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Biomedical subjects

G Lee

Publications and source records attributed to G Lee.

At least 433 records · Page 24Linked to original sources
PubMed1981

Evaluation of platelet kinetics following porcine and mechanical valve replacement.

Because thromboembolic pathogenesis in mechanical prosthetic valves (MP) might involve selective MP platelet consumption with consequent reduced platelet survival, it has been suggested that lowered platelet half-life (T 1/2) detection provides identification of postoperative thrombotic risk. Porcine heterografts (PH) possess less thromboembolic hazards than MP; thus, comparative evaluation of PH versus MP platelet T 1/2 is germane to the test's thrombotic predictive value, yet platelet kinetics in PH require elucidation. Accordingly, 51chromium platelet T 1/2 was determined in 16 patients with substituted valves (10 PH and 6 MP). Average platelet T 1/2 in PH (2.9 +/- 0.6 d) was similar (p greater than 0.05) to MP (3.2 +/- 0.6 d), and both were considerably lower (p less than 0.05) than platelet T 1/2 in normal subjects (NL, 5.1 +/- 0.5 d). Furthermore, platelet T 1/2 was below the lowest NL platelet T 1/2 (4.0 d) in seven PH and three MP patients. Thus, frequency and extent of decreased platelet survival in PH are common and equal to MP. These results indicate that platelet half-life does not afford thromboembolic predictability in patients with mechanical valves and, instead, favors prosthetic-induced physical trauma causing abnormal platelet survival.

Adult↗
PubMed1981

Ambulatory prazosin treatment of chronic congestive heart failure: development of late tolerance reversible by higher dosage and interrupted substitution therapy.

To evaluate whether long-term administration of the oral vasodilator, prazosin, in the ambulatory therapy of chronic refractory congestive heart failure (CHF) results in gradual attentuation of its marked salutary peripheral circulatory relaxing actions, 16 coronary heart failure patients receiving chronic prazosin, 16 mg daily, were assessed for the development of vasodilator tolerance for 12 months. In six of these patients such tolerance was documented after 7 months which was readily surmountable, thereby allowing continuation of effective chronic prazosin therapy. Each of the six tolerance patients underwent four forearm plethysmography studies: prior to chronic prazosin (study I; 4.0 mg study dose), after 7 months prazosin (study II; 4.0 mg), repeated following 1 additional week on higher effective prazosin dose of 32 mg daily (study III; 8.4 mg), and following 2 weeks of prazosin withdrawal (study IV; 4.0 mg). The prazosin study dose increased forearm blood flow, decreased forearm vascular resistance and venous tone in studies I, III, and IV; these variables were unchanged by prazosin in study II. Despite vasodilator tolerance to the initial daily dosage at 7 months (study II), symptomatic effectiveness and improved cardiac performance were sustained throughout the entire 12 months of chronic prazosin therapy by increasing dosage (study III) and brief interruption of the vasodilator (study IV) (NYHA class IV pre-prazosin symptoms improved to class 2.7 at 3 months, class 2.4 at 6 months, and class 2.5 at 12 months chronic prazosin). This study showed that prazosin vasodilator tolerance occurred in approximately one third of CHF patients after several months of chronic prazosin therapy. More importantly, however, the present investigation demonstrated that chronic prazosin symptomatic efficacy can be maintained in such CHF patients by overcoming tolerance with higher effective prazosin dosage or brief prazosin discontinuation.

Administration, Oral↗
PubMed1981

Effects of diltiazem-induced calcium blockade upon exercise capacity in effort angina due to chronic coronary artery disease.

Few data are available regarding the effects of calcium blockade upon exercise tolerance in patients with stable effort angina due to coronary artery disease (CAD). Therefore we compared the effects of the calcium blocking agent, diltiazem (D), to placebo (P) in 12 patients with chronic effort angina and catheterization documented fixed CAD. The 8-week total protocol consisted of a 1-week baseline period followed by the double-blind randomized crossover alternate 1-week administration of P and D in doses of 120, 180, and 240 mg. Maximal exercise tests (MET) were performed at the end of each 1-week period, while rest radionuclide ventriculography (RVG) was obtained during 240 mg D and corresponding crossover P. Resting heart rate decreased from baseline and initial P at D doses of 60 and 240 mg, but not from P during crossover period. No changes were observed at any dose of D either at rest or during MET in systolic blood pressure or rate . pressure double product. D at 240 mg, but not lower doses, increased MET duration (437 vs 490 seconds, p less than 0.01) and time to angina (383 vs 441 seconds, p less than 0.01). Ejection fraction by RVG was greater with D than P (0.54 vs 0.50, p less than 0.05). Thus these data indicate that calcium blockade with diltiazem provides antianginal efficacy by reducing myocardial oxygen demand, and increases exercise tolerance without depression of myocardial performance in effort angina patients with fixed chronic CAD.

Aged↗
PubMed1981

Experimental reversal of acute coronary thrombotic occlusion and myocardial injury in animals utilizing streptokinase.

Fresh autologous thrombus, 1.0 to 1.5 ml, was injected into the left anterior descending and/or left diagonal coronary arteries of 19 open-chest dogs to produce evolving acute myocardial infarction (AMI). Thrombotic obstruction was documented by coronary angiography. Multilead epicardial ECGs showed ST segment elevations of affected left ventricular (LV) areas within 2 minutes after thrombus injection, and LV segmental wall cyanosis with hypocontraction was observed within 10 minutes in the myocardial areas supplied by the thrombosed artery. Ten animals then received an initial dose of streptokinase (STK), 250,000 U (intravenous), followed by STK, 1000 to 3000 U/min (intracoronary), while nine control dogs untreated with STK received normal saline infusion. All but one STK-treated animal (all nine animals receiving intracoronary STK) had reestablishment of blood flow in the previously occluded vessels within 1 1/2 hours, disappearance of ventricular cyanosis, return of normal LV contractile function, and normalization of elevated ST segments within 1 hour after intracoronary STK therapy. In contrast, in the non-STK-treated control group, all animals had continued coronary obstruction, progressive ST elevations, and worsening LV cyanosis and hypocontraction until death or for more than 3 hours post thrombus; three control animals died of ventricular fibrillation (VF) within 1 hour of thrombus occlusion, three more died of VF within 2 hours post thrombus, and only three survived beyond 2 hours post thrombus. Postmortem examination of non-STK-treated animals revealed extensive residual coronary thrombus. All intracoronary STK-treated animals evidenced absence of residual coronary thrombus at postmortem examination. These data provide clinically relevant evidence that early intracoronary STK effects thrombolysis in AMI by reopening coronary vessels occluded by fresh thrombus, thereby protecting myocardium from further ischemia and necrosis, preserving LV function, and also reversing cardiac muscle injury.

Animals↗
PubMed1981

Efficacy of percutaneous transluminal coronary recanalization utilizing streptokinase thrombolysis in patients with acute myocardial infarction.

Since coronary thrombosis is a principal factor in the evolving necrotic process in the majority of patients with acute myocardial infarction (AMI), a prospective study was conducted in 25 AMI patients who underwent expeditious coronary arteriography. Of these patients, 22 with totally occluding thrombus also received early streptokinase (STK) administration. STK was given by intracoronary (20 patients) or systemic (two patients) infusion, 2000 to 50,000 IU/min, to a total dose of 125,000 to 500,000 IU within 10 hours of AMI symptom onset. Eighteen patients had angiographically visualized successful coronary thrombolysis; the shorter the interval between onset of symptoms to treatment, the more rapid was the clot dissolution. Successful thrombolysis occurred concomitantly with readily managed reperfusion ventricular tachyarrhythmias in nearly all patients. In addition, STK recanalization resulted in relief of ongoing chest pain in 10 of 12 patients, 10 of 16 evidenced immediate normalization of hyperacute ST segment abnormalities, and 8 of 14 demonstrated subsequent improvement of angiographically visualized left ventricular (LV) ejection fraction. In the percutaneous transluminal coronary recanalization (PTCR) procedure, the step of using a soft-tipped guide wire itself was transiently useful in only one of seven patients in whom this was attempted; reocclusion took place without added STK therapy. Nitroglycerin (NTG) alone produced only slight distal patency in but 1 of 19 patients with coronary occlusion given the nitrate. Importantly, in 14 control AMI patients receiving conventional treatment without STK, 10 showed angiographically complete occlusion of the coronary artery supplying the infarct region 1 month after infarction, thereby excluding spontaneous clot lysis mimicking STK-PTCR-induced reperfusion. These data support the concept that coronary occlusion by thrombosis is inherently involved with AMI and that rapid PTCR application of intracoronary STK provides potent thrombolysis, superior to that provided by NTG and guide wire passage in reestablishing coronary flow with attendant salvage of jeopardized myocardium and with subsequently improved LV function.

Adult↗
PubMed1981

Monoclonal rat antibodies to murine IgM determinants.

A series of 6 hybrid clones are described which produced antibodies directed to murine IgM. These were derived by immunizing rats with W279 B-lymphoma cells and then fusing the immune spleen cells to enzyme-deficient murine plasmacytoma cell lines. Immunoenzymatic techniques were used to select clones producing desirable antibodies to cell surface or soluble antigens. Antibodies from 3 of the clones (293.14, 414.18 and 307.5) preferentially bound to idiotypic determinants of W279 immunoglobulin whereas the remaining 3 clones made antibodies which bound to various myeloma and normal cell surface IgM molecules. One IgM-specific clone (287.2) produced antibody of relatively low avidity. The two other clones (81.20 and 331.12) which secreted anti-mu antibodies appeared to be directed to determinants which differed in glutaraldehyde lability and expression in F(ab')2 preparations.

Animals↗
PubMed1981

Hemodynamic effects of morphine and nalbuphine in acute myocardial infarction.

Hemodynamic effects of morphine and the new narcotic analgesic, nalbuphine, were compared in a randomized, double-blind study in 15 patients with acute myocardial infarction (11 men and four women, average age 56.2 yr) and normal group mean hemodynamic function. During a 1-hr evaluation the hemodynamic effects were small but there were changes in several parameters. Morphine reduced heart rate (78 to 72 bpm, p less than 0.01) and diastolic and mean arterial pressures (69 to 64 mm Hg, p less than 0.05; and 91 to 84 mm Hg, p less than 0.05); nalbuphine was associated with a decrease in heart rate (82 to 72 bpm, p less than 0.01), decrease in cardiac index, which remained within the normal range (3.16 to 2.75 l/min/m(2), p less than 0.01), and an increase in systemic vascular resistance (1,204 to 1,461 dynes . sec . cm(-5), p less than 0.05). Neither drug altered systolic arterial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, stroke index, stroke work index, or pulmonary vascular resistance. Echocardiographic assessment revealed diminution of left ventricular mean velocity of circumferential fiber shortening after nalbuphine (1.26 to 1.08 circ/sec, p less than 0.05). Both drugs induced small reductions in respiratory rate and arterial pH and increases in PAO2. There were no changes in PaO2. Because of the absence of clinically important deleterious effects on cardiac pump function, nalbuphine merits further investigation as an analgesic in acute myocardial infarction.

Adult↗
PubMed1981

Aortic input impedance in man: acute response to vasodilator drugs.

In 18 patients who underwent coronary arteriography, aortic velocity and pressure data were obtained during a control state and during either isoproterenol infusion at 1, 2 and 3 micrograms/min or graded nitroprusside infusion (average peak dose 60 micrograms/min). Impedance moduli and phase angles were derived to 10 Hz for controls states, isoproterenol at 2 micrograms/min, and at peak nitroprusside effect. Averaged control data included a mean resistance of 1460 dyn-sec-cm-5 and a characteristic impedance of 88 dyn-sec-cm-5 The characteristic impedance did not correlate with age (r = 0.21), coronary artery disease score (r = 0.17) or mean aortic pressure (r = -0.01). In 11 patients, isoproterenol induced a 38% reduction in mean resistance and a 10% reduction in mean aortic pressure. There was slight reduction in characteristic impedance and phase angles became less negative, to 2 Hz. In seven patients, nitroprusside induced a 38% reduction in mean resistance and a 22% reduction in mean aortic pressure. Impedance moduli decreased to 1.8 Hz and phase angles became less negative, to 3 Hz. Based on the different cardiovascular actions of these two drugs, the data suggest that vasodilators do not induce significant changes in the aortic impedance spectrum when not associated with a decrease in mean aortic pressure.

Adult↗
PubMed1981

Cellular interactions affecting the maturation of murine B lymphocyte precursors in vitro.

Clonable B cells arose in liquid cultures of slg+ cell-depleted bone marrow suspensions, and a majority of these derived from rapidly sedimenting (presumably large) precursors. Such immature (pre-B) cells were not demonstrable in adult lymph nodes. The development of functional B cells in vitro depended on adherent cells present in adult bone marrow or peritoneal exudates and in the presence of optimal numbers of these accessory cells; not FCS or 2-ME or LPS were essential for B cell maturation. In contrast, the ability of fetal liver cell suspensions to generate B cells in culture was not affected by the removal of adherent cells or addition of macrophages, and LPS consistently reduced numbers of colony-forming B cells recovered. A type of nonadherent cell present in the bone marrow of adult CBA/N mice dramatically enhanced B cell maturation in normal CBA/H-T6T6 fetal liver cell cultures. These results indicate that 2 types of accessory cells may augment transition of pre-B cells to functional B cells in culture. One is adherent and can be replaced by macrophages, whereas the other is nonadherent and is present in limiting numbers in embryos. When fetal liver cultures were incubated with optimal numbers of adult accessory cells, the rate of emergence of B cells was dependent on the gestational age of the donor embryo. This suggests that B cell formation in utero may be limited by the availability of B cell precursors as well as nonadherent accessory cells. The possibility exists that fetal pre-B cells typify intermediates in the B lineage which are infrequent in adult marrow. Alternatively, B cells may be produced in adult life through processes that do not precisely recapitulate embryonic events.

Animals↗