Search PubMed⌕ Search

Biomedical subjects

M Lesch

Publications and source records attributed to M Lesch.

At least 109 records · Page 6Linked to original sources
PubMed1977

Administration of nitrous oxide in normal subjects. Evaluation of systems of gas delivery for their clinical use and hemodynamic effects.

Nitrous oxide (concentrations of 30 to 50%) was administered to 22 healthy volunteer subjects via nasal prongs, rebreathing mask, and an airlines mask to assess the efficiency of systems of delivery and the hemodynamic effects. The end-expired concentration of nitrous oxide, expressed as a percentage of the inspired concentration of nitrous oxide, was 19% for nasal prongs, 34% for the rebreathing mask, and 95% for the airlines mask (most accurate delivery). The pulse rate fell from a mean of 79+/-3 beats per minute to 67+/-2 with nasal prongs, to 64+/-2 with the rebreathing mask, and to 64+/-2 with the airlines mask. Both systolic and diastolic pressures fell from means of 122+/-4 and 74+/-2 mm Hg, respectively, to 98+/-3 mm Hg and 64+/-2 mm Hg, respectively, with the airlines apparatus. The fall in systolic blood pressure (slope, -0.79) exceeded that in the diastolic (slope, -0.35). In additional eight normal subjects, administration of 30% nitrous oxide via airlines mask produced identical changes in blood pressure and pulse rate, but there was no effect from 30 minutes of administration of 30% nitrous oxide on the end-systolic volume index, cardiac index, ejection fraction, normalized wall velocity determined echocardiographically, ejection time, or the ratio of preejection period to ejection time.

Adult↗
PubMed1976

Reflex increase in coronary vascular resistance in patients with ischemic heart disease.

To assess possible coronary vasoconstriction in patients with ischemic heart disease, we measured coronary vascular resistance in 12 patients with normal hearts and 12 with coronary disease before and during the initial 50 seconds of cold pressor test, a stimulus known to produce systemic vasoconstriction. Control coronary vascular resistance was similar in the two groups, and although it did not change in patients with normal vessels, it rose by 27 per cent (P less than 0.005) in the group with coronary disease during the cold pressor test. In three of 12 patients with coronary disease coronary flow actually declined despite an increase in arterial pressure; in four, angina was precipitated. Phentolamine abolished increases in arterial pressure and coronary vascular resistance during the test in three patients with coronary disease. Adrenergically mediated coronary vascular tone may be an important determinant of coronary blood flow and may contribute to ischemia in patients with coronary disease.

Adrenergic alpha-Antagonists↗
PubMed1976

Inotropic agents and infarct size. Theoretical and practical considerations.

Recent data demonstrating the ability of interventions that alter the balance between myocardial oxygen demand and supply to affect infarct size are reviewed. The effects of inotropic agents on the determinants of myocardial oxygen consumption and coronary blood flow are discussed relative to the potential of these drugs to decrease or increase infarct size in the experimental animal and in man. The applicability of the animal data to the clinical situation is discussed and, on the basis of these considerations, guidelines are presented for the use of inotropic agents in patients with acute myocardial infarction.

Acute Disease↗
PubMed1976

Correlation of acute myocardial infarct scintigraphy with postmortem studies.

Acute myocardial infarct scintigraphy with technetium-99m-pyrophosphate was performed in a patient with an acute massive transmural infarct. The patient died 12 hours later, and postmortem tracer studies demonstrated a tracer concentration ratio of 13:1 between acutely infarcted myocardium and normal myocardium remote from the infarct. The concentration of tracer in tissue bordering on the infarct but without histologic evidence of acute infarction was 1.5 times that in normal tissue remote from the infarct. In vitro scintigraphy of the excised heart revealed a pattern of tracer distribution similar to that of scintiscans obtained before death. The biologic distribution of 99mTc-pyrophosphate, with large tracer concentrations only within the acutely infarcted tissue, suggests that acute myocardial infarct scintigraphy can be used to estimate the extent of an acute myocardial infarct.

Acute Disease↗
PubMed1976

Evaluation of radiopharmaceuticals for the detection of acute myocardial infarction in man.

The accuracy of the scintigraphic diagnosis of acute myocardial infarction with 99mTc-pyrophosphate, 99mTc-tetracycline and 99mTc-glucoheptonate was assessed in 63 patients, 43 of whom had clinical evidence of acute myocardial infarction. In 15, studies with both 99mTc-tetracycline and 99mTc-pyrophosphate were performed. Accuracy was greatest with 99mTc-pyrophosphate (17/17 true positives, 8/10 true negatives) contrasted with 99mTc-tetracycline (12/25 true positives, 6/11 true negatives) and 99mTc-glucoheptonate (3/13 true positives, 2/2 true negatives). 99mTc-pyrophosphate was the most sensitive tracer for the detection of acute myocardial infarction. The diagnostic accuracy with 99mTc-glucoheptonate was poor.

Acute Disease↗
PubMed1976

Mechanism of the inhibition of myocardial protein synthesis during oxygen deprivation.

Inhibition of protein synthesis during anoxia in the isolated rabbit right ventricular papillary muscle preparation is totally reversible for up to 2 h if glucose concentration is increased during anoxia. The degree of inhibition of protein synthesis during anoxia is, however, not altered by the presence of increased glucose. Thus inhibition of myocardial protein synthesis induced by anoxia need not be related to irreversible disruption of cellular integrity but may represent metabolic regulation of the synthesis. Tissue content of ATP, ADP, AMP, CP, and lactate and phenylalanine incorporation into protein were measured in individual papillary muscles incubated with varying degrees of O2 deprivation and varying substrates and metabolic inhibitors to determine if the inhibition during anoxia could be ascribed to alterations in tissue high-energy phosphate, adenine nucleotide levels, or rate of metabolic flux through the glycolytic and/or Krebs cycle. Protein synthesis was inhibited in muscles incubated in 15 mM glucose during anoxia despite the fact that in the presence of increased glucose, tissue levels of ATP, ADP, and AMP were equal to that of controls. Protein synthesis was normal in muscles made sufficiently hypoxic so that ATP and CP were significantly decreased and lactate increased. Inhibition of Krebs cycle activity with pentenoate failed to effect the rate of protein synthesis. We conclude that anoxic inhibition of myocardial protein synthesis is due neither to high-energy phosphate depletion nor inhibition of Krebs cycle acitivity. The possibility remains that the inhibition may be related to accumulation of glycolytic intermediates or by-products other than lactate.

Adenosine Diphosphate↗
PubMed1976

Alterations of myocardial amino acid metabolism in chronic ischemic heart disease.

Arteriovenous differences (A-V) of all naturally occurring amino acids, lactate, and oxygen were measured simultaneously with coronary sinus blood flow (CSBF) in 8 normal subjects and 11 patients with coronary artery disease at rest and during pacing stress. Mean values for CSBF and myocardial oxygen consumptions (MVO2) for the two groups were similar at rest and during pacing, although mean CSBF and MVO2 increased significantly in both groups in the paced as compared to the rest state. Alanine (ala) was the only amino acid released by the myocardium, while only glutamic acid(glu) demonstrated uptake. Mean A-V ala was negative at rest in the control and coronary disease groups (-4.8+/-3.8 vs. -22.0+/-3.0 nmol/ml, respectively), but was significantly more negative in the coronary group (P less than 0.001) and not statistically different than zero in the normals. A-V ala became significantly negative with pacing in the normals (-10.0+/-4.3 nmol/ml), remained unchanged in the coronary group (-23.0+/-2.9 nmol/ml), and was significantly more negative in the coronary group (P less than 0.05). Calculation of data on the basis of net ala flux ([A-V] X [CSBF X hematocrit]) yielded similar results as that obtained with A-V differences. A-V glu was significantly positive in normals (27.7 +/- 8.9 nmol/ml, P less than 0.01) and coronary patients (59.9 +/- 8.9 nmol/ml, P less than 0.01) at rest but significantly greater in the latter group (P less than 0.001). With pacing, A-V glu remained significantly greater than zero in coronary patients (35.3 +/- 6.3 nmol/ml) and decreased to zero in the normals (4.3 +/- 11.8 nmol/ml). Calculation of net glu flux (nmol/min) at rest yielded data similar to that based on A-V difference. With pacing, net glu flux in the coronary patients did not decrease due to the augmentation of CSBF. No relation between A-V glu or ala and CSBF, MVO2 or A-V lactate was noted. The data demonstrate that specific alterations of myocardial amino acid metabolism characterize patients with chronic ischemic heart disease.

Adult↗
PubMed1976

The scintigraphic demonstration of acute myocardial infarcts.

The feasibility of acute infarct scintigraphy for the clinical evaluation of patients with known or suspected acute myocardial infarction is established. Further development of this methodologic approach may result in even better agents for the visualization of infarcts. Radiotracers with high affinity for the infarct, rapid blood clearance, and low concentrations in surrounding organs, such as liver and bone, would be more suitable than available radiopharmaceuticals for acute myocardial infarct scintigraphy. Ultimately, labeling these tracers and ultra-short-lived radionuclides will enable rapid sequential imaging to assess changes in the extent of infarction and to determine the efficacy of therapies aimed at limiting infarct size.

Acute Disease↗
PubMed1975

Natural history of S-T segment elevation after acute myocardial infarction.

Clinical, electrocardiographic and cineventriculographic data in two patient groups were analyzed to define the natural history of S-T segment elevation after myocardial infarction. In sixteen of 22 patients (73 percent) with acute inferior myocardial infarction, S-T segment elevation was present on hospital admission, persisting in 1 (5 percent) by the 2nd week. S-T segment elevation was present on admission in 18 of 23 patients (78 per cent) with acute anterior myocardial infarction and persisted in 13 after 1 week and in 9 of 14 (64 percent) during a follow-up period of 1 to 6 months. S-T segment elevation lasting more than 2 weeks after myocardial infarction did not resolve. Compared with patients with inferior myocardial infarction or anterior infarction without persistent S-T segment elevation, patients with anterior infarction and persistent S-T segment elevation had a higher level of mean maximal serum creatine phosphokinase (CPK), more severe left ventricular decompensation and a greater frequency of death in the early follow-up period. In a separate series of 95 patients with cineangiographically documented coronary artery disease, 40 of 65 patients (62 percent) with advanced anterior and apical asynergy had persistent S-T segment elevation. By contrast, only 1 of 30 (3 percent) with coronary disease and normal ventriculograms had persistent S-T segment elevation. We concluded that (1) the natural history of S-T segment elevation after myocardial infarction is resolution within 2 weeks in 95 percent of inferior but in only 40 percent of anterior infarctions; (2) S-T segment elevation persisting more than 2 weeks after myocardial infarction does not resolve; (3) persistent S-T segment elevation is associated with clinically more severe myocardial infarction; and (4) in patients with coronary artery disease, persistent S-T segment elevation after myocardial infarction is a specific but insensitive index of advanced asynergy.

Creatine Kinase↗