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Biomedical subjects

G Lee

Publications and source records attributed to G Lee.

At least 487 records · Page 27Linked to original sources
PubMed1978

Structural basis for the changing physical properties of human pulmonary vessels with age.

Circumferential strips of pulmonary vessel wall were obtained at necropsy from the major arterial and venous branches at the lung hilum in patients aged 7-87 years. The extensibility of these strips was measured using the tension balance method of Harris et al. (British Heart Journal, 1965, 27, 651-659). The vessels were then bisected, and half of each strip was submitted for structural analysis using morphometric methods on paraffin sections stained to show the collagen, elastin, and muscle content. The other halves of the formalin-fixed vessel strips were examined chemically to determine their collagen content by estimation of the total hydroxyproline content. The thickness of the vessel media was measured microscopically on all of the sections examined. Quantitative measurements were made on 42 arteries and 37 veins. Contrary to expectation, there was a steady fall in medial collagen content with increasing age in arteries and veins. The decrease in collagen content was similar in the morphometric and chemical studies and was statistically significant. The thickness of the vessel media did not change significantly with age. The pulmonary artery and vein strips were less extensible in the older age groups, the main change occurring in the elastic phase of the vascular stress/strain curves. It is suggested that changes in the elastic tissue at a molecular and lamellar level are responsible for the increasing stiffness of pulmonary vessels rather than changes in the medial collagen content.

Adolescent↗
PubMed1978

Hemodynamic evaluation in acute myocardial infarction.

Bedside right heart catheterization in patients with acute myocardial infarction and hemodynamic dysfunction provides a rational basis for therapy aimed at maximizing cardiac performance and limiting infarct size. Readily performed and associated with minimal risk, this diagnostic approach is primarily indicated when myocardial infarction is associated with evidence of hemodynamic dysfunction. It affords precise information on cardiac performance and prognosis, allows identification of specific complications such as ventricular septal defect and acute mitral regurgitation, and is of critical importance in selection of therapy. Hemodynamic monitoring is also essential for safe, effective application of certain forms of treatment such as vasodilator therapy for the failing ventricle.

Acute Disease↗
PubMed1978

Alterations in ventricular mass and performance induced by exercise training in man evaluated by echocardiography.

Few data are available regarding the effects of exercise training upon cardiac structure and performance in man. We evaluated the echograms of 24 normals before (PRE) and after (POST) 11 weeks of endurance exercise training. Conditioning consisted of a walk-jog-run protocol at 70% maximal heart rate for one hour four days per week. Training reduced heart rate and increased maximal duration and estimated oxygen consumption of treadmill exercise. Compared to PRE, the echogram in the POST training period revealed an increased left ventricular (LV) end-diastolic dimension (EdD), a decreased end-systolic dimension (EsD) and thus an increased stroke volume (EdD3-EsD3) and shortening fraction (EdD-EsD)/EdD). Cardiac output (CO) and peripheral vascular resistance (BP/CO X 80) were identical PRE and POST conditioning. Importantly, an increase in mean fiber shortening velocity was observed POST training as were increases in LV wall thickness, ECG voltage of S in V1 + R in V5, and LV mass. Thus endurance training was accompanied by increases in both LV dimension and mass as well as LV shortening fraction and contraction velocity as observed by echocardiogram.

Adult↗
PubMed1978

Relationships of the structure and function of the interferon receptor to hormone receptors and establishment of the antiviral state.

This report describes similarities between the structure and function of the interferon receptor and receptors for glycoprotein hormones and several bacterial toxins. Specifically, it describes several common molecular and mechanistic elements, including: (a) the presence of a glycoprotein as well as a ganglioside component in the receptor; (b) changes in membrane structure as a consequence of interferon action; (c) interferon-induced intracellular cyclic adenosine 3':5'-monophosphate changes; and (d) alterations in the flux of certain ions across the membrane. Since interferon has an antiviral effect, these results define a relationship between hormonal perturbation of cellular events and the ability of an agent to prevent or suppress viral infections of cells. Further definition of these relationships should be important to our understanding of the oncogenic state, of hormonal effects on the oncogenic state, and of other human diseases in which hormonal perturbations of non-target tissues or cross-reactivity of receptors could be pathogenic.

Binding Sites↗
PubMed1978

Effects of acute ethanol on the contractile state of normal and failing cat papillary muscles.

The direct effects of 100, 300 and 500 mg/100 ml ethanol on contractility of isolated, supported right ventricular papillary muscles were evaluated from 10 normal or failing cat hearts. In isometrically contracting muscles, 500 mg% ethanol decreased maximum tension in normal and failing hearts from 7.1 to 4.3 g/mm2 (P less than 0.001) and 3.4 to 2.3 (P less than 0.01) respectively, and lowered maximum tension rise from 30.4 to 20.2 g/mm2/sec (P less than 0.001) and 10.2 to 0.8 (P less than 0.01), without alterations of time to peak tension. In isotonically contracting muscles, 500 mg% ethanol reduced contractile element velocity at 0.5 g/mm2 load in normal and failing ventricles from 1.27 to 0.97 L/sec (P less than 0.001) and 0.59 to 0.39 (P less than 0.001) respectively. Thus, clinically meaningful doses of ethanol clearly, exerted dose-related negative inotropic actions on both normal and failing myocardium, thereby indicating that ethanol ingestion may exacerbate heart failure in diseased hearts.

Animals↗