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Biomedical subjects

M Feola

Publications and source records attributed to M Feola.

At least 55 records · Page 3Linked to original sources
PubMed1977

The terminal pathway of the lymphatic system of the human heart.

Aantomical dissections in 9 human cadavers revealed the terminal pathway of the lymphatic system of the left ventricle to be constituted mainly by channels emptying into the right angulus venosus (junction of the internal jugular and subclavian veins) at the base of the right side of the neck. This observation has clinical implications because it has been shown that a sampling of cardiac lymph provides the best method for analyzing myocardial metabolic abnormalities and that drainage of cardiac lymph alleviates the myocardial changes produced by ischemic injury.

Adult↗
PubMed1977

Early prostaglandin release from the ischemic myocardium in the dog.

Cellular consequences of myocardial ischemia were studied in anesthetized dogs. Confirmation of myocardial ischemia was provided by electrocardiographic and biochemical indexes. Prostaglandin F2alpha release into coronary venous blood was significantly elevated during myocardial ischemia, whereas indomethacin treatment prevented this increase in coronary venous prostaglandin F2alpha concentrations. No significant increase in prostaglandin E2 release was observed in response to myocardial ischemia, but indomethacin treatment significantly reduced coronary venous prostaglandin E2 concentrations below those of control values. Within one hour after occlusion of the coronary artery, the S-T segment was significantly altered, and coronary venous prostaglandin F2alpha had increased significantly above the control concentration. These changes persisted during four hours of myocardial ischemia. Plasma creatine phosphokinase activity increased significantly after two hours of myocardial ischemia and remained elevated for the subsequent two hours of ischemia. After four hours of myocardial ischemia, myocardial creatine phosphokinase activity of ischemic myocardium was significantly reduced, and labilization of myocardial treatment prevented increases in prostaglandin release but did not influence other biochemical changes or the electrocardiographic response to ischemia. Thus, prostaglandin release by ischemic myocardial tissue is an early response to the ischemic stimulus.

Animals↗
PubMed1976

Monitoring tissue oxygenation of the heart after myocardial revascularization.

A polarographic technique capable of simultaneous monitoring of myocardial tissue oxygen tension (MPO2) and intramyocardial electrograms by way of the same electrodes has been developed. Initially, the method was evaluated in dogs to verify the appropriateness of the directional changes of MPO2 in function of selected determinants of myocardial oxygen supply (regional coronary blood flow, arterial blood oxygen tension) and demand (heart rate, force of ventricular contraction). A combined reduction of MPO2 and elevation of the S-T segment in the corresponding electrograms was observed only when a 50 percent or greater reduction of blood flow to the sampled area was effected. Subsequently, in nine patients undergoing aortocoronary bypass surgery, MPO2 was measured from 48 areas for 2 weeks postoperatively. In 11 normal and 31 revascularized areas, MPO2 increased during the postoperative period. In four areas subsequently found to be supplied by occluded grafts MPO2 decreased from 12.7 +/- 3.1 (mean +/- standard error) to 10.1 +/- 3.3 mm Hg (P less than 0.05). In two areas, MPO2 decreased during the 3rd postoperative day from 16 to 3 and from 14 to 4.2 mm Hg, respectively. This reduction was attended by a significant rise in the S-T segment of the corresponding electrograms. This finding preceded by 24 hours standard electrocardiographic evidence of myocardial infarction. This technique appears to be sensitive and reliable, and thereby capable of enhancing the management of patients during the high risk early postoperative period after coronary bypass surgery.

Animals↗
PubMed1976

Glucocorticoid protection of the myocardial cell membrane and the reduction of edema in experimental acute myocardial ischemia.

A possible protective effect of glucocorticoids on the ischemic myocardium was investigated in in situ dog hearts subjected to regional ischemia and in isolated rat hearts subjected to global ischemia. In the whole-animal preparation, the left anterior descending coronary artery (LAD) was occluded for 3 hours, or for 2 1/2 hours followed by 30 minutes of reperfusion. Dexamethasone phosphate was randomly administered (20 mg. per kilogram intravenously) after 15 minutes of ischemia. Its effects were studied on the following: (1) myocardial cell membrane integrity, using electron microscopic examination of tissue biopsies treated with colloidal lanthanum; (2) myocardial water content, measuring the wet/dry weight of myocardial tissue; (3) ischemic injury, by a count of fuchsinophilic cells at light microscopy. In isolated rat hearts, ischemia was produced by a 60 per cent reduction of coronary flow. Randomized hearts were perfused for 2 hours with dexamethasone, 15 mg. per milliliter in buffered salt solution. Study included determination of tissue water content and coronary vascular resistance. Lanthanum was confined to the extracellular spaces in normal dog myocardium, but it was found all intracellularly after 3 hours of ischemia or after reperfusion. This was associated with morphologic changes characteristic of irreversible cell injury. In the hearts treated with dexamethasone, lanthanum remained excluded from the cells, water content was less (p less than 0.005), and fuchsinophilia less severe (p less than 0.005). Likewise, water content was less (p less than 0.005) and the increase in coronary vascular resistance resulting from ischemia less severe (p less than 0.005) in the dexamethasone-treated isolated rat hearts. Thus dexamethasone administered in pharmacologic doses, early, appeared to stabilize the cell membrane, limit myocardial edema, and reduce the severity of injury, both during ischemia and upon reperfusion.

Acute Disease↗
PubMed1975

Cardiac lymph flow and composition in acute myocardial ischemia in dogs.

Cardiac lymph was obtained from 12 normal dogs (group 1) for two consecutive 2-h control periods and from 7 dogs (group 2) for 2 h before and 2 h after occlusion of the circumflex branch of the left coronary artery. Lymph composition was studied with reference to pH, red blood cell (RBC) concentration, total protein content, potassium and sodium ion concentrations, and creatine phosphokinase (CPK) and acid phosphatase enzyme activities. No significant difference was noted in any variable between the two groups during the firts 2-h period. In group 1, no significant changes occurred in any variable as a result of the passage of time alone. In group 2, 2 h of myocardial ischemia produced increases of 53.3 plus or minus 5.1% in lymph flow, 67 plus or minus 5% in protein content, and 418 plus or minus 27% in the RBC concentration, suggesting increased blood capillary permeability. Lactate rose 120.5 plus or minus 27%, potassium concentration increased 16.9 plus or minus 2.4%, acid phosphatase increased 30 plus or minus 3%, and CPK rose 61.6 pluse or minus 10.9%, suggesting ischemic injury of myocardial cells. These changes in lymph were statistically significant (P LESS THAN 0.05) and reflect both capillary and myocardial cell abnormalities.

Animals↗
PubMedDate not supplied

A novel hemoglobin-adenosine-glutathione based blood substitute: evaluation of its effects on human blood ex vivo.

Chemically modified hemoglobin (Hb) solutions are under current investigation as potential red cell substitutes. Researchers at Texas Tech University have developed a novel free Hb based blood substitute product. This blood substitute is composed of purified bovine Hb cross-linked intramolecularly with o-adenosine-5'-triphosphate and intermolecularly with o-adenosine, and conjugated with reduced glutathione (GSH). In this study, we compared the effects of our novel blood substitute and unmodified (U) Hb, by using allogenic plasma as the control, on human blood components: red blood cells (RBCs), platelets, monocytes (Mo), and low-density lipoproteins (LDLs). The pro-oxidant potential of both Hb solutions on RBCs was examined by the measurement of osmotic and mechanical fragility, conjugated dienes (CD), lipid hydroperoxides (LOOH), thiobarbituric acid reactants (TBAR-S), isoprostanes (8-iso PGF2alpha) and intracellular GSH. The oxidative modification of LDLs was assessed by CD, LOOH, and TBAR-S, and the degree of apolipoprotein (apo) B cross-linking. The effects of Hb on platelets have been studied by monitoring their responses to the aggregation agonists: collagen, ADP, epinephrine, and arachidonic acid. Monocytes were cultured with Hb solutions or plasma and tested for TNF-alpha and IL-1beta release, then examined by electron microscopy. Results indicate that native UHb initiates oxidative stress of many blood components and aggravates inflammatory responses of Mo. It also caused an increase in RBC osmotic and mechanical fragility (p < 0.001). While the level of GSH was slightly changed, the lipid peroxidation of RBC increased (p < 0.001). UHb was found to be a stimulator of 8-iso PGF2alpha synthesis, a potent modulator of LDLs, and an effective potentiator of agonist induced platelet aggregation. Contrarily, our novel blood substitute did not seem to induce oxidative stress nor to increase Mo inflammatory reactions. The osmotic and mechanical fragility of RBCs was similar to that of the control. Such modified Hb failed to alter LDLs, increase the production of 8-iso PGF2alpha, but markedly inhibited platelet aggregation. The effect of this novel blood substitute can be linked with the cytoprotective and anti-inflammatory properties of adenosine, which is used as a cross-linker and surface modifier, and a modification procedure that lowers the hemoglobin pro-oxidant potential.

Adenosine↗
PubMedDate not supplied

An improved blood substitute. In vivo evaluation of its hemodynamic effects.

The purpose of the present study was to assess the ability of an improved free hemoglobin based blood substitute to serve as a resuscitative fluid in the treatment of hemorrhagic shock. Comparison studies were performed by using blood autotransfusion as a positive control. The hemodynamic parameters studied included cardiac index, mean arterial pressure, pulse pressure, heart rate, stroke volume index, and total peripheral resistance. Tissue oxygenation was measured in the biceps femori muscle by polarography. Hemorrhagic shock (at 40% of the total blood volume) in anesthetized rats caused severe disturbances in hemodynamic parameters and tissue oxygenation. Shock was characterized by a 66% drop in cardiac index, a 67% drop in mean arterial pressure with a significant increase in total peripheral resistance, and a 78% reduction in tissue oxygenation, all lasting 30 min. Resuscitation from shock with the blood substitute was effective in restoring hemodynamic parameters, producing vasodilation, and improving tissue oxygenation. Autotransfusion with blood also restored hemodynamics. However, lower tissue oxygenation and lack of vasodilation were noted. Therefore, the modified hemoglobin solution yielded better results than blood in the resuscitation of rats after hemorrhagic shock. The vasodilatory activity and the reduction of vasoconstriction that followed hemorrhage can be primarily linked with adenosine, which possesses vasodilatory and anti-inflammatory properties, and is used in our technology as an intermolecular cross linking reagent and hemoglobin surface modifier.

Animals↗