Biomedical subjects
Publications and source records attributed to L Wiener.
A parent education booklet describing Pneumocystis carinii pneumonia (PCP) was prepared by the Pediatric Branch of the National Cancer Institute. In addition to information about prophylaxis and treatment of PCP, the booklet discusses overall care of children infected with human immunodeficiency virus.
14C-labelled proteins from E. coli 30S ribosomal subunits were isolated by HPLC, and selected groups of these proteins were reconstituted with 32P-labelled 16S RNA. The isolated reconstituted particles were partially digested with ribonuclease A, and the RNA fragments protected by the proteins were separated by gel electrophoresis and subjected to sequence analysis. Protein S7 alone gave no protected fragments, but S7 together with S14 and S19 protected an RNA region comprising the sequences 936-965, 972-1030, 1208-1262 and 1285-1379 of the 16S RNA. Addition of increasing amounts of protein S9 to the S7/S14/S19 particle resulted in a parallel increase in the protection of the hairpin loop between bases 1262 and 1285. The results are discussed in terms of the three-dimensional folding of 16S RNA in the 30S subunit.
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The plasma levels of thromboxane B2 (TxB2) were determined by radioimmunoassay in 6 consecutive patients with Prinzmetal's angina and in 9 healthy volunteers. In the normal group TxB2 was not detectable (= 0.5 pmoles/ml), while in patients with variant angina TxB2 was consistently detected (1.5-140 pmole/ml).
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The influence of the Valsalva maneuver (VM) on myocardial ischemia was evaluated in 24 patients with coronary heart disease. Clinical and hemodynamic responses to the VM were studied during acute ischemia manifested by angina pectoris with transient left ventricular (LV) dysfunction and compared with responses during nonischemic intervals. In the absence of evidence for acute ischemia (angina and increased LV end-diastolic pressure), six patients had abnormal hemodynamic responses to the VM. Five had lack of systolic pressure overshoot and in one, systolic pressure did not decline during straining. When the VM was performed during an ischemic episode, 14 patients had abnormal responses (12 with lack of overshoot in phase IV and two with lack of systolic pressure decline in phase II). In 18 patients a prompt decline in LV end-diastolic pressure occurred with the disappearance of angina during the VM. These changes uniformly occurred during the latter part of straining (VM phase II) as cardiac size and systolic pressure declined. No adverse effects occurred when a VM was performed during acute ischemia. Our observations suggest that the VM abruptly reduces determinants of cardiac oxygen demand, relieving acute ischemia without harmful effects.
Experiments were conducted in anesthetized open-chest dogs subjected to occlusion of the left anterior descending coronary artery for three hours. The oxygenation of myocardial tissue was monitored by a polarographic technique capable of recording simultaneously the oxygen tension (Po2) of myocardial tissue and electrograms. Ischemic injury was monitored by means of ST-segment elevations on myocardial and epicardial electrograms. The volume of the myocardial infarct was measured at the end of each experiment by incubation of transverse slices of left ventricle in a solution of nitroblue tetrazolium and by separation of the unstained (ischemic) from the stained (normal) portions. In one group of dogs, hemodilution was performed after 15 minutes of ischemia by exchanging blood with a stroma-free hemoglobin solution (from a hematocrit reading of 45 +/- 3 percent to 23 +/- 2 percent). Changes occurring in this group were compared with those occurring in dogs that did not undergo hemodilution, underwent hemodilution with dextran 75, or were transfused with whole blood. Hemodilution with hemoglobin reduced aortic and left ventricular filling pressures while increasing coronary blood flow, increased myocardial Po2 from 2 +/- 2 mm Hg to 8 +/- 2 mm Hg (P less than 0.005), lowered the ST-segment elevation of both myocardial and epicardial electrograms, and reduced the volume of the myocardial infarct. These effects were unmatched by hemodilution with dextran or infusion of whole blood.
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The operative mortality rate of aortocoronary bypass surgery in 23 patients with poor left ventricular function (ejection fraction 0.30 or less) operated on in 1973-74 was 34.7 percent. The incidence rate of operative myocardial infarction was 30.4 percent. In an attempt to improve survival, intraaortic balloon counterpulsation was used therafter in 25 similar patients. Counterpulsation was instituted preoperatively and continued intra- and postoperatively for 2 to 5 days. Preoperative studies revealed an "unloading" effect of the left ventricle, with significant reductions of systolic arterial blood pressure, end-diastolic pulmonary arterial pressure and end-diastolic left ventricular volume and pressure. Metabolic improvement was demonstrated by the lesser production of myocardial lactate after pacing-induced tachycardia when the ventricle was balloon-assisted. Intraoperatively, blood flow through the vein graft was found to increase with counterpulsation. The rate of operative myocardial infarction was reduced to 4 percent and the mortality rate to 8 percent. In patients who have sustained a significant loss of functioning myocardium, the beneficial hemodynamic and metabolic effects of intraaortic balloon counterpulsation appear to prevent furhter, possibly critical, myocardial damage in the perioperative period.
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A polarographic technique capable of simultaneous monitoring of myocardial tissue oxygen tension (MPO2) and intramyocardial electrograms by way of the same electrodes has been developed. Initially, the method was evaluated in dogs to verify the appropriateness of the directional changes of MPO2 in function of selected determinants of myocardial oxygen supply (regional coronary blood flow, arterial blood oxygen tension) and demand (heart rate, force of ventricular contraction). A combined reduction of MPO2 and elevation of the S-T segment in the corresponding electrograms was observed only when a 50 percent or greater reduction of blood flow to the sampled area was effected. Subsequently, in nine patients undergoing aortocoronary bypass surgery, MPO2 was measured from 48 areas for 2 weeks postoperatively. In 11 normal and 31 revascularized areas, MPO2 increased during the postoperative period. In four areas subsequently found to be supplied by occluded grafts MPO2 decreased from 12.7 +/- 3.1 (mean +/- standard error) to 10.1 +/- 3.3 mm Hg (P less than 0.05). In two areas, MPO2 decreased during the 3rd postoperative day from 16 to 3 and from 14 to 4.2 mm Hg, respectively. This reduction was attended by a significant rise in the S-T segment of the corresponding electrograms. This finding preceded by 24 hours standard electrocardiographic evidence of myocardial infarction. This technique appears to be sensitive and reliable, and thereby capable of enhancing the management of patients during the high risk early postoperative period after coronary bypass surgery.
A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome;16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block. Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.
A possible protective effect of glucocorticoids on the ischemic myocardium was investigated in in situ dog hearts subjected to regional ischemia and in isolated rat hearts subjected to global ischemia. In the whole-animal preparation, the left anterior descending coronary artery (LAD) was occluded for 3 hours, or for 2 1/2 hours followed by 30 minutes of reperfusion. Dexamethasone phosphate was randomly administered (20 mg. per kilogram intravenously) after 15 minutes of ischemia. Its effects were studied on the following: (1) myocardial cell membrane integrity, using electron microscopic examination of tissue biopsies treated with colloidal lanthanum; (2) myocardial water content, measuring the wet/dry weight of myocardial tissue; (3) ischemic injury, by a count of fuchsinophilic cells at light microscopy. In isolated rat hearts, ischemia was produced by a 60 per cent reduction of coronary flow. Randomized hearts were perfused for 2 hours with dexamethasone, 15 mg. per milliliter in buffered salt solution. Study included determination of tissue water content and coronary vascular resistance. Lanthanum was confined to the extracellular spaces in normal dog myocardium, but it was found all intracellularly after 3 hours of ischemia or after reperfusion. This was associated with morphologic changes characteristic of irreversible cell injury. In the hearts treated with dexamethasone, lanthanum remained excluded from the cells, water content was less (p less than 0.005), and fuchsinophilia less severe (p less than 0.005). Likewise, water content was less (p less than 0.005) and the increase in coronary vascular resistance resulting from ischemia less severe (p less than 0.005) in the dexamethasone-treated isolated rat hearts. Thus dexamethasone administered in pharmacologic doses, early, appeared to stabilize the cell membrane, limit myocardial edema, and reduce the severity of injury, both during ischemia and upon reperfusion.
Comparative hemodynamic effects of placebo and 10 mg of oral isosorbide dinitrate were studied in patients with significant coronary artery disease (larger than or equal to 75 per cent lumen narrowing) proved angiographically. Isosorbide dinitrate or placebo was given to eight and 10 patients, respectively, in a double-blind fashion. Cardiac performance at rest and during supine leg exercise was evaluated before and 60 minutes after drug administration. In the resting state, isosorbide dinitrate compared to placebo significantly reduced the left ventricualr (systolic and diastolic), mean pulmonary artery and mean aortic pressures, cardiac index, stroke index, left ventricular work index, stroke work index, and mean systolic ejection rate. Isosorbide dinitrate also significantly reduced left ventricular (systolic and diastolic and mean pulmonary artery pressures during exercise. This study indicates that 10 mg of isosorbide dinitrate has a significant influence on ischemic left ventricular dysfunction 60 minutes after its oral administration.
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