Effects of Bariatric Surgery on Human Small Artery Function

Abstract

ObjectivesThe aim of this study was to investigate the effects of bariatric surgery on small artery function and the mechanisms underlying this.BackgroundIn lean healthy humans, perivascular adipose tissue (PVAT) exerts an anticontractile effect on adjacent small arteries, but this is lost in obesity-associated conditions such as the metabolic syndrome and type II diabetes where there is evidence of adipocyte inflammation and increased oxidative stress.MethodsSegments of small subcutaneous artery and perivascular fat were harvested from severely obese individuals before (n = 20) and 6 months after bariatric surgery (n = 15). Small artery contractile function was examined in vitro with wire myography, and perivascular adipose tissue (PVAT) morphology was assessed with immunohistochemistry.ResultsThe anticontractile activity of PVAT was lost in obese patients before surgery when compared with healthy volunteers and was restored 6 months after bariatric surgery. In vitro protocols with superoxide dismutase and catalase rescued PVAT anticontractile function in tissue from obese individuals before surgery. The improvement in anticontractile function after surgery was accompanied by improvements in insulin sensitivity, serum glycemic indexes, inflammatory cytokines, adipokine profile, and systolic blood pressure together with increased PVAT adiponectin and nitric oxide bioavailability and reduced macrophage infiltration and inflammation. These changes were observed despite the patients remaining severely obese.ConclusionsBariatric surgery and its attendant improvements in weight, blood pressure, inflammation, and metabolism collectively reverse the obesity-induced alteration to PVAT anticontractile function. This reversal is attributable to reductions in local adipose inflammation and oxidative stress with improved adiponectin and nitric oxide bioavailability.

Lack of direct effect of adiponectin on vascular smooth muscle cell BKCa channels or Ca2+ signaling in the regulation of small artery pressure-induced constriction

“…2009; Aghamohammadzadeh et al. 2013). However, in obese patients the ability of PVAT to release adiponectin and thus ameliorate constriction is lost; and this has been proposed as a potential mechanism contributing to the development of obesity related hypertension (Gao 2007).…”

“…Furthermore, a follow‐up study suggested that functional recovery of PVAT following bariatric surgery may be in part due to restoration of adiponectin in the PVAT itself (Aghamohammadzadeh et al. 2013). Adiponectin is a 30kD protein which is released exclusively from adipocytes, and traditionally has been studied in relation to its beneficial anti‐inflammatory and metabolic effects, thought to be mediated through activation of AMP Kinase (Iwabu et al.…”

Perivascular adipose tissue: role in the pathogenesis of obesity, type 2 diabetes mellitus and cardiovascular pathology.

“…Согласно данным ряда исследований, в периваску-лярной жировой ткани пациентов после бариатриче-ских операций наблюдается постепенное уменьшение размера адипоцитов, снижение уровня воспаления, восстановление антиконтрактильных свойств и увели-чение концентрации оксида азота и адипонектина [42].…”

Vitamin D controls resistance artery function through regulation of perivascular adipose tissue hypoxia and inflammation

“…In addition, PVAT produces transferable vasoactive substances including adipocyte-derived relaxing factors and adipocyte-derived contractile factors (2). The effect of PVAT on arterial reactivity has been examined in human small arteries obtained from subcutaneous adipose tissue biopsies using wire myography (3, 4). PVAT-containing arteries displayed a blunted response to vasoconstrictor agonist stimulation compared to arteries without PVAT from healthy lean subjects.…”

“…PVAT-containing arteries displayed a blunted response to vasoconstrictor agonist stimulation compared to arteries without PVAT from healthy lean subjects. Importantly, the anti-contractile effect of PVAT was lost in arteries taken from subjects with metabolic syndrome (3, 4). Obese subjects tend to have lower levels of serum 25-hydroxyvitamin D (25(OH)D) (5).…”