Acute effects of Helicobacter pylori extracts on gastric mucosal blood flow in the mouse

Henriksnäs, Johanna; Atuma, Christer; Phillipson, Mia; Sandler, Stellan; Engstrand, Lars; Holm, Lena

doi:10.3748/wjg.15.219

Cited by 8 publications

(5 citation statements)

References 28 publications

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“…Judaki et al [18] reported more prominent vascular changes in patients with H. pylori-positive chronic gastritis than in H. pylori-negative chronic gastritis. Some studies have also reported decreased gastric microcirculation in patients with H. pylori infection [12,20]. These findings all show that both micro-and macrovascular changes occur in the presence of H.…”

Section: Discussionmentioning

confidence: 55%

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Evaluation of celiac artery blood flow in children with chronic active gastritis

Akbulut¹,

Özkan²,

Işık³

et al. 2021

Pamukkale Medical Journal

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Section: Discussionmentioning

confidence: 55%

“…Platelet activating factor (PAF) released from mast cells and some other inflammatory cells is a potent vasoconstrictor. PAF causes early leukocyte migration and hypoperfusionin gastrointestinal microcirculatory [12]. Although few mast cells can be seen in normal mucosa, the level increases in the presence of inflammation [13].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of celiac artery blood flow in children with chronic active gastritis

Akbulut¹,

Özkan²,

Işık³

et al. 2021

Pamukkale Medical Journal

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show abstract

“…An additional study confirmed these findings and identified significant albumin leakage, which suggested damage to the endothelium [27]. H. pylori infection in mice resulted in a 30% reduction in mucosal blood flow as evaluated by laser Doppler [46]. Clinically, H. pylori infection was associated with a decrease in mucosal blood flow in patients who had undergone endoscopic mucosal resection [47].…”

Section: Acute Infectionsmentioning

confidence: 71%

Imaging of the Intestinal Microcirculation during Acute and Chronic Inflammation

Dickson

Malitan

Lehmann

2020

Biology

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Because of its unique microvascular anatomy, the intestine is particularly vulnerable to microcirculatory disturbances. During inflammation, pathological changes in blood flow, vessel integrity and capillary density result in impaired tissue oxygenation. In severe cases, these changes can progress to multiorgan failure and possibly death. Microcirculation may be evaluated in superficial tissues in patients using video microscopy devices, but these techniques do not allow the assessment of intestinal microcirculation. The gold standard for the experimental evaluation of intestinal microcirculation is intravital microscopy, a technique that allows for the in vivo examination of many pathophysiological processes including leukocyte-endothelial interactions and capillary blood flow. This review provides an overview of changes in the intestinal microcirculation in various acute and chronic inflammatory conditions. Acute conditions discussed include local infections, severe acute pancreatitis, necrotizing enterocolitis and sepsis. Inflammatory bowel disease and irritable bowel syndrome are included as examples of chronic conditions of the intestine.

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“…These systems are part of the pathogen protection against nitrosative stress . Likewise, Hp may exhibit a direct effect on the reduction in gastric mucosal blood flow by inhibiting NO production by iNOS, thereby decreasing the vasodilatory and mast cell–stabilizing action of NO . Moreover, several Hp virulence agents contribute to its ability to evade the immune system and disrupt host cells.…”

Section: Hp In No‐related Glaucoma Pathophysiologymentioning

confidence: 99%

Impact of nitric oxide's bidirectional role on glaucoma: focus onHelicobacter pylori–related nitrosative stress

Papaefthymiou

Doulberis

Katsinelos

et al. 2019

Annals of the New York Academy of Sciences

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Nitric oxide (NO), a small molecule generated ubiquitously, targets a plethora of tissues to regulate both physiological and pathophysiological functions. NO overproduction, stimulated by microenvironmental conditions, is the main component that dysregulates the tight balance between its beneficial and damaging roles in ocular homeostasis. Considering the protective functions of NO against glaucoma, its endogenous release facilitates aqueous humor drainage and regulates ocular blood flow, maintaining a normal intraocular pressure. NO overproduction generates free radicals, such as peroxynitrite, which induce a vicious circle of vascular disharmony and dysregulation, transient ischemia, nitrosative stress, neuronal degeneration, and permanent glaucomatic injury. Helicobacter pylori (Hp) is considered a burdening factor of glaucoma. NO overproduction and possible systematic dispersion in Hp infection (Hp‐I) could suggest a potential pathophysiological bridge between these conditions. In this review, we aim to elucidate the role of NO in glaucoma with respect to Hp‐I, with the aim to stimulate further studies.

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Acute effects of Helicobacter pylori extracts on gastric mucosal blood flow in the mouse

Abstract: A H pylori water extract reduces gastric mucosal blood flow acutely through iNOS- and nerve-mediated pathways.

Cited by 8 publications

References 28 publications

Evaluation of celiac artery blood flow in children with chronic active gastritis

Evaluation of celiac artery blood flow in children with chronic active gastritis

Imaging of the Intestinal Microcirculation during Acute and Chronic Inflammation

Impact of nitric oxide's bidirectional role on glaucoma: focus onHelicobacter pylori–related nitrosative stress

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