Obesity is independently associated with increased cardiovascular risk. However, since established obesity clusters with various cardiovascular risk factors, configuring the metabolic syndrome, the early effects of obesity on vascular function are still poorly understood. The current study was designed to evaluate the effect of early obesity on coronary endothelial function in a new animal model of swine obesity. As to method, juvenile domestic crossbred pigs were randomized to either high-fat/high-calorie diet (HF) or normal chow diet for 12 wk. Coronary microvascular permeability and abdominal wall fat were determined by using electron beam computerized tomography. Epicardial endothelial function and oxidative stress were measured in vitro. Systemic oxidative stress, renin-angiotensin activity, leptin levels, and parameters of insulin sensitivity were evaluated. As a result, HF pigs were characterized by abdominal obesity, hypertension, and elevated plasma lysophosphatidylcholine and leptin in the presence of increased insulin sensitivity. Coronary endothelium-dependent vasorelaxation was reduced in HF pigs and myocardial microvascular permeability increased compared with those values in normal pigs. Systemic redox status in HF pigs was similar to that in normal pigs, whereas the coronary endothelium demonstrated higher content of superoxide anions, nitrotyrosine, and NADPH-oxidase subunits, indicating increased tissue oxidative stress. In conclusion, the current study shows that early obesity is characterized by increased vascular oxidative stress and endothelial dysfunction in association with increased levels of leptin and before the development of insulin resistance and systemic oxidative stress. Vascular dysfunction is therefore an early manifestation of obesity and might contribute to the increased cardiovascular risk, independently of insulin resistance.

Although bactibilia is an important condition of acute cholecystitis, its effect on the course and outcome of the infectious gallbladder disease has rarely been studied, particularly in relation to the laparoscopic procedure. The current study attempts to learn more about the inter-relationship between bactibilia and laparoscopic cholecystectomy during acute cholecystitis. Demographic, preoperative, operative, and postoperative data were prospectively collected in every patient with acute cholecystitis treated in the department of surgery at the Bnai Zion Medical Center, Israel. Intraoperative biliary samples were collected under aseptic conditions at the time of operation for bacteriologic examination and were routinely cultured in aerobic and anaerobic media for 3 days. The study population was divided into culture-positive and culture-negative groups, and the collected parameters were compared between the groups. Age over 60 years, a palpable gallbladder, temperature over 37.5 degrees C, a white blood cell (WBC) count of more than 12,000/cc(3), and serum alkaline phosphatase higher than 100 U/dL were all found to be factors capable of predicting bactibilia. Bactibilia was a significant factor associated with total, as well as infectious, operative complications. Bactibilia is considered to indicate an advanced stage of acute cholecystitis. In cases of laparoscopic cholecystectomy for infectious gallbladder disease, bactibilia is strongly associated with total, as well as local, infectious complications. Preoperative conditions such as older age, elevated temperature, a palpable gallbladder, elevated WBC count, and elevated serum levels of alkaline phosphatase can serve as predictors of bactibilia and its consequent complications. Although the sensitivity and specificity of the predictive factors for bactibilia are limited to 63% and 67%, respectively, in their presence during acute cholecystitis, conservative wide-spectrum antibiotics as the first-line therapy is appropriate, and, upon regimen failure, laparoscopic surgery by an experienced surgeon is indicated as the adjusted therapy.

The current study demonstrates a differential structure of the adventitial VV in different vascular beds. This intra- and intervessel heterogeneity in VV anatomy is a phenotypic variability that might determine a differential local response to systemic risk factors and, thereby, variable propensity for vascular disease among different vascular beds.

Objective-Vasa vasorum (VV) neovascularization is a key feature of early atherosclerosis and adds substantial endothelial exchange-surface to the coronary vessel wall. Thus, it is conceivable that VV neovascularization favors the entry of pro-inflammatory and pro-atherosclerotic blood components into the coronary vessel wall. We sought to investigate the effects of Thalidomide (Th) a potent anti-angiogenic drug on vasa vasorum (VV) neovascularization, vessel wall inflammation and neointima formation in early experimental atherosclerosis.Methods and Results-Female domestic swine, 3-months old, were fed normal (N, n=12) or high-cholesterol diet (HC, n=12) for 3 months. In each group six pigs were randomized to 200 mg Thalidomide daily for the diet period (N+Th, HC+Th). LADs were scanned with micro-CT (20μm cubic voxel size) to determine VV spatial density (#/mm²). Fresh-frozen coronary tissue was used for Western Blotting (VEGF, TNF-α , LOX-1, IkBα and Gro-α ) and electrophoretic mobility shift assay (EMSA, NFkB). Treatment with Thalidomide preserved VV spatial density (2.7±0.3 (N), 6.4 ±0.7 (HC), 3.5±0.8 (HC+Th); p=ns HC+Th vs. N) and inhibited the expression of VEGF, TNF-alpha and LOX-1 but not NFkB activity in the coronary vessel wall. Immunofluorescense analyses revealed co-localization of vWF but not SMA and NFkB, TNF-α as well as VEGF in HC and HC+Th coronaries. Intima-media thickness was significantly inhibited in HC+Th compared to HC. Serum levels of hs-CRP and TNF-α did not differ among the groups.Conclusions-Our study supports a role of VV neovascularization in the development of and a therapeutic potential for anti-angiogenic intervention in early atherosclerosis.

ObjectiveWe hypothesized that ultrasound (US)-guided technique of the supra- and infraclavicular and axillary approaches of brachial plexus block (BPB) will produce a high quality of surgical anesthesia for operations below the shoulder independently of the approach and body mass index (BMI). Intercostobrachial and medial brachial cutaneous nerves will be blocked separately because they are not a part of the brachial plexus.MethodsThis is a prospective randomized observer-blinded study. The three approaches of the US-guided BPB without neurostimulation were compared for quality, performance time, and correlation between performance time and BMI. Intercostobrachial and medial brachial cutaneous nerve blocks were used in all patients.ResultsA total of 101 patients were randomized into three groups: SCL (supraclavicular), ICL (infraclavicular), and AX (axillary). Seven patients were excluded due to various factors. All three groups were similar in demographic data, M:F proportion, preoperative diagnosis and type of surgery, anesthesiologists who performed the block, and surgical staff that performed the surgical intervention. The time between the end of the block performance and the start of the operation was also similar. The quality of the surgical anesthesia and discomfort during the operation were identical following comparison between groups. No direct positive correlation was observed between BMI and the block performance time. The time for the axillary block was slightly longer than the time for the supra- and infraclavicular approaches, but it had no practical clinical significance. Transient Horner syndrome was observed in three patients in the SCL group. No other adverse effects or complications were observed.ConclusionsAll three approaches can be used for US-guided BPB with similar quality of surgical anesthesia for operations of below the shoulder. A block of the intercostobrachial and medial brachial cutaneous nerves is recommended. Obesity is not a significant factor in relation to the time of US-guided BPB performance, or the quality of surgical anesthesia. (ClinicalTrials.gov number, NCT01442558.)