PubMed Health⌕ Search

Biomedical subjects

T J Tsagaris

Publications and source records attributed to T J Tsagaris.

11 recordsLinked to original sources
PubMed1979

Comparative effect of counterpulsation and bypass on left ventricular myocardial oxygen consumption and dynamics before and after coronary occlusion.

In this preparation counterpulsation effect was found equivalent to 42 +/- 7% of complete left ventricular bypass before, and 46 +/- 9% post-coronary occlusion. We conclude that counterpulsation is effective mainly by reducing a major determinant of myocardial oxygen consumption, i.e., afterload, whereas left ventricular bypass by reducing primarily preload results in secondary afterload reduction when peripheral resistance is unchanged. At the higher left ventricular bypass levels, reduction of myocardial oxygen consumption is far greater than during balloon counterpulsation. Acute functional loss of myocardium does not alter the effect of these assist methods regarding the reduction of myocardial oxygen consumption. Whether selection of either method for clinical application should be made only on the basis of its capability for reduction of myocardial oxygen consumption remains to be justified by conclusive demonstration of beneficial effect of reduction of myocardial oxygen consumption in the specific circulatory disorders.

Animals↗
PubMed1979

Rest and exercise hemodynamic studies in patients with isolated aortic stenosis.

Hemodynamic data obtained during rest and exercise in 22 patients with aortic stenosis were analyzed. Mean aortic valve gradient for the group did not change significantly during exercise but there was large individual variability. Aortic valve flow increased during exercise in all but 2 patients. There was no correlation between change in gradient and change in flow during exercise. Although the mean calculated aortic valve area for the group did not change significantly during exercise, the calculated area was larger during exercise in most patients. Change in the calculated valve area correlated best with changes in aortic valve flow, left ventricular stroke work index, and the product of left ventricular systolic pressure and stroke volume. This suggests that in some patients there may be a dynamic component to aortic valve obstruction that may vary with changing hemodynamics.

Adult↗
PubMed1978

Effect of activation sequence on MVO2 before and after coronary ligation.

In pentobarbital-anesthetized, open-chest dogs with fixed heart rate, cardiac output, and systemic arterial pressure, ectopic ventricular activation originating from apical as compared to basilar regions of either ventricle was associated with small (3--5%) but significantly (P less than 0.005) lower myocardial O2 consumption (MVO2) and thus higher left ventricular (LV) efficiency without change in LV end-diastolic pressure (LVEDP), work index (LVWI), and LV dP/dt. Data obtained during epicardial and corresponding endocardial activation did not differ. During normal ventricular activation, MVO2 remained unchanged but LVEDP was significantly (P less than 0.005) lower, thus yielding higher LVWI and efficiency. MVO2 differences among ectopic sites were abolished after coronary artery occlusion, whereas data obtained during endocardial and epicardial on normal and ectopic activation were not affected. Thus, normal activation resulting in lower LVEDP is most efficient; apical ventricular activation is less efficient at the same MVO2P basilar is the least efficient, because both MVO2 and LVEDP are higher. Ventricular activation sequence changes do not constitute a substantial determinant of MVO2.

Animals↗
PubMed1978

A comparison of hemodynamic and angiographic indices of left ventricular performance in patients with coronary artery disease.

We compared ejection fraction, left ventricular end-diastolic pressure, cardiac index and the relation of left ventricular stroke work index to left ventricular end-diastolic pressure during rest and exercise in 60 patients with coronary artery disease. Left ventricular end-diastolic pressure was usually normal at rest (48/60) and abnormal during exercise (46/60) and did not correlate with ejection fraction. Cardiac index was insensitive, usually remaining normal until ejection fraction was less than 0.40. Patients with a normal left ventricular stroke work index response to exercise had higher ejection fractions than those with an abnormal response (p is less than 0.05). However, 9 patients with normal ejection fractions had an abnormal exercise response. This may reflect loss of left ventricular reserve, abnormal compliance or clinically silent ischemia during exercise. Different indices of left ventricular performance may be widely disparate in coronary artery disease, and abnormalities are frequently apparent only during exercise.

Adult↗
PubMed1978

Intermittent severe mitral regurgitation.

The findings in two patients with hemodynamic evidence of intermittent severe mitral regurgitation with cyclic variation in right and left ventricular pressures are presented. Both patients had aortic and mitral valvular regurgitation of unknown etiology without definite evidence of papillary muscle dysfunction. The basis for the variation in the degree of mitral regurgitation is unclear.

Aortic Valve Insufficiency↗
PubMed1976

Degradation of prostaglandin E2 and F2alpha by the canine liver.

Degradation of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha) by the liver was determined in 16 dogs. PGE2 (8 dogs) or PGF2 alpha (8 dogs) was infused into the left ventricle at rates of 3.75, 7.5, 15, 37.5, and 75 mug/min. Blood samples obtained simultaneously from the portal vein (PV), hepatic vein (HV), and abdominal inferior vena cava (IVC) at each infusion rate were tested for PGE or PGF concentration by radioimmunoassy. During PGE2 infusion the mean PGE concentrations in the PV were 0.60, 1.05, 1.40, 2.29, 4.80, and 7.29 ng/ml at each infusion rate, Corresponding concentrations in the HV were 0.51, 0.62, 0.71, 0.96, 1.94, and 2.62 ng/ml, and in the IVC 0.51, 0.95, 1.31, 1.96, 4.31, AND 5;18 NG/ML. During PGF2 alpha infusion, the mean PGF concentrations in the PV were 0.32, 0.59, 0.73, 1.73, 4.11, and 7.11 ng/ml at the respective infusion rates; Corresponding concentrations in the HV were 0.26, 0.24, 0.33, 0.48, 0.49, and 0.96 ng/ml, and in the IVC 0.32, 0.50, 0.61, 1.10, 2.40, and 4.17 ng/ml. Thus, these data indicate that the canine liver has substantial, but not unlimited, capacity for degradation of PGE2 and PGF2 alpha in the portal circulation. Whether or not PGE or PGF levels in the PV may exceed this capacity during periods of stress or whether this enzymatic mechanism may be suppressed by either physiological or pharmacological factors is not known.

Animals↗
PubMed1975

Endotoxin-induced prostaglandin E and F release in dogs.

Prostaglandin E and F (PGE and PGF) levels in sequential blood samples obtained simultaneously from the renal and portal veins and aorta during endotoxin shock in dogs were determined by radioimmunoassay. Four groups of dogs were studied. In five control dogs in which no endotoxin was given, PGE and PGF levels did not change significantly at 0, 15, 30, 60, and 90 min. In eight dogs given endotoxin alone, PGE and PGF levels did not change in the aorta. In samples taken from the portal vein there was a significant rise in PGE and PGF 15 min after endotoxin, whereas renal vein PGE and PGF did not become significantly elevated until 60 and 90 min after endotoxin. In six dogs pretreated with acetylsalicylic acid and six dogs pretreated with indomethacin, PGE and PGF levels did not change after endotoxin. Indomethacin modified the delayed hemodynamic effects of endotoxin whereas acetylsalicylic acid did not. Neither drug blocked the immediate hemodynamic effects of endotoxin. Endotoxin-induced PGE and PGF release is probably due to increased synthesis. The mechanism whereby synthesis is stimulated and the extent to which vasomotor tone is influenced by PGE and PGF during endotoxin shock cannot be determined from our data.

Animals↗
PubMed1975

Prostaglandin F and E levels during endotoxin-induced pulmonary hypertension in calves.

Prostaglandin F and E (PGF and PGE) concentrations in sequential blood samples obtained simultaneously from the pulmonary artery (PA) and pulmonary vein (PV) during endotoxin-induced pulmonary hypertension in calves were determined by radioimmunoassay. Three groups of calves were studied. In nine control calves in which no endotoxin was given PA pressure and PGF and PGE concentrations in four pairs of samples taken at 0, 5, 15, and 45 min did not change. In 17 calves given 1 mg E. coli endotoxin, PGF concentrations were increased significantly in the PV and to a lesser degree in the PA in the 15-and 45-min samples. The increased PGF concentration in the 15-min sample corresponded to an increased PA pressure of 74 plus or minus 4 mmHg (mean plus or minus SE). In three of the endotoxin-treated calves studied a second time and three separate calves indomethacin pretreatment completely blocked the hemodynamic effect of endotoxin as well as PGF release. PGE concentrations did not change in either group. These data suggest that endotoxin-induced pulmonary hypertension may be mediated by PGF, a known pulmonary pressor agent in the bovine, and that blockade of this effect by indomethacin may be due to inhibition of prostaglandin synthesis and/or release.

Animals↗