Role of gastric distention in angina pectoris

1963 ◽  
Vol 11 (2) ◽  
pp. 253-258 ◽  
Author(s):  
Adan Nigaglioni ◽  
David Finkelstein ◽  
Henry L. Bockus
Keyword(s):  
Angina Pectoris ◽  
Gastric Distention

Understanding the role of Inflammasome in Angina Pectoris

2020 ◽  
Vol 21 ◽  
Author(s):  
Ishita Sharma ◽  
Tapan Behl ◽  
Simona Bungau ◽  
Monika Sachdeva ◽  
Arun Kumar ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Angina Pectoris ◽  
Nlrp3 Inflammasome ◽  
Vital Role ◽  
Death Process ◽  
Cell Death Process ◽  
Artery Disease ◽  
Species Production ◽  
Pro Inflammatory Cytokines

Abstract:: Angina pectoris, associated with coronary artery disease, a cardiovascular disease where, pain is caused by adverse oxygen supply in myocardium, resulting in contractility and discomfort in chest. Inflammasomes, triggered by stimuli due to infection and cellular stress have identified to play a vital role in the progression of cardiovascular disorders and thus, causing various symptoms like angina pectoris. Nlrp3 inflammasome, a key contributor in the pathogenesis of angina pectoris, requires activation and primary signaling for the commencement of inflammation. Nlrp3 inflammasome elicit out an inflammatory response by emission of pro inflammatory cytokines by ROS (reactive oxygen species) production, mobilization of K+ efflux and Ca2+ and by activation of lysosome destabilization that eventually causes pyroptosis, a programmed cell death process. Thus, inflammasome are considered to be one of the factors involved in the progression of coronary artery diseases and have an intricate role in development of angina pectoris.

DIFFERENTIATION OF ESOPHAGEAL PAIN FROM ANGINA PECTORIS: ROLE OF THE ESOPHAGEAL ACID PERFUSION TEST

Medicine ◽  
1962 ◽  
Vol 41 (2) ◽  
pp. 143-162 ◽  
Author(s):  
LIONEL M. BERNSTEIN ◽  
ROBERT C. FRUIN ◽  
RALPH PACINI
Keyword(s):  
Angina Pectoris ◽  
Acid Perfusion ◽  
Acid Perfusion Test

Triggering of transient LES relaxations in ferrets: role of sympathetic pathways and effects of baclofen

2000 ◽  
Vol 279 (1) ◽  
pp. G157-G162 ◽  
Author(s):  
Esther Staunton ◽  
Scott D. Smid ◽  
John Dent ◽  
L. Ashley Blackshaw
Keyword(s):  
Gastroesophageal Reflux ◽  
Lower Esophageal Sphincter ◽  
Glucose Infusion ◽  
Gastric Distention ◽  
Low Level ◽  
Before And After ◽  
Esophageal Sphincter ◽  
Splanchnic Mechanoreceptors ◽  
High Level

Activation of gastric vagal mechanoreceptors by distention is thought to be the trigger for transient lower esophageal sphincter relaxations (TLESR), which lead to gastroesophageal reflux. The contribution of higher-threshold gastric splanchnic mechanoreceptors is uninvestigated. GABABreceptor agonists, including baclofen, potently reduce triggering of TLESR by low-level gastric distention. We aimed to determine first whether this effect of baclofen is maintained at high-level distention and second the role of splanchnic pathways in triggering TLESR. Micromanometric/pH studies in conscious ferrets showed that intragastric glucose infusion (25 ml) increased triggering of TLESR and reflux. Both were significantly reduced by baclofen (7 μmol/kg ip) ( P < 0.05). When 40 ml of air was added to the glucose infusion, more TLESR occurred than with glucose alone ( P < 0.01). These were also reduced by baclofen ( P < 0.001). TLESR after glucose/air infusion were assessed before and after splanchnectomy (2–4, 9–11, and 23–25 days), which revealed no change. Baclofen inhibits TLESR after both low- and high-level gastric distention. Splanchnic pathways do not contribute to increased triggering of TLESR by high-level gastric distention.

Role of stomach in regulation of activities of hypothalamic feeding centers

1961 ◽  
Vol 201 (4) ◽  
pp. 593-598 ◽  
Author(s):  
K. N. Sharma ◽  
B. K. Anand ◽  
S. Dua ◽  
Baldev Singh
Keyword(s):  
Blood Glucose ◽  
Electrical Activity ◽  
High Voltage ◽  
Glucose Utilization ◽  
Irregular Waves ◽  
Gastric Distention ◽  
Implanted Electrodes ◽  
Gastric Contractions ◽  
Balloon System

Gastric distention was produced through a water-filled-balloon system and the electrical activity of the hypothalamic "satiety" and "feeding" centers were recorded electroencephalographically through stereotaxically implanted electrodes. Gastric distention leads to production of high voltage irregular waves and occasional spikes, selectively in the region of the satiety centers. Gastric hunger contractions do not change the electrical activity of either feeding or satiety centers. Glucagon does not produce any direct effect on the hypothalamic centers or stomach contractions. Later, when glucagon raises blood glucose and arteriovenous Δ-glucose, activity of satiety centers increases and gastric contractions are inhibited. After lesions of satiety centers, rise in blood glucose with glucagon does not inhibit gastric contractions. Therefore, the inhibition of gastric hunger contractions is a result of activation of satiety centers by increased glucose utilization.

Mo-P4:235 A possible role of lipopolisaccharide-binding protein in infection related angina pectoris

2006 ◽  
Vol 7 (3) ◽  
pp. 98
Author(s):  
T. Recheinski ◽  
A. Grebowska ◽  
M. Kurpesa ◽  
M. Krzeminska-Pakula ◽  
W. Rudnicka ◽  
...  
Keyword(s):  
Angina Pectoris ◽  
Binding Protein

The role of the stomach in the control of appetite and the secretion of satiation peptides

2012 ◽  
Vol 302 (6) ◽  
pp. E666-E673 ◽  
Author(s):  
Robert E. Steinert ◽  
Anne C. Meyer-Gerspach ◽  
Christoph Beglinger
Keyword(s):  
Peptide Yy ◽  
Potential Interaction ◽  
Feedback Signal ◽  
Similar Degree ◽  
Short Term ◽  
Gastric Distention ◽  
Liquid Meal ◽  
Intraduodenal Infusion ◽  
Glucagon Like Peptide 1

It is widely accepted that gastric parameters such as gastric distention provide a direct negative feedback signal to inhibit eating; moreover, gastric and intestinal signals have been reported to synergize to promote satiation. However, there are few human data exploring the potential interaction effects of gastric and intestinal signals in the short-term control of appetite and the secretion of satiation peptides. We performed experiments in healthy subjects receiving either a rapid intragastric load or a continuous intraduodenal infusion of glucose or a mixed liquid meal. Intraduodenal infusions (3 kcal/min) were at rates comparable with the duodenal delivery of these nutrients under physiological conditions. Intraduodenal infusions of glucose elicited only weak effects on appetite and the secretion of glucagon-like peptide-1 (GLP-1) and peptide YY (PYY). In contrast, identical amounts of glucose delivered intragastrically markedly suppressed appetite ( P < 0.05) paralleled by greatly increased plasma levels of GLP-1 and PYY (≤3-fold, P < 0.05). Administration of the mixed liquid meal showed a comparable phenomenon. In contrast to GLP-1 and PYY, plasma ghrelin was suppressed to a similar degree with both intragastric and intraduodenal nutrients. Our data confirm that the stomach is an important element in the short-term control of appetite and suggest that gastric and intestinal signals interact to mediate early fullness and satiation potentially by increased GLP-1 and PYY secretions.

scholarly journals The role of prostacyclin during exercise in patients with chronic angina pectoris.

1988 ◽  
Vol 29 (4) ◽  
pp. 401-413 ◽  
Author(s):  
Akira KURITA ◽  
Bonpei TAKASE ◽  
Akimi UEHATA ◽  
Kimio SATOMURA ◽  
Hiroko SUGAWARA ◽  
...  
Keyword(s):  
Angina Pectoris ◽  
Chronic Angina
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