Biomedical subjects
Publications and source records attributed to D T Mason.
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The effects of acute exposure of rat heart mitochondria to ethanol (87, 65, and 45 mM) and acetaldehyde (3, 1, and 0.3 mM) were studied using both glutamate and pyruvate/malate substrates. Mitochondria assayed with pyruvate/malate substrate showed no apparent effects of acute exposure to or 30 min preincubation with ethanol at the three concentrations tested. With glutamate substrate, acute ethanol at 87 and 65 mM produced significant decreases in respiratory control ratio (RCR). With 65 and 45 mM acute ethanol, mitochondrial oxygen consumption (QO2) was significantly decreased. Acute acetaldehyde significantly decreased RCR and QO2 of mitochondria tested with both substrates. The depressive effect was more pronounced with pyruvate/malate substrate than with glutamate substrate. With pyruvate/malate substrate, the ADP/O ratio was also decreased with 3 and 1 mM acetaldehyde. Preincubation with acetaldehyde had no effect on mitochondrial function except for significantly decreased RCR after preincubation with 3 mM acetaldehyde followed by assay with glutamate substrate. The data indicate a depressant effect of acetaldehyde and ethanol on cardiac mitochondria that may contribute to abnormal cardiac biochemistry and function characteristic of alcoholic cardiomyopathy.
The vasodilators produce disparate modifications of cardiac function depending on the differing alterations of preload versus impedance: nitrates principally cause venodilation; nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation; while hydralazine predominantly effects arterial dilation. Combined nitroprusside and dopamine or dobutamine synergistically enhance low cardiac output and decrease raised left ventricular end-diastolic pressure. Ambulatory oral vasodilator therapy is provided by long-acting nitrates, hydralazine and prazosin alone, combined nitrate-hydralazine and combined prazosin-hydralazine. It is truly remarkable how quickly systemic vasodilators have become established as an important new medical advance in acute and chronic congestive heart failure treatment. In the future, as more experience is gained with the vasodilators and as newer such agents become available, the systemic vasodilators likely will be utilized as often as digitalis in the standard treatment of congestive heart failure.
Although glutaraldehyde-preserved porcine aortic Hancock heterografts have lower thromboembolism incidence than mechanical aortic valves, Hancock xenografts provide less functional aortic outflow orifices and thereby greater transvalvular gradients than mechanical prostheses. The newly developed aortic Carpentier-Edwards porcine heterografts comprise a thin-walled Elgiloy flexible metal stent covered with Teflon which provides somewhat wider internal orifices than aortic Hancock valves of the same external annulus diameter. Since aortic Carpentier-Edwards xenografts have not been clinically evaluated previously, the present study assessed cardiac function and heterograft performance (1.7 months postoperation) and clinical status (4.2 months postoperation) of 19 patients with severe aortic stenosis and/or regurgitation prior to surgery. Left ventricular end-diastolic pressures decreased (17 to 9 mm Hg), cardiac index remained normal, and clinical symptomatology diminished markedly. Mean peak transxenograft systolic pressure was only 16 mm Hg (valve area 1.73 cm2), without meaningful regurgitation. Thus aortic Carpentier-Edwards bioprostheses provide generally excellent heterograft function which appears more favorable than previous reports of Hancock xenografts.
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To evaluate the relationship between myocardial infarction and angina pectoris, history of symptomatic coronary heart disease was analyzed in 146 patients who had had documented myocardial infarction. There were 126 males and 70 females of mean age 55 years (range 32 to 70 years). Infarction had occurred 6 to 63 months prior to the study (mean: 30 months). Angina pectoris occurred at some time during the clinical course of 75 patients (51%), and 71 patients (49%) had not experienced angina. In the majority of the group with angina (n = 39; 52%) the symptom had not been present before infarction, appearing initially thereafter. Angina was present both before and after infarction in 31 patients (41%). In only 5 patients (7%) was precedent angina lost after infarction. Angina was, therefore, present in 70 of 146 patients (48%) after, compared to 36 patients (25%) before, infarction and in 86% (31/36) of patients with angina before infarction it persisted following the attack. Prior angina following myocardial infarction was not related to increased activity since in the majority of patients activity level was less after than before infarction. Post-infarction cardiac failure, which developed in 9 patients who had prior angina, was not associated with abolition of angina in any of this group. It is concluded that: 1. angina is frequent after myocardial infarction, 2. when present before infarction it usually persists thereafter, 3. angina commonly appears as a new symptom after infarction when not previously present and 4. disappearance of angina after infarction is distinctly uncommon.
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The most commonly used methods to study the mechanisms of hypocholesterolemic action of therapeutic agents generally determine the turnover of total (exchangeable) cholesterol pools in the body. This approach is based on the view that whatever increases the total load of cholesterol in the body will increase the levels of plasma cholesterol, and vice versa. Despite the importance of this assumption it has never been tested, and there is no evidence to indicate that it is valid under all conditions. This "overload" hypothesis dates from the times before the importance of plasma lipoproteins was recognized and their role in the transport of lipids was well understood. However, it is becoming increasingly clear that the levels of plasma cholesterol are determined more directly by the "transport" of cholesterol into and out of plasma compartment by lipoproteins than by the synthesis, absorption and elimination of cholesterol from the total body pools. Any effects that the latter parameters of cholesterol metabolism have on the levels of plasma cholesterol must be mediated through changes in synthesis and the subsequent metabolism of plasma lipoproteins. In other words, in any equation relating changes in the levels of plasma cholesterol to the changes in synthesis, absorption and elimination of cholesterol from the body pools we must consider the "transport" of cholesterol by lipoproteins and their metabolism.
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The effect on sinus rhythmicity and automaticity of complete digitalization in a 24 hour period was observed in 14 patients with sick sinus syndrome. Sinus nodal function was evaluated in these patients by assessing sinus nodal recovery time and by treadmill exercise testing and 24 hour Holter monitoring, before and after digoxin administration. Corrected sinus nodal recovery times ranged from 240 to 2,065 msec (average 714) before digoxin and were shortened to 250 to 1,260 msec (average 565) after the glycoside. Further, digoxin induced accelerated infra sinus escape pacemaker activity in five patients: junctional and ventricular in one and atrial in four. Spontaneous sinus rate evaluated with Holter monitoring revealed an average of 56 beats/min (range 43 to 69) before digitalis that was unchanged (average 58 beats/min; range 48 to 74) after digoxin therapy. Similarly, the sinus nodal response to exercise was unaffected after digitalization (average 118 beats/min both before and during digitalis therapy). It is concluded that digoxin does not exert adverse effects on sinus nodal function in patients with sick sinus syndrome. The glycoside can be used safely in these patients when indicated for cardiac pump dysfunction or for control of tachyarrhythmia.
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Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).
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1. In a homologous radioimmunoassay for canine ventricular myosin light chains, the following percentages of cross-reactivities were obtained using the dog as a reference: human, 28%; sheep, 21%; cat, 8%; guinea-pig, 7%; rabbit, 5%; and rat, 4%. 2. In a homologous double diffusion immunoassay using specific gamma G to canine cardiac myosin heavy chains, dog cardiac myosin showed immunological identity with human and sheep cardiac myosin but partial identity with myosins of other species. 3. On a 5-20% polyacrylamide gradient, light chain C1 was electrophoretically distinct in some species; light chain C2 was electrophoretically identical in all species. 4. The K+-activated myosin ATPase of small animals was higher than that of larger animals at an alkaline pH; the same was true for Ca2+-activated myosin when assayed at pH 6.3.