Cardiovascular Autonomic Response to Food Ingestion in Patients with Gastritis: A Comparison Between <i>Helicobacter pylori</i>‐Positive and ‐Negative Patients

Lugon, Jocemir Ronaldo; Moreira, Mauro Diniz; Almeida, José Mentor Ramos de; Silva, Agostinho Soares; Esberard, Eliane Cathala Bordalo; Santos, Kelb Bousquet; Carvalho, Angela Gouvêa; Mendes, Luciana Claudia; Nóbrega, Antônio Cláudio Lucas da

doi:10.1111/j.1523-5378.2006.00397.x

Cited by 7 publications

(7 citation statements)

References 24 publications

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“…However, a recent study has shown an inverse correlation between the severity of gastritis and circulating levels of ghrelin, which gradually decrease after bacterial eradication (23). Others have shown that subjects with H. pylori infection have blunted sympathetic reactivity and an exacerbated vagal response to feeding (16). In our study, we found that plasma ghrelin levels were higher in infected mice and normalized after bacterial eradication, while leptin levels were unchanged by H. pylori infection.…”

Section: Discussionsupporting

confidence: 68%

Role of gut-brain axis in persistent abnormal feeding behavior in mice following eradication of Helicobacter pylori infection

Berčík

Verdú²,

Foster³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Here, we investigate the role of the gut-brain axis in gastric dysfunction during and after chronic H. pylori infection. Control and chronically H. pylori-infected Balb/c mice were studied before and 2 mo after bacterial eradication. Gastric motility and emptying were investigated using videofluoroscopy image analysis. Gastric mechanical viscerosensitivity was assessed by cardioautonomic responses to distension. Feeding patterns were recorded by a computer-assisted system. Plasma leptin, ghrelin, and CCK levels were measured using ELISA. IL-1␤, TNF-␣, proopiomelanocortin (POMC), and neuropeptide Y mRNAs were assessed by in situ hybridizations on frozen brain sections. Gastric inflammation was assessed by histology and immunohistochemistry. As shown previously, H. pylori-infected mice ate more frequently than controls but consumed less food per bout, maintaining normal body weight. Abnormal feeding behavior was accompanied by elevated plasma ghrelin and postprandial CCK, higher TNF-␣ (median eminence), and lower POMC (arcuate nucleus) mRNA. Infected mice displayed delayed gastric emptying and visceral hypersensitivity. Eradication therapy normalized gastric emptying and improved gastric sensitivity but had no effect on eating behavior. This was accompanied by persistently increased TNF-␣ in the brain and gastric CD3 ϩ T-cell counts. In conclusion, chronic H. pylori infection in mice alters gastric emptying and mechanosensitivity, which improve after bacterial eradication. A feeding pattern reminiscent of early satiety persists after H. pylori eradication and is accompanied by increased TNF-␣ in the brain. The results support a role for altered gut-brain pathways in the maintenance of postinfective gut dysfunction.inflammation; gut-brain axis; gastric emptying; visceral sensitivity FUNCTIONAL GI DISORDERS SUCH as irritable bowel disease (IBS) and functional dyspepsia (FD) have traditionally been viewed as psychosomatic. The concept that previous infection can trigger the development of functional GI disease is now accepted. A large cohort study identified bacterial gastroenteritis as the most significant risk factor identified to date for the development of IBS (24). IBS symptoms have been reported to develop in a significant proportion of subjects with documented Campylobacter, Salmonella, E. coli, or Shigella infection (12,32,37). A similar case has been also made for functional dyspepsia (18,33). These studies were restricted to acute enteric infections.Accumulating evidence suggests that changes in the bacterial content in the gut can affect the central nervous system (CNS) (10, 13). Most of these studies have dealt with the effect of acute infection and early CNS changes that occurred before the onset of the inflammatory response to the infection. The effect of chronic GI infection and inflammation on the CNS has not yet been investigated. Previous studies suggested that vagal sensory afferents are responsible for the rapid changes that occur in the brain within hours of a GI infection (13). However, multiple...

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Section: Discussionsupporting

confidence: 68%

Role of gut-brain axis in persistent abnormal feeding behavior in mice following eradication of Helicobacter pylori infection

Berčík

Verdú²,

Foster³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…It is worth noting that since the validation of the 4sET two decades ago (Araújo et al 1992), our research group (Almeida et al 2004;Araújo et al 1992Araújo et al ,2003Nóbrega and Araújo 1993;Nóbrega et al 1994a;Oliveira et al 2006;Ricardo et al 2005;Teixeira et al 2007) and others (KnopXi and Bar-Or 1999;Lugon et al 2006) have been using the 4sET in physiological and clinical investigations.…”

Section: Samplementioning

confidence: 96%

Similar cardiac vagal withdrawal at the onset of arm and leg dynamic exercise

et al. 2007

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Electrocardiogram RR intervals duration reduce rapidly in the first seconds of dynamic exercise mainly due to a cardiac vagal withdrawal. However, it remains unclear if this response varies between exercises performed with different body segments (i.e. arm vs. leg). Our aim was to compare the vagal withdrawal at the onset of arm and leg dynamic exercise. Cardiac vagal withdrawal was assessed by the 4-s exercise test (4sET), a pharmacologically validated and highly reliable procedure. Initially, 60 healthy subjects performed the 4sET using arms (ARM 4sET) and legs (LEG 4sET), in a random order. Later, 20 of them repeated the testing, controlling for cycling rate and time of exercise onset within a RR interval, potential intervenient variables. Similar results were found for ARM and LEG 4sET considering the RR interval duration obtained immediately before the onset of exercise (RRB) (mean +/- SEM; 852 +/- 23 vs. 857 +/- 23 ms; P = 0.55), the shortest RR interval duration during exercise (RRC) (570 +/- 10 vs. 563 +/- 10 ms; P = 0.22) and the cardiac vagal index (CVI), which is the ratio between RRB and RRC (1.49 +/- 0.03 vs. 1.52 +/- 0.03; P = 0.10). Furthermore, high intraclass correlation coefficients were found (RRB r (i) = 0.94, P < 0.001; RRC r (i) = 0.85, P < 0.001; CVI r (i) = 0.81, P < 0.001). We conclude that similar cardiac vagal withdrawal was induced by 4-s fast unloaded cycling exercise performed with arms or legs.

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“…Vagal nerve predominance, as diagnosed by heart rate variability analyses, was also recognized as a risk factor for duodenal ulcer development [2,[38][39]121] . Lugon et al [122] reported blunted sympathetic reactivity and an exacerbated vagal response to feeding in H. pyloripositive subjects. However, Katoh et al [36] have shown that H. pylori eradication in duodenal ulcer patients does not change nocturnal sympatheticotonia or parasympatheticotonia, which may be the cause for persistently increased gastric acid secretion, gastric mucosal vasoconstriction and ulcer recurrence [38,121] , though the time course between eradication and ANS evaluation may have been too short to reveal statistically significant differences.…”

Section: H Pylori and Ans Activitymentioning

confidence: 98%

Brain-gut axis in the pathogenesis ofHelicobacter pyloriinfection

Budzyński¹

2014

WJG

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Helicobacter pylori (H. pylori) infection is the main pathogenic factor for upper digestive tract organic diseases. In addition to direct cytotoxic and proinflammatory effects, H. pylori infection may also induce abnormalities indirectly by affecting the brain-gut axis, similar to other microorganisms present in the alimentary tract. The brain-gut axis integrates the central, peripheral, enteric and autonomic nervous systems, as well as the endocrine and immunological systems, with gastrointestinal functions and environmental stimuli, including gastric and intestinal microbiota. The bidirectional relationship between H. pylori infection and the brain-gut axis influences both the contagion process and the host's neuroendocrine-immunological reaction to it, resulting in alterations in cognitive functions, food intake and appetite, immunological response, and modification of symptom sensitivity thresholds. Furthermore, disturbances in the upper and lower digestive tract permeability, motility and secretion can occur, mainly as a form of irritable bowel syndrome. Many of these abnormalities disappear following H. pylori eradication. H. pylori may have direct neurotoxic effects that lead to alteration of the brain-gut axis through the activation of neurogenic inflammatory processes, or by microelement deficiency secondary to functional and morphological changes in the digestive tract. In digestive tissue, H. pylori can alter signaling in the brain-gut axis by mast cells, the main brain-gut axis effector, as H. pylori infection is associated with decreased mast cell infiltration in the digestive tract. Nevertheless, unequivocal data concerning the direct and immediate effect of H. pylori infection on the brain-gut axis are still lacking. Therefore, further studies evaluating the clinical importance of these host-bacteria interactions will improve our understanding of H. pylori infection pathophysiology and suggest new therapeutic approaches.

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Cardiovascular Autonomic Response to Food Ingestion in Patients with Gastritis: A Comparison Between Helicobacter pylori‐Positive and ‐Negative Patients

Abstract: Supporting the observations that motivate the study, our findings indicate blunted sympathetic reactivity and exacerbated vagal response to feeding in H. pylori-positive patients.

Cited by 7 publications

References 24 publications

Role of gut-brain axis in persistent abnormal feeding behavior in mice following eradication of Helicobacter pylori infection

Role of gut-brain axis in persistent abnormal feeding behavior in mice following eradication of Helicobacter pylori infection

Similar cardiac vagal withdrawal at the onset of arm and leg dynamic exercise

Brain-gut axis in the pathogenesis ofHelicobacter pyloriinfection

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