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Biomedical subjects

C Smithen

Publications and source records attributed to C Smithen.

18 recordsLinked to original sources
PubMed1976

Aspirin therapy in angina pectoris: effects on platelet aggregation, exercise tolerance, and electrocardiographic manifestations of ischemia.

If altered platelet function contributes to poorly perfused zones of myocardium in patients with angina pectoris, then specific antiplatelet therapy might improve cardiovascular function and exercise performance. Exercise tolerance on a bicycle ergometer, heart rate-blood pressure product, and ischemic ECG changes at exercise end-point were compared before and during oral aspirin therapy (2.4 Gm. per day for 2 weeks) in 11 normal subjecs and in 11 patients with stable angina pectoris. Platelet aggregation threshold in response to ADP and epinephrine was measured. Untreated patients had increased platelet aggregability when compared to normal subjects...

Adult↗
PubMed1975

Variant angina pectoris.

A patient with variant angina pectoris due to a pedunculated calcific mass extending from the aortic valve and resulting in intermittent obstruction of the left coronary ostia is reported. No atherosclerotic disease was demonstrated by coronary angiography. During attacks, marked ST segment elevation and episodes of tachycardia were associated with a moderate rise in pulmonary artery pressure. Replacement of the calcified aortic valve resulted in total relief of symptomatology.

Angina Pectoris↗
PubMed1975

Noninvasive assessment of clinical response to oral propranolol therapy.

Nineteen patients with severe but stable angina pectoris entered a double blind controlled study to evaluate the effect of orally administered propranolol on exercise tolerance measured with a bicycle ergometer, and left ventricular function measured by echocardiography and systolic time intervals. In the group treated with propranolol the dose was increased from 80 to 320 mg/day. Studies including determination of propranolol blood levels were obtained before treatment and for each dose of propranolol. With propranolol, 80 mg/day, total work performance increased by 128 percent from 765 plus or minus 125 before treatment to 1,792 plus or minus 285 kilopond-meters (mean plus or minus standard error) (P less than 0.01). With 160 mg of propranolol daily, total work performance decreased, but remained higher than at control levels. In the group given propranolol, left ventricular function decreased progressively with increasing doses of the drug. As measured from the echocardiogram, maximal endocardial posterior wall velocity decreased 42 percent, from 72 plus or minus 7 to to 41 plus or minus 4 mm/sec (P less than 0.02); ejection fraction decreased 13 percent, from 0.68 plus or minus 0.01 to 0.59 plus or minus 0.01; and end-diastolic bolume increased 28 percent, from 79 plus or minus 11 to 102 plus or minus 9 ml/m2 (P less than 0.05). The preejection period and the ratio between preejection period and left ventricular ejection time significantly increased with progessive dose increments. There was no correlation between blood level of propranolol and improved work performance. Exercise tolerance was maximally improved with doses of 80 to 160 mg/day. At higher dose levels left ventricular function deteriorated and exercise work decreased. Noninvasive assessment of left ventricular function proved more valuable than determination of drug blood levels in managing patients with angina pectoris and provided a guide to optimal adjustment of dosage.

Adult↗
PubMed1975

Metabolic and hemodynamic consequences of mannitol following myocardial anoxia.

The mechanism of action of hyperosmolal mannitol was evaluated by hemodynamic and metabolic studies in 79 isovolumic nonrecirculating paced perfused rat hearts during sequential 15-min periods of aerobic, anoxic, and reoxygenated perfusion. Hyperosmolality induced by addition of mannitol significantly decreased myocardial water content (wet/dry wt ratio). It improved recovery of hemodynamic function during reoxygenation. With isomolal perfusion (290 mosmol/kg) left ventricular systolic peak pressure (LVSP) decreased 32% (127 +/- 5 to 86 +/- 6 mmHg) and maximum dP/dt fell 50% (3,513 +/- 328 to 1,758 +/- 172 mmHg/s) during the postanoxic recovery period. With hyperosmolal perfusion (350 mosmol/kg), LVSP decreased 23% (132 +/- 5 to 102 +/- 7 mmHg) and dP/dt fell 21% (3,817 +/- 215 to 2,998 +/- 234 mmHg/s) (P less than .01). Hyperosmolal perfusion did not affect postanoxic total coronary flow, lactate and glucose metabolism, tissue glycogen, creatine phsophate, or adenine nucleotide concentrations. Coronary perfusion with hypersmolal solution aided recovery, enhanced postanoxic myocardial performance, and minimized tissue swelling. The most tenable explanation for the locus of action of hyperosmolal mannitol during anoxia under our experimental conditions is its direct effect on myocardial water content.

Adenosine Triphosphate↗
PubMed1975

Effects of mannitol on cardiac ultrastructure and microcirculation following anoxia.

Electron microscopic and microcirculatory effects of hyperosmolal mannitol were evaluated in the isolated perfused isovolumic rat heart. Specimens for ultrastructural examination were obtained in 26 experiemnts after 15 min of sequential aerobic, anoxic, and reoxygenated perfusion using an isosmolal perfusate of Krebs-Ringer-Henseleit bicarbonate buffer (KRB) (osmolality equals 290 mosmol/kg) vs. a hyperosmolal solution of KRB + mannitol (equals 350 mosmol/kg). No significant changes were noted during aerobic perfusion. Anoxic hearts perfused with isosmolal KRB demonstrated the most severe ultrastructural alterations including: mitochondrial swelling with disruption of cristae, myofibrillar fusion and contraction bands, and subsarcolemmal edema and vacuolization. These subcellular changes were not only partially reversed by oxygenated isosmolal perfusion but were significantly reversed during both the anoxic and reoxygenation perfusion periods with mannitol added. Following silicone rubber injection of the microcirculation, only focal capillary endothelial cell swelling was noted, and no difference in arteriolar or capillary filling was observed with either perfusate. Thus, mannitol significantly reversed the postanoxic ultrastructural changes consistently observed in the absence of increased osmolality. No gross effect on vascular patency could be demonstrated.

Animals↗
PubMed1975

Protective role of increased myocardial glycogen stores induced by propranolol.

Glycogen is an essential substrate during myocardial anoxia. Since porpranolol may maintain myocardial glycogen levels after acute stress by blockade of catecholamine-induced glycogenolysis, we evaluated the effect of propranolol treatment in the isolated perfused isovolumic paced rat heart. Forty-one rats were studied after 10 min of ice-water immersion: half were pretreated with propranolol, 20 mg/kg/day x3, and half with saline. Glycogen content of unperfused propranolol-treated hearts exceeded controls by 46% (146 +/- 9 vs. 100 +/- 4 mumoles/g dry wt, p less than 0.02), and this difference persisted during aerobic perfusion. Propranolol did not affect adenine nucleotide concentration or left ventricular hemodynamics. Following 5 min of anoxic perfusion, propranolol hearts showed improved ventricular performance concomitant with enhanced glycogenolytic flux and lactate production. Propranolol augmented high energy phosphate production (ATP/AMP = 5.19 +/- 0.42 vs. 3.39 +/- 0.42, p less than 0.02) and increased coronary flow (22.1 +/- 1.6 vs. 16.6 +/- 1.4 ml/min, p less than 0.02) during anoxia. Thus, propranolol supported glycogen stores following acute stresses, enhanced glycogenolytic energy production, increased coronary flow, and improved ventricular function during subsequent anoxia.

Animals↗
PubMed1975

Hemodynamic, metabolic, and ultrastructural consequences of hyperosmolal mannitol after myocardial anoxia.

Recovery from anoxia has been evaluated in the isovolumic nonrecirculating paced perfused rat heart. Seventy studies were performed consisting of 1) 15 min of aerobic perfusion (AP), 2) AP + 15 min of anoxic perfusion, 3) AP + 15 min of anoxic perfusion + 15 min of reoxygenation. Krebs-Ringer-bicarbonate + 5 mM glucose (KRB) was compared with KRB + mannitol (osmolality, +60 mOsm). Mannitol decreased myocardial water content. It improved recovery of hemodynamic function after reoxygenation. With KRB alone left ventricular systolic peak pressure (LVSp) decreased by 32 percent and maximum dP/dt by 50 percent. With mannitol added LVSp decreased 18 percent and dP/dt 21 percent (p less than 0.01). No effect on energy metabolism was demonstrated. KRB and mannitol did not differentially affect total coronary flow, lactate, and glucose extraction, tissue glycogen, creatine phosphate, or adenine nucleotide concentrations. No significant difference in capillary filling was demonstrated by microfil injection. Mannitol appears to improve LV function by direct myocardial osmotic action unrelated to enhanced energy production.

Adenosine Diphosphate↗
PubMed1972

Venous graft surgery in treatment of coronary heart disease.

Sixty-seven patients have had aortocoronary venous graft bypass surgery by one surgeon for the relief of symptoms of severe coronary heart disease, including eight emergency operations. The overall operative, hospital, and late mortality was low in patients with favourable myocardial function and no previous myocardial infarction. There was a 7% mortality in patients with a normal preoperative chest radiogram, 8% mortality when the left ventricular end-diastolic pressure was normal preoperatively, and a 5% mortality in patients who had normal left ventricular angiograms. The overall mortality in all elective operations for cardiac pain resistant to medical treatment was 15.8%. 89% of survivors improved; 67% are pain-free. Exercise tolerance in survivors is increased by 135%, atrial pacing results are improved by 10%. Left ventricular end-diastolic pressure is unchanged. Left ventricular function on angiography is improved. The improvement in left ventricular function assessed objectively correlates positively with vein-graft patency, as does freedom from angina pectoris.

Adult↗