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Biomedical subjects

R M Effros

Publications and source records attributed to R M Effros.

85 records · Page 5Linked to original sources
PubMed1976

Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition.

Myocardial cell pH was measured with 5, 5 dimethyl-2, 4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular and water indicators were made into the left anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady state distribution of DMO between cells and plasma was calculated from the mean transit times of the indicator. Normal myocardial cell pH averaged 6.94 and changed by 58% of the concomitant alterations in plasma pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a balloon tip catheter in the left anterior descending coronary artery resulted in progressive decreases in cell pH to 6.59 by 1 hour. Infusions of sodium carbonate diminished intracellular acidosis. Hemodynamic studies during 4 hours of ischemia with blood pH at 7.55 to 7.60 indicated a significantly reduced left ventricular end-diastolic pressure and increased stroke volume by comparison with findings in animals given infusions of saline solution. Ventriculograms revealed improved wall motion in the ischemic segment after infusion of alkali. Precordial mapping showed a significant reduction in the number of leads with S-T segment elevation as well as in the sum of S-T segment elevations, but R wave amplitudes did not differ from those in control studies. Calculations of extracellular space, tissue water and cation content revealed a reduced gain of cell sodium ion and loss of cell potassium ion during ischemia after alkali treatment. The latter may account for the S-T segment responses, whereas enhanced ventricular performance may be related to reduced competition of hydrogen ion with calcium ion for binding sites on contractile protein.

Acidosis↗
PubMed1975

In vivo myocardial cell pH in the dog. Response to ischemia and infusion of alkali.

Myocardial cell pH has been measured with 5,5-dimethyl-2,4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular, and water indicators were made into the anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady-state distribution of DMO between cells and plasma was calculated from the indicator mean transit times, and the plasma pH. Myocardial cell pH was determined from the distribution value and plasma pH. Normal myocardial cell pH averaged 6.94. Changes in myocardial cell pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a coronary artery balloon resulted in progressive decreases in cellular pH to average values of 6.83 within the initial 15 min and to 6.59 within the interval between 20 and 70 min. Infusions of Na2CO3 tended to diminish intracellular acidosis although these infusions had little effect on the difference in pH between the myocardial cell and extracellular fluid.

Acid-Base Equilibrium↗
PubMed1974

Osmotic extraction of hypotonic fluid from the lungs.

After injections of sucrose, NaCl, and urea solutions, the flow of tissue fluid from the lungs amounted to 0.182, 0.216, and 0.152 x 10(-3) ml/s per mosmol/kg of concentration difference between plasma and tissues in each gram of wet tissue weight. The extracted fluid contained less than 20% of the Na(+), K(+) and urea concentrations of the plasma. It was concluded that this fluid was distinctly hypotonic in comparision with the fluids of the plasma and tissue compartments both before and after the injection of hypertonic solutions. The presence of low solute concentrations in the extracted fluid is attributed to the passage of this fluid across cellular membranes, which are relatively impermeable to small hydrophilic solutes. Movement of fluid out of the junctions appears to be less than that through the endothelial cells. It is suggested that the injected solutes rapidly leak into the junctions and consequently induce relatively little movement of water or tissue solutes out of the junctions. Concentrations of tritiated water and [(14)C]antipyrine in the extracted fluid are essentially the same as base-line plasma concentrations when the animals have been primed with these tracers. It is therefore likely that these tracers can readily traverse cellular membranes. Red cell transit through the lungs is impaired by hypertonic solutions of sucrose and NaCl with transient increases in pulmonary arterial hemoglobin concentrations of as much as 35% of base-line values.

Animals↗
PubMed1969

The in vivo pH of the extravascular space of the lung.

The partition of 5,5-dimethyloxazolidine-2,4-dione (DMO) and of 11 amines between the vascular and extravascular spaces of the lung has been determined by the multiple indicator dilution technique. Four amines (nicotine, pentylamine, quinine, and benzylamine) were found to have pH-sensitive tissue to blood concentration ratios. Of these, tritiated nicotine appears to be the nost satisfactory indicator of tissue pH and values for the pH of the pulmonary extravascular space (pH(e)) have been calculated from the nicotine data. At an arterial pH (pH(art)) between 7.38 and 7.43 pH(e) averaged 6.69 +/-0.07. Changes in pH(e) usually paralleled but were consistently less than concomitant changes in pH(art). Alterations in P(CO2) at constant pH(art) regularly produced relatively small, parallel changes in extravascular hydrogen ion concentrations. Local alterations in tissue pH due to P(CO2) changes are apparently buffered quite rapidly and the pH(e) of the lung seems more closely linked to pH(art) than the cellular pH of other tissues.DMO, guanidine, methylamine, morphine, and atropine were confined to the vascular volume during the first circulation and could not be used to measure tissue pH. Histamine appeared to be bound to a pH-insensitive site. The extravascular distributions of antipyrine and aniline were unresponsive to alterations in arterial pH, presumably because they are essentially uncharged at pH levels found in the lung.

Amines↗