.

Purpose: A recent study showed by in vitro experiment that exercise enhances myocardial tolerance to ischemia-reperfusion (I-R) injury via an opioid receptor-dependent mechanism. However, in an in vivo model, peripheral mechanisms could interfere in this response, and whether or not opioid system would still contribute to cardioprotection remains to be determined. Methods: Male Wistar rats (250-300g) were randomly assigned to 4 groups: Sedentary I-R (n = 10); Sedentary Sham I-R (n = 10); Exercise I-R (n = 10); Naloxone (a non-selective opioid receptor antagonist) + Exercise I-R (n = 10). Exercise groups performed 4 consecutive days of treadmill training (60 min at 70% of VO2max obtained in a graded exercise test). I-R injury consisted of 30 min interventricular coronary occlusion followed by 60 min of reperfusion. Infarct size, as a percentage of the area at risk, was determined by triphenyltetrazolium and Evans blue staining. Results: In baseline, there were no differences between groups. During ischemia and reperfusion, Sedentary I-R presented significantly lower systolic blood pressure compared to Sedentary Sham I-R and Exercise I-R, as showed in the graph below. Exercise I-R group presented a smaller infarct size (21.88±4.53%) compared to Sedentary I-R (38.64±5.00%; p