Experiments conducted in recent years on animals and research works worldwide show a linkage between calprotectin and occurrence and development of the abdominal aortic aneurysm (AAA). Additionally, a correlation between the level of the receptor for advanced glycation end products (RAGE) and the diameter of the abdominal aorta was found. The purpose of this study was to investigate whether calprotectin and the RAGE plasma level may be a biomarker of human AAA occurrence. We determined two groups of research participants: a group of 32 patients aged 53–88 undergoing primary endovascular aneurysm repair and a control group of 43 volunteers aged 59–82 without the AAA. All the patients from the study group had their blood samples drawn in order to determine the level of calprotectin and RAGE in plasma. The second follow-up examination was carried out after three months. The concentration of calprotectin and RAGE in plasma was determined with the use of the immunoenzymatic method (ELISA). The study showed that patients with the AAA had significantly higher mean calprotectin and RAGE plasma levels (p = 0.0001 and p = 0.0002, respectively) as compared to the control group. After the AAA repair operations, the level of concentration of the calprotectin decreased significantly (p = 0.0002). So far, no studies on the connection between the increase of the calprotectin and RAGE in the patient’s plasma with the AAA have been published. Calprotectin may be a promising biomarker related to the occurrence of AAA. Larger studies are needed to fully elucidate and confirm the role of calprotectin in the development and progression of the aneurysm.

An abdominal aortic aneurysm (AAA) is a dilatation of the abdominal aorta greater than 50% of the diameter of a healthy aorta. Previous experimental studies confirm the effect of calprotectin (CAL) on the onset of arterial pathology. It has been suggested that low levels of soluble receptors for advanced glycation end products (RAGEs) increase levels of cytokines that lead to the inhibition of matrix metalloproteinases (MMPs), affecting AAA formation. This study aimed to analyze the correlation of levels of RAGE and CAL with AAA diameter. A group of 32 patients aged 50–75 with diagnosed AAA was enrolled in the study. This group of patients was further divided into three subgroups based on AAA diameter: (1) <4.5 cm, (2) 4.5–5.5 cm, (3) >5.5 cm. Peripheral blood was drawn from all participants on admission to measure the serum CAL and RAGE levels. An enumeration survey was performed three months after AAA surgical treatment. CAL and RAGE plasma levels were measured with the enzyme-linked immunosorbent assay (ELISA). The median CAL levels were 2273.0 ng/mL before and 1217.0 ng/mL after treatment. There was a statistically significant decrease in CAL levels following the surgical treatment (p = 0.003). The correlation analysis between CAL levels and RAGE levels before and after surgical treatment showed no statistically significant correlations. In addition, there were no statistically significant correlations between CAL and RAGE levels with AAA size. In conclusion, CAL levels appear to be a significant marker in patients with AAA. There is an almost twofold decrease in CAL levels after AAA excision.

â-adrenergic antagonists influence abdominal aorta contractility by mechanisms not involving â-adrenergic receptors. Folia Biologica (Kraków) 62: 243-250. â-adrenergic receptors (â-AR) are widely distributed in the cardiovascular system, where they considerably contribute to the control of its functions. â-blockers are commonly used in the treatment of disorders of the circulatory system. They act primarily by inhibiting cardiac â-receptors. However, there are also reports of pleiotropic action of â-blockers as well as of new compounds created to study â 3 adrenergic receptors. The study aimed to investigate additional mechanisms of action of â-AR inhibitors in the rabbit abdominal aorta with emphasis on their action on á-adrenergic receptors and calcium influx. Responses to propranolol, betaxolol, metoprolol and SR59230A were evaluated in phenylephrine and PGF 2alpha precontracted aortic rings. The effect of propranolol on the phenylephrine concentration-contraction curve was examined. Propranolol ($10 FM) and SR59230A ($0.1 FM) induced relaxations in phenylephrine-precontracted rings, while betaxolol and metoprolol had little effect. The â-AR inhibitors produced further contraction of tissues preincubated with PGF 2alpha , excluding SR59230A, which after initial contraction, elicited marked relaxation at a concentration above 1 ìM. 100 FM of propranolol caused a significant rightward shift of the concentration-contraction curve to phenylephrine with no reduction in the maximum response. Incubation of aortic rings in phentolamine reduced the maximal contraction to propranolol; verapamil pretreatment by contrast enhanced contractile response. In conclusion, SR59230A and propranolol most probably act as á 1-AR competitive antagonists in the presence of phenylephrine in rabbit abdominal aortic rings. After á-ARs blockade, propranolol exerts a weak relaxing activity connected with Ca 2+ channel inactivation. SR59230A at a high concentration acts on the rabbit aorta by an additional mechanism needing further investigation.

Background: Abdominal aortic aneurysm (AAA) remains a surgical challenge. There are many recognizable markers associated with the formation of AAA. Previous experiments carried out on animal models have shown a correlation between serum calprotectin and the occurrence of AAA. Objective: This study aimed to evaluate the level of calprotectin as a potential diagnostic biomarker in patients with diagnosed AAA. Method: The study group consisted of 75 patients aged 35–75 years who were assigned to two groups: a control group (n=43) of healthy subjects without AAA and a study group (n=32) of patients with a diagnosed AAA. The first calprotectin test was performed upon patient admission to the hospital, and the second control test was performed after three months. The concentration of calprotectin in plasma was determined using the immunoenzymatic method (ELISA) with the commercially available Assaypro Kit (AssayMax™ Human Calprotectin ELISA Kit), as well as the sandwich method with polyclonal antibodies to human calprotectin and peroxidase enzyme. Results & Discussion: Serum calprotectin levels in AAA patients were three times higher than in healthy subjects (p<0.05). A statistically significant a twofold decrease in calprotectin concentration was observed after AAA surgery in comparison with the control group (p<0.05). Conclusion: Calprotectin levels can be an important marker in the detection of AAA. In conclusion, AAA patients showed a threefold increase in serum calprotectin level and a twofold decrease in this marker after AAA surgery.

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