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Biomedical subjects

C R Lacy

Publications and source records attributed to C R Lacy.

26 records · Page 2Linked to original sources
PubMed1992

Arterial blood nicotine concentration and coronary vasoconstrictive effect of low-nicotine cigarette smoking.

Low-nicotine cigarettes have been advertised to the public as less harmful to the cardiovascular system. We studied the effects of smoking two low-nicotine cigarettes on arterial and venous blood nicotine levels, hemodynamics, and coronary vascular tone in 12 patients referred for diagnostic coronary arteriography. All were chronic smokers as evidenced by their elevated baseline arterial and venous cotinine blood levels (139 +/- 30 ng/ml and 155 +/- 34 ng/ml, respectively). High-resolution coronary angiograms were evaluated "blindly" before and after smoking. An electronic caliper was used to measure the diameter of disease-free coronary segments of the left anterior descending and circumflex arteries. Arterial nicotine levels rose from 5 +/- 1 ng/ml at baseline to 37 +/- 7 ng/ml (p less than 0.01) after the first cigarette was smoked and to 45 +/- 8 ng/ml (p less than 0.01) after the second cigarette. Venous nicotine levels rose from 8 +/- 2 ng at baseline to 15 +/- 3 ng/ml (p less than 0.05) after the first cigarette and to 20 +/- 3 ng/ml (p less than 0.01) after the second cigarette. After the first cigarette heart rate increased 8 +/- 2 beats/min (p less than 0.003) and double product 1229 +/- 400 beats/min x mm Hg (p less than 0.02). Compared to baseline values, after the second cigarette heart rate increased 9 +/- 1 beats/min (p less than 0.001) and double product 1767 +/- 486 beats/min x mm Hg (p less than 0.01). Systolic, diastolic, and mean blood pressure did not change significantly after either the first or second cigarette.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1990

Angiotensin-converting enzyme inhibitors: a comparative review.

The chemistry, pharmacology, pharmacokinetics, adverse effects, and dosages of the three currently available angiotensin-converting enzyme (ACE) inhibitors are reviewed. This class of agents effectively inhibits the conversion of angiotensin I to the active vasoconstrictor angiotensin II, a hormone that also promotes, via aldosterone stimulation, increased sodium and water retention. The ACE inhibitors, therefore, are capable of lowering blood pressure primarily by promoting vasodilatation and reducing intravascular fluid volume. Captopril, the first orally active, commercially available ACE inhibitor, is a sulfhydryl-containing compound. Captopril was followed by the introduction of enalapril and lisinopril, two non-sulfhydryl ACE inhibitors. The pharmacokinetic profiles of these three ACE inhibitors differ. Captopril has rapid onset with relatively short duration of action, whereas enalapril and lisinopril have slower onset and relatively long duration of action. Captopril is an active ACE inhibitor in its orally absorbable parent form. In contrast, enalapril must be deesterified in the liver to the metabolite enalaprilat in order to inhibit the converting enzyme; this accounts for its delayed onset of action. Lisinopril does not require metabolic activation to be effective; however, a slow and incomplete absorption pattern explains the delay in onset of activity. Captopril and its disulfide metabolites are primarily excreted in the urine with minor elimination in the feces. Approximately two-thirds of an administered enalapril dose is excreted in the urine as both the parent drug and the metabolite enalaprilat; the remainder of these two substances are excreted in the feces. Lisinopril does not undergo measurable metabolism and approximately one-third is excreted unchanged in the urine with the remaining parent drug being excreted in the feces. The ACE inhibitors lower systemic vascular resistance with a resultant decrease in blood pressure. Their efficacy is comparable to diuretics and beta-blockers in treating patients with mild, moderate, or severe essential and renovascular hypertension. In those patients with severe congestive heart failure (CHF) the ACE inhibitors produce a reduction in systemic vascular resistance, blood pressure, pulmonary capillary wedge pressure, and pulmonary artery pressure. These drugs may produce improvement in cardiac output and stroke volume and, with chronic administration, may promote regression of left ventricular hypertrophy. The antihypertensive effects of the ACE inhibitors are enhanced when these agents are combined with a diuretic. Captopril and enalapril have been shown to be of particular benefits as adjunctive therapy in patients with congestive heart failure, both in terms of subjective improvement of patient symptoms, and in improving overall hemodynamic status.(ABSTRACT TRUNCATED AT 400 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

The relationship of plasma renin activity to clinic and ambulatory blood pressure in elderly people with isolated systolic hypertension.

Eighty-one untreated elderly patients with clinic-defined isolated systolic hypertension (ISH) and 39 normotensive elderly subjects underwent 24-h ambulatory blood pressure monitoring. Before the ambulatory blood pressure monitoring, EDTA-anticoagulated venous blood was obtained from seated subjects for determination of plasma renin activity. Ambulatory blood pressure and heart rates were determined at 15-30-min intervals by a validated, portable non-invasive technique (Spacelabs 5200). Ambulatory blood pressure variability was defined for each subject as the standard deviation and the coefficient of variation of the ambulatory blood pressure. The mean awake systolic blood pressure was much lower than the clinic-determined value in the ISH group (P less than 0.001), but only slightly so in the normotensive group. Forty-two per cent of the clinic-defined ISH group had mean awake ambulatory systolic blood pressures below the 90th percentile of the normotensive group. A discrepancy between office and ambulatory blood pressures was not associated with blood pressure variability, heart rate or plasma renin activity.

Aged↗
PubMed1987

DPI 201-106 for severe congestive heart failure.

DPI 201-106 is a new oral inotropic agent that exerts its effects through a novel mechanism of action, namely, by enhancing sensitivity of myofilaments to calcium and prolonging inward sodium current. In a double-blind, randomized, placebo-controlled fashion, single oral doses (80 and 100 mg) of DPI 201-106 were administered to 15 patients with severe congestive heart failure. Dose-dependent increases in cardiac index (25%, p = 0.016), left ventricular stroke work index (24%, p = 0.018), left ventricular stroke volume index (32%,p = 0.005) and QTc interval (7%, p = 0.009) were observed. Significant effects on heart rate and systemic arterial pressure were not observed. Positive correlations of QTc interval with DPI plasma level (r = 0.64, p = 0.0001), stroke work index (r = 0.47, p = 0.0001) and ventricular ectopic activity on ambulatory electrocardiography (r = 0.49, p = 0.0001) were observed. Maximum changes occurred approximately 3 to 4 hours after ingestion and lasted more than 8 hours. Plasma drug levels were consistent with a 2-compartment model exhibiting first-order absorption and elimination kinetics. DPI 201-106 produced hemodynamic improvement in patients with severe congestive heart failure.

Adult↗
PubMed1984

Atenolol, nadolol, and pindolol in angina pectoris on effort: effect of pharmacokinetics.

The duration of action of three beta blockers (atenolol in nine patients, nadolol in 18 patients, and pindolol in 11 patients) administered once a day was studied in three cohorts of patients with angina on effort. Compared with single-blind run-in placebo, all three beta blockers decreased angina frequency (p less than 0.01), exercise tolerance (p less than 0.01), heart rate recorded by ambulatory ECG, and submaximal heart rate when a treadmill exercise stress test was performed 3 hours after administration of the daily dose (p less than 0.0001). Twenty-four hours after the dose, the percentage of the maximal heart rate-attenuating effect was highest for nadolol (pharmacokinetic half-life, 15.5 hours), followed by atenolol and then by pindolol (half-life, 5.5 hours). A linear relationship between the logarithm of plasma concentration of beta blocker and the heart rate at submaximal exercise (r = 0.72 and p = 0.0001 for nadolol; r = 0.50 and p = 0.0001 for pindolol) was observed. The data suggest that in the treatment of angina on effort, beta blockers should be prescribed according to their pharmacokinetic properties to achieve adequate suppression of the heart rate during exercise.

Adrenergic beta-Antagonists↗