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Biomedical subjects

D T Mason

Publications and source records attributed to D T Mason.

At least 109 records · Page 6Linked to original sources
PubMed1982

Long-term hemodynamic and clinical efficacy of captopril therapy in ambulatory management of severe chronic congestive heart failure.

The 6-month extended vasodilator efficacy of the oral angiotensin converting enzyme (ACE) inhibitor, captopril (CPT), was evaluated by sequential cardiac catheterization, nuclear scintigraphy, echocardiography, treadmill exercise, and symptomatology in nine patients with severe chronic left ventricular (LV) failure (CHF). CPT lowered LV filling pressure (from 23 to 14 mm Hg acutely (p less than 0.001) and to 14 mm Hg (p less than 0.01) with continuous 6-month therapy; concomitantly CPT raised cardiac index from 2.03 to 2.46 L/min/m2 initially (p less than 0.02) and to 2.33 L/min/m2 (p less than 0.02) at 6 months. Simultaneously CPT raised LV ejection fraction from 0.21 to 0.25 acutely (p less than 0.01) and to 0.30 (p less than 0.001) and to 60 mm (p less than 0.001) at 6 months. These beneficial actions of CPT on LV pump function raised treadmill exercise duration (from 339 to 426 seconds initially (p less than 0.05) and to 499 seconds (p less than 0.05) at 6 months, while considerably reducing CHF symptomatology (p less than 0.001). Thus ACE inhibition by CPT provides markedly beneficial sustained hemodynamic and clinical improvement in advanced LV failure without fluid accumulation or late vasodilator drug tolerance.

Aged↗
PubMed1982

Maturational changes in cardiac muscle myosin adenosine triphosphatase activity relative to hemodynamic alterations in newborn lambs.

We performed a chronologic investigation of left (LV) and right (RV) ventricular myosin ATPase activity and hemodynamics in newborn lambs. We found an elevation in myosin ATPase activity for the LV, which was achieved by 6 to 8 weeks of age and which correlated directly with increasing ventricular stroke work. Myosin ATPase activity did not increase with age for the RV, a finding which was associated with a postnatal decrease in ventricular stroke work. These findings may represent an important postnatal adaptation of newborn myocardium to the demands of extrauterine life.

Adenosine Triphosphatases↗
PubMed1982

Assessment of oral quinidine effects on sinus node function in sick sinus syndrome patients.

The effects of therapeutic doses of orally administered quinidine sulfate on sinus rhythmicity and automaticity were observed in 11 patients with sick sinus syndrome (SSS). Evaluation of sinus node (SN) function was undertaken by assessing sinus nodal recovery time (SNRT), treadmill exercise testing, and 24-hour ambulatory ECG monitoring before and after quinidine administration (25 mg/kg) (range 800 to 1600 mg daily). Corrected SNRT ranged from 100 to 1320 msec (average 551) before quinidine and was not significantly (p greater than 0.05) altered after quinidine to 346 to 660 msec (average 481). Further, quinidine did not induce accelerated infrasinus pacemaker activity. Spontaneous sinus rate evaluated with ambulatory monitoring revealed average rate of 57 bpm (range 53 to 63) before quinidine without significant increase to average 59 bpm (range 52 to 80) after quinidine therapy. Similarly, the maximal SN response to exercise was not significantly affected by quinidine (average 129 bpm before and 129 bpm after drug therapy). It is concluded that therapeutic doses of quinidine do not exert adverse effects on SN function in SSS patients. Chronic oral quinidine therapy can therefore be used safely with caution in patients with chronic SN disease when indicated for control of tachyarrhythmias.

Administration, Oral↗
PubMed1982

Cardiocirculatory actions of trimazosin and sodium nitroprusside in ischemic heart disease.

Although postload-reducing drugs are effective vasodilators in chronic congestive heart failure, the clinical application of the approach to ambulatory patient management remains difficult. We compared the hemodynamic effects of the new oral systemic vasodilator trimazosin (TZ) with those of nitroprusside (NP). Both TZ (172 mg) and NP (46 microgram/min) decreased mean blood pressure modestly (P less than 0.001), while causing considerable decline in elevated left ventricular filling pressure (TZ from 30 to 24 mm Hg; NP from 31 to 20 mm Hg; both P less than 0.001). TZ also raised the low cardiac index (CI) of 2.02 to 2.59 1/min/M2 (P less than 0.001), whereas NP elevated CI from 2.16 to 2.96 1/min/M2 (P less than 0.001). Both drugs lowered (P less than 0.05) total systemic vascular resistance and pressure time/minute while enhancing (P less than 0.01) stroke work index. The drugs diminished forearm venous tone (P less than 0.02) and forearm vascular resistance (P less than 0.01) concomitantly with elevation of forearm blood flow (P less than 0.05). Thus, TZ induced qualitatively similar marked augmentation of cardiac function to that by NP. These encouraging hemodynamic findings indicate that TZ may be beneficial to patients undergoing ambulatory vasodilator therapy of severe chronic congestive heart failure.

Adult↗
PubMed1982

Beta-adrenergic receptors in chronic alcoholic rat hearts.

Properties of cardiac beta-adrenergic receptors from chronic alcoholic and control rats were studied to determine whether alterations in the receptor contribute to the decreased responsiveness of isolated working alcoholic rat hearts to beta-adrenergic stimulation. The receptors, assessed in crude membrane fractions by the binding of (-)[3H]dihydroalprenolol, did not differ significantly in either number or affinity in alcoholic rats (22.5 +/- 1.9 fmol . mg protein-1; Kd = 0.49 +/- 0.03 nmol . litre-1; n = 7) compared with control rats (25.9 +/- 1.3 fmol . mg protein-1; Kd = 0.55 +/-0.04 nmol . litre-1; n = 7). Competition experiments indicated that there was no difference in the binding affinity of (-)isoprenaline for the alcoholic and control rat heart receptors, nor in the affinity of (-)propranolol for he alcoholic and control rat heart receptors. In the presence of 5' -guanylylimidodiphosphate, the affinity of (-)isoprenaline for the receptors was decreased the same amount in the alcoholic and control rat hearts. These results suggest that the beta-adrenergic subsensitivity of chronic alcoholic rat hearts is mediated by a biochemical mechanism other than a direct alteration of the beta-adrenergic receptor or coupling between the receptor and adenylate cyclase.

Alcoholism↗
PubMed1982

Importance of neuroendocrine regulators of vascular tone and integral adrenoreceptor interaction during oral vasodilator therapy of severe congestive heart failure with prazosin.

The cardiocirculatory actions of the oral vasodilator prazosin were evaluated by cardiac catheterization, forearm plethysmography, echocardiography, treadmill exercise, and symptoms in patients with advanced long-standing congestive heart failure. The administration of oral prazosin (2-7mg) reduced forearm venous tone and forearm vascular resistance. Concomitantly, mean systemic arterial pressure and left ventricular filling pressure decreased, and the cardiac index increased. These effects of a single dose of prazosin on left ventricular function were rapid in onset, maximal at 1 h, and sustained for the entire 6-h period of observation. After 2 weeks of outpatient therapy with 2-7 mg of prazosin four times daily, echographic end-diastolic dimension decreased, whereas the duration of treadmill exercise increased. Symptoms (dyspnea, fatigue, angina) were diminished throughout the course of prazosin therapy, and there was an improvement in the New York Heart Association functional class from 3.7 to 2.2. Thus, prazosin possesses sustained nitroprusside-like balanced dilator actions on the systemic arterial and venous beds, which are effectively translated into the beneficial hemodynamic effects of augmenting cardiac output and relieving excessive left ventricular end-diastolic pressure. The delayed vasodilator tolerance that occurs in 30% of the patients is prevented by the prior use of aldosterone antagonists, and is easily treated when present. Subacute hemodynamic suppression of beneficial prazosin vasodilator actions is transient and does not preclude successful sustained prazosin therapy of severe heart failure.

Heart Failure↗
PubMed1982

The hemodynamic actions of prenalterol in left ventricular failure.

The hemodynamic effects of prenalterol, a parenteral cardioselective beta 1-receptor agonist, were evaluated by cardiac catheterization in patients with refractory severe congestive heart failure (CHF). Prenalterol (PN) (4 mg i.v.) did not alter (p greater than 0.05) heart rate (HR), mean blood pressure (MBP) or left ventricular filling pressure (LVFP). Concomitantly PN markedly augmented cardiac index (CI) from 1.9 to 2.6 l/min/m2 (p less than 0.01) and substantially elevated stroke index (SI) from 24 to 30 ml/beta/m2 (p less than 0.001). In addition PN raised stroke work index (SWI) from 21 to 26 g . m/m2 (p less than 0.005) and decreased total systemic vascular resistance (TSVR) from 1702 to 1260 dyn . s. cm-5 (p less than 0.001). An important finding was that the heart rate x systolic blood pressure product was unchanged (p greater than 0.05) and precipitation of cardiac dysrhythmias or myocardial ischemia were not observed. Further PN 1 mg, 4 mg and 8 mg i.v. was sequentially injected and peak hemodynamic effects were determined 10 min after drug administration. PN 1 mg raised CI from 2.1 to 2.5 1/min/m2 (p less than 0.01), elevated SI from 24 to 29 ml/beat/m2 (p less than 0.01), and augmented SWI from 21 to 25 g . m/m2 (p less than 0.01), however, TSVR declined from 1702 to 1392 dyn . s. cm-5. Subsequent incremental PN doses of 4 and 8 mg did not provide (p greater than 0.05) additional enhancement of cardiac function. Thus, prenalterol produced markedly beneficial enhancement of cardiocirculatory function without untoward effects and may be useful in the management of patients with severe congestive heart failure. Moreover, dose-response analysis indicates these salutary improvements can be maximally produced by the small dose of 1 mg obviating the need for larger doses.

Adrenergic beta-Agonists↗
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

Cardiocirculatory and myocardial energetic effects of prostaglandin E1 in severe left ventricular failure due to chronic coronary heart disease.

The cardiocirculatory actions of brief (69 +/- 5 minutes) infusions of prostaglandin E1 were evaluated in nine chronic coronary heart disease patients with severe left ventricular (LV) failure caused by previous myocardial infarction. Prostaglandin E1 infusion did not alter heart rate (HR) and produced modest declines in mean systemic blood pressure (BP) (85 +/- 6 to 76 +/- 5 mm Hg, P less than 0.025) and LV filling pressure (19 +/- 3 to 15 +/- 2 mm Hg, P less than 0.01). Simultaneously, prostaglandin E1 augmented LV pump function raising cardiac index from 1.9 +/- 0.2 to 2.5 +/- 0.1 L/min/m2 (p less than 0.005), elevating stroke index from 28 +/- 2.4 to 35 +/- 2.9 ml/beat/m2 (p less than 0.01), and increasing stroke work index from 26 +/- 4.3 to 30 +/- 4.4 gm . m/m2 (p less than 0.02). Additionally, total systemic vascular resistance decreased from 1862 +/- 192 to 1282 +/- 100 dynes-sec-cm-5 (p less than 0.02) and double product LV aerobic index of HR . systolic BP diminished from 9492 +/- 666 to 8278 +/- 492 (p less than 0.02). Concomitantly, in the forearm, vascular resistance fell, blood flow rose, and venous tone remained unchanged. These results indicate that prostaglandin E1 is a potent systemic arteriolar dilator with markedly beneficial effects on cardiac function in chronic coronary patients having severe ischemic LV failure refractory to conventional therapy.

Adult↗
PubMed1981

Beneficial effects of nitroprusside administration on left ventricular dysfunction and myocardial ischemia in severe aortic stenosis.

Although surgical therapy is effective for reducing excessive left ventricular (LV) afterload in valvular aortic stenosis (AS), salutary short-term medical treatment has been lacking. Since we have shown LV systolic pressure (SP) is altered concordant with arterial SP in AS by vasopressors, the present study evaluated efficacy of nitroprusside (NP) on LV function, energetics, and perfusion in 15 severe AS patients. NP infusion (average 33 micron/min) proved beneficial in each: LVSP 192 mm Hg was reduced to 164; arterial SP decrement equaled LVSP change; LV end-diastolic pressure 19 mm Hg declined to 10: cardiac index (2.73 L/min/m2) and heart rate were unaltered; total systemic vascular resistance 1433 dsc-5 decreased to 1201; elevated LV stroke work index 92 gm.m/m2 was diminished to 74. Simultaneously, LV O2 consumption fell, LV diastolic flow was unchanged, while subendocardial perfusion increased. Thus cautious NP therapy with careful monitoring provided marked reduction of LV affected and improved LV function, energetics, and coronary flow distribution.

Aged↗