Effects of magnetic resonance imaging on polymorphonuclear neutrophil adhesion.

BACKGROUND: Limited research has been performed concerning the effects of MR imaging on the immune system. In this study the influence of MR imaging exposure on polymorphonuclear neutrophil (PMN) adhesion was evaluated. MATERIAL AND METHODS: In vivo and in vitro studies were performed in 10 patients undergoing an MR imaging procedure, PMN adhesion to a plastic surface, as well as the expression of adhesion molecules beta 2-integrins CD11b, CD18, and L-selectin on the surface of PMN were estimated. RESULTS: Exposure to MR imaging significantly increased adhesion of isolated PMNs to plastic surfaces. PMNs from blood samples obtained from patients undergoing MR imaging as well as from blood samples placed beside patients during MR imaging did not differ from controls in adhesion to plastic surfaces. Similarly, plasma from three tested samples did not change control PMN adhesion to plastic surface. Expression of beta 2-integrins (CD11, CD18) was significantly increased in samples left beside patients during MR imaging, while significantly decreased in samples obtained from patients after MR imaging exposure when compared to control samples. Expression of the surface adhesion molecule L-selectin on the surface of PMN decreased significantly in blood samples left beside patients during MR imaging. CONCLUSION: The results indicate that the PMN adhesion properties increase under the influence of MR imaging exposure. This phenomenon may be the result of direct stimulation of polymorphonuclear neutrophils by the exposure to MR imaging.

The effects of dipyridamole stress test on plasma levels of soluble adhesion molecules intracellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin and L-selectin in patients with ischemic heart disease and patients with syndrome X.

BACKGROUND: Adhesion of activated leukocytes to the endothelium as a result of myocardial ischemia/reperfusion has been shown to be involved in the development of tissue injury. Leukocyte adhesion to the endothelium occurs via adhesion molecules expressed on the surface of both cell types. Upon cell activation these proteins may be released into the circulation and measured in a soluble form. AIM: To verify whether the dipyridamole stress test, performed in patients with ischemic heart disease (IHD) and in patients with syndrome X, modifies plasma levels of the soluble adhesion molecules vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), E-selectin and L-selectin. METHODS: Plasma levels of the soluble endothelial adhesion molecules ICAM-1, VCAM-1 and E-selectin, as well as of the soluble leukocyte adhesion molecule L-selectin, were measured in venous blood samples taken before and 7 min after administration of dipyridamole in patients with IHD, patients with syndrome X and healthy individuals. Myocardial perfusion was evaluated using single photon emission tomography. The plasma levels of soluble VCAM-1, ICAM-1, E-selectin and L-selectin were all measured using enzyme-linked immunosorbent assays. RESULTS: After infusion of dipyridamole, plasma levels of ICAM-1 increased significantly in patients with IHD, whereas they remained unchanged in patients with syndrome X and in the control group. In patients with IHD, the initial plasma levels of VCAM-1, E-selectin and L-selectin, before administration of dipyridamole, were higher than those observed in patients with syndrome X and than those in the control group. Plasma levels of soluble VCAM-1, E-selectin and L-selectin decreased significantly in patients with IHD following the dipyridamole stress test, whereas they remained unchanged in patients with syndrome X, and in the control group. CONCLUSION: In patients with IHD, administration of dipyridamole induces myocardial ischemia resulting in modification of plasma levels of the soluble adhesion molecules.

Soluble adhesion molecules in reperfusion during coronary bypass grafting.

OBJECTIVE: Adhesion of activated leukocytes to the endothelial cells as a result of myocardial ischaemia/reperfusion during open chest coronary artery surgery has been shown to be involved in the development of tissue damage. Activated leukocytes adhere to endothelium via adhesion molecules expressed by both cell types, resulting in the impairment of coronary capillary flow. Upon cell activation, adhesion proteins may be released in the soluble form to circulating blood. The purpose of our study was to verify whether myocardial ischaemia/reperfusion occurring during coronary artery bypass grafting results in release of the soluble adhesion molecules VCAM-1, ICAM-1, E-selectin and L-selectin into the circulation. METHODS: Plasma levels of the soluble adhesion molecules were measured in vein, arterial and coronary sinus blood samples taken from 15 patients undergoing coronary artery bypass grafting (CABG). Blood samples for estimations were collected during the procedure: before aorta cross-clamping, at the beginning of reperfusion and 30 min after reperfusion. Soluble adhesion molecules levels were measured by standard ELISA assays. RESULTS: Mean plasma levels of soluble VCAM-1 in arterial samples increased significantly at the beginning of reperfusion and 30 min after reperfusion. In contrast, soluble L-selectin plasma levels in arterial samples remained unchanged. In coronary sinus samples, levels of soluble ICAM-1 significantly increased 30 min after reperfusion. Moreover, in coronary sinus samples collected 30 min after reperfusion, soluble ICAM-1 levels were significantly higher than in arterial samples obtained at the same time. The mean concentration of soluble E-selectin in samples obtained from coronary sinus decreased significantly 30 min after reperfusion. Moreover, plasma levels of soluble E-selectin in coronary sinus samples obtained 30 min after reperfusion were significantly decreased compared with these observed in arterial samples collected at the same time. CONCLUSIONS: The reperfusion of ischaemic myocardium during CABG results in a significant increase in plasma levels of the soluble endothelial adhesion molecules VCAM-1 and ICAM-1 and significant decrease in soluble E-selectin plasma levels. L-selectin plasma levels during CABG procedure remain unchanged. We propose that the increased plasma concentrations of soluble VCAM-1 and ICAM-1 are a result of endothelial cell activation during ischaemia/reperfusion following bypass surgery.

Increased release of the soluble form of the adhesion molecules L-selectin and ICAM-1 but not E-selectin during attacks of angina pectoris.

Myocardial ischemia leads to the activation of neutrophils as well as endothelial cells. The interaction between these cells is dependent on certain adhesion glycoproteins which are expressed on their surface. Adhesion of neutrophils to endothelium, mediated by adhesion molecules, has been shown to result in coronary capillary plugging and impairment of coronary blood flow. In certain conditions, upon cell activation, adhesion proteins may be released in soluble form into the circulating blood. The purpose of our study was to verify whether myocardial ischemia occurring during angina episodes results in the release of the soluble adhesion molecules, L-selectin, E-selectin, and intracellular adhesion molecule-1 (ICAM-1), into the circulation. Plasma samples were collected by venepuncture from 15 patients admitted to the emergency room with chest pain caused by attacks of angina pectoris and 15 patients with noncardiac chest pain. To confirm the diagnosis, all patients underwent an exercise stress test and, if not conclusive, 99mTc MIBI SPECT or coronary arteriography. Another set of plasma samples were taken from each patient in the absence of chest pain. In addition, blood for analysis was obtained from 15 sex-and age-matched healthy subjects. Soluble adhesion molecules plasma levels were measured by standard enzyme-linked immunosorbent assay. In patients with angina pectoris, plasma levels of soluble L-selectin estimated during chest pain were significantly higher than in the control group and decreased in the absence of chest pain. Similarly, the mean concentration of soluble ICAM-1 at the time of angina onset was significantly elevated in the patients in comparison with the control group and remained higher, although not significantly, in the absence of chest pain. In patients with noncardiac chest pain, plasma levels of soluble L-selectin did not differ significantly from those observed in control subjects. In this group of patients, the plasma levels of soluble ICAM-1 estimated during pain onset and in the absence of this symptom were not significantly elevated. On the contrary, the mean values of soluble E-selectin in the patients with ischemic cardiac pain during chest pain and in the absence of this symptom, as well as those in the patients with noncardiac chest pain during or without symptoms, remained unchanged in comparison with the control group. During attacks of angina pectoris an increase in the plasma levels of the soluble adhesion molecules, ICAM-1 and L-selectin, was noted, possibly reflecting activation of neutrophils and endothelial cells during myocardial ischemia. However, E-selectin plasma levels remained unchanged in response to myocardial ischemia.

The influence of electrical cardioversion on superoxide anions (O2-) production by polymorphonuclear neutrophils, hydrogen peroxide (H2O2) plasma level and malondialdehyde serum concentration.

We studied the influence of electrical cardioversion on unstimulated and stimulated superoxide anion production by polymorphonuclear neutrophils in 22 patients with atrial flutter or atrial fibrillation. We also estimated hydrogen peroxide plasma level, as well as malondialdehyde serum concentration, in these subjects. We noted an increase in spontaneous production of superoxide anions from 14.9 +/- 1.8 nmol/10(6) neutrophils per 20 min to 21.37 +/- 2.7 nmol/10(6) neutrophils per 20 min (P = 0.002) in neutrophils obtained after electrical cardioversion. Similarly, stimulated production of O2- also increased after electrical cardioversion (41.8 +/ 3.4 nmol/10(6) neutrophils per 20 min vs. 59.0 +/- 5.9 nmol/10(6) neutrophils per 20 min, P = 0.0027). Moreover, hydrogen peroxide plasma level increased significantly after electrical cardioversion (39.9 +/- 6.2 mumol/l vs. 53.4 +/- 7.6 mol/l, P = 0.003). Serum malondialdehyde concentration also increased after countershock (2.56 +/- 0.26 nmol/ml vs. 2.94 +/- 0.26 nmol/ml, P = 0.023). These results seem to indicate that electrical cardioversion may lead to polymorphonuclear neutrophils activation, increased H2O2 production and lipid peroxidation.

Effects of magnetic resonance imaging on polymorphonuclear neutrophil functions.

RATIONALE AND OBJECTIVES: Limited research has been performed on the effects of magnetic resonance (MR) imaging on the immune system. To our knowledge, there are no reported studies of MR imaging effects on the polymorphonuclear neutrophil (PMN) system. Therefore, we evaluated the influence of MR imaging exposure on PMNs. METHODS: In vivo and in vitro studies were performed on 36 patients undergoing MR imaging. The following were estimated in blood samples: leukocyte and PMN count, PMN phagocytosis and bactericidal capacity, percentage of cells with expression of surface receptor for the Fc fragment of immunoglobulin G (IgG), PMN superoxide, hydrogen peroxide production, and plasma lysozyme activity. Another sample of patients was used to eliminate temperature as an influence on changes in PMN functions. RESULTS: Both in vitro and in vivo MR imaging led to a decrease in PMNs and an increase in PMN phagocytosis, bactericidal capacity, hydrogen peroxide production, and percentage of cells with expression of surface receptor for Fc IgG. Superoxide anion production did not change significantly. Elevated temperature, stress, and anxiety were excluded as influences on our results. CONCLUSION: The PMN system is affected seriously by MR imaging.

Comparison of the influence of stress exercise test and transesophageal cardiac pacing on polymorphonuclear neutrophils functions.

Peripheral polymorphonuclear neutrophils (PMN) number, percent of PMN bearing IgG Fc receptors as well as PMN adherence were evaluated in 29 patients submitted to an exercise test. The peripheral PMN count significantly increased at the maximal work load. The increase in number of neutrophils bearing IgG Fc receptors was also noticed at that point, while PMN adherence to nylon wool columns did not change significantly. Nine subjects were additionally submitted to diagnostic transesophageal atrial pacing with a rate similar to maximal heart rate observed during the exercise test. It was revealed that atrial pacing in these patients had no influence on the peripheral PMN count, PMN adherence as well as number of neutrophils bearing IgG Fc receptors. We conclude, that granulocytosis observed during exercise can not be solely attributed to the increased heart rate and increased cardiac output but other mechanisms like muscle work play a significant role in this process.