Disease relevance of Hyperemia

• In addition to reduction of mortality and prolongation of survival time, supplemental Vit A moderated weight loss, adrenal gland hyperemia, thymus involution, and lymphopenia--all signs of radiation toxicity [1].
• We recently demonstrated in isolated, perfused hearts that radiolabeled pyruvaldehyde bis(N4-methylthiosemicarbazonato)copper(II) (Cu-PTSM) is well extracted throughout a range of conditions including ischemia, hypoxia, and hyperemia [2].
• Adenosine deaminase caused a 33 +/- 7 to 39 +/- 3% decrease in reactive hyperemia blood flow following coronary occlusions of 5-20 seconds duration, respectively, while 8-phenyltheophylline produced a 40 +/- 6 to 62 +/- 8% decrease in reactive hyperemia [3].
• Right coronary reactive hyperemia and the maximal coronary vasodilator response to adenosine were examined in conscious, normal dogs and dogs with right ventricular (RV) hypertrophy [4].
• After hypoxemia, reactive hyperemia associated with a significant increase in urinary prostaglandin excretion (PGE and PGF2 alpha) was observed in near-term fetuses but not in young fetuses [5].

Psychiatry related information on Hyperemia

• BACKGROUND: The purpose of the present study was to determine interactive and main effects of the eNOS T-786C gene polymorphism and habitual physical activity level on forearm vascular resistance (FVR) and forearm blood flow (FBF) at rest and during 3 min of reactive hyperemia [6].

High impact information on Hyperemia

• Using [(13)N]ammonia, we measured myocardial blood flow at rest, during adenosine-induced hyperemia, and in response to sympathetic stimulation induced by cold pressor testing [7].
• Vasodilation occurred with a latency of only 1-2 s, and both indomethacin and the cyclooxygenase-1 inhibitor SC-560 blocked the photolysis-induced hyperemia [8].
• Glycogen depletion of hepatocytes and hyperemia, and white pulp depletion of the spleen were the only changes induced by Aroclor 1254 [9].
• After indomethacin, this increase in prostaglandin production was not observed and reactive hyperemia was significantly reduced [10].
• Indomethacin, an inhibitor of prostaglandin synthetase, reduced reactive hyperemia at 10, 15, and 20 s to 15 plus or minus 5, 33 plus or minus 11, and 47 plus or minus 17 ml, respectively (P smaller than 0.05) [10].

Chemical compound and disease context of Hyperemia

• Endogenous nitric oxide, H1 receptors, and capsaicin-sensitive afferent nerves are not involved in this protective hyperemia [11].
• Within 1 min of contact, ethanol caused diffuse mucosal hyperemia [12].
• CONCLUSIONS: Both prostacyclin and NO contributed to splanchnic hyperemia in portal-hypertensive rats [13].
• Key mechanisms contributing to enteral nutrient-induced intestinal adaptation include nonspecific luminal stimulation and that provided by specific nutrients, "functional workload" induced by polymeric nutrients, potential stimulation of pancreaticobiliary secretions, secretion of humoral mediators, and induction of intestinal hyperemia [14].
• The results of this study may have important implications in steatorrheal diseases in that, atropine may alleviate the diarrhea induced by the presence of excess lipid in chyme without compromising the intestinal hyperemia and enhanced oxygen delivery required to meet the increased metabolic demands during nutrient absorption [15].

Biological context of Hyperemia

• There were no sex differences in response to intra-arterial nitroglycerin or digoxin or to reactive hyperemia, procedures that do not act through adrenergic receptors [16].
• Prostaglandin E2 (25 ng), a hyperemia inducer in microcirculation, augmented the permeability activity 12-fold, suggesting the presence of an up-regulation system in vivo [17].
• The reactive hyperemia response of the patients resembled responses obtained in normal fingers during decrease in local perfusion blood pressure, during local cooling or after infiltration of norepinephrine around the digital arteries [18].
• Exposure of anthracene treated skin to long-wave ultraviolet radiation (UVA) will produce hyperemia, increased vascular permeability, burning and itching [19].
• BACKGROUND/AIM: Portal hypertension is characterized by splanchnic hyperemia due to a reduction in mesenteric vascular resistance [20].

Anatomical context of Hyperemia

• Therefore, this study examines the effect of SP on capsaicin-induced mucosal hyperemia and mast cells [21].
• Only after 1-2 days of the initial insult, were signs of classical inflammation observed, including increases in colonic myeloperoxidase activity (neutrophil infiltration) and colon weight as well as hyperemia and mucosal ulcerations [22].
• We measured brachial artery diameters noninvasively using a 7.5-MHz ultrasound machine at rest, during reactive hyperemia, and after sublingual nitroglycerin administration [23].
• Proximal and distal poststenotic Doppler coronary flow velocities were measured (left anterior descending coronary artery, 16; right coronary artery, 10; left circumflex artery, 7 patients) before and during peak maximal hyperemia with intracoronary adenosine (8 to 12 micrograms) [24].
• With a recently developed high-resolution ultrasound system, diameters of radial artery were measured at rest, during reactive hyperemia (with increased flow causing endothelium-mediated dilation), and during sodium nitroprusside, causing endothelium-independent dilation [25].

Gene context of Hyperemia

• Role of inducible nitric oxide synthase and cyclooxygenase-2 in endotoxin-induced cerebral hyperemia [26].
• First, in the central nervous system, COX-2 is expressed under normal conditions and contributes to fundamental brain functions, such as synaptic activity, memory consolidation, and functional hyperemia [27].
• The inhibition of nitric oxide (NO) synthase by NG-nitro-L-arginine methyl ester attenuated the gastroprotection and gastric hyperemia induced by CCK while the concurrent treatment with L-arginine, but not D-arginine restored the protective activity of CCK and the accompanying increase in gastric blood flow [28].
• Rather, leptin induced hyperemia and leakage in the follicle, as well as the proteinase ADAMTS-1 (a disintegrin and metalloproteinase with a thrombospondin-like motif), which facilitates extrusion of the follicular content [29].
• Collectively, these findings suggest that Ang II impairs functional hyperemia by activating AT1 receptors and inducing ROS production via a gp91phox containing NADPH oxidase [30].

Analytical, diagnostic and therapeutic context of Hyperemia

• The single-pass extraction fraction averaged 64.2 +/- 9.7% in control, 65.3 +/- 9.1% in ischemia, 70.0 +/- 4.4% in reperfusion, and 46.5 +/- 7.4% in dipyridamole-induced hyperemia groups [31].
• METHODS AND RESULTS: In 25 patients with postangioplasty restenosis of the left anterior descending artery, ECG-gated digital subtraction coronary angiograms were recorded at baseline and during hyperemia (12 mg papaverine IC) before and after balloon predilatation (PTCA), after implantation of a Palmaz-Schatz stent, and after 6 months [32].
• METHODS AND RESULTS: In 12 open-chest dogs, MCE was performed and myocardial blood flow (MBF) was measured by use of radiolabeled microspheres at baseline and during phenylephrine-induced coronary hyperemia [33].
• METHODS AND RESULTS: Myocardial blood flow (MBF) was quantified with [13N]ammonia and positron emission tomography (PET) at rest, during cold pressor testing (endothelium-dependent vasomotion), and during dipyridamole-induced hyperemia in 16 long-term smokers and 17 nonsmokers [34].
• METHODS AND RESULTS: In 60 patients accepted for percutaneous transluminal coronary angioplasty (PTCA) of single-vessel disease, with a positive exercise test (ET) < 24 hours before PTCA, FFR was determined during adenosine-induced hyperemia just before and 15 minutes after angioplasty [35].

References