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Biomedical subjects

O J Hartling

Publications and source records attributed to O J Hartling.

At least 37 records · Page 2Linked to original sources
PubMed1987

First-pass radionuclide determination of cardiac output: an improved gamma camera method.

A technique for noninvasive determination of cardiac output by aid of first-pass radionuclide cardiography is described. After intravenous injection of 10-15 mCi technetium-99m-(99mTc) labeled red blood cells the method requires acquisition of a first passage time-activity curve recorded with a gamma camera over the left ventricle, the background corrected left ventricular count rate recorded after complete mixing of the tracer in the circulation, and determination of the distribution volume of the tracer. The method was applied in 14 patients with heart disease of various origins and evaluated against the conventional tracer dilution technique with arterial sampling of blood activity. Cardiac output determinations by external counting ranged from 2.30 to 8.56 l/min, mean +/- s.d. 4.50 +/- 1.66 l/min and by arterial blood sampling from 1.88 to 8.96 l/min, mean +/- s.d. 4.52 +/- 1.71 l/min. An excellent correlation was demonstrated between the two techniques, r = 0.978 (p less than 0.001). When no background subtraction was applied to the left ventricular counts at equilibrium, radionuclide cardiac output values were approximately 40% higher than those obtained by arterial sampling. The new first-pass radionuclide cardiographic technique may prove a useful tool in the noninvasive evaluation of cardiac function, especially in patients with arrhythmias and/or valvular incompetence.

Adult↗
PubMed1986

Controlled double blind trial of nisoldipine in the treatment of idiopathic Raynaud's phenomenon.

In a controlled double blind trial the symptomatic effect of the calcium channel blocker nisoldipine was assessed in 19 patients with idiopathic Raynaud's phenomenon. Nisoldipine significantly reduced the frequency of attacks (p less than 0.05), whilst having a non-significant tendency (p less than 0.10) to reduce the severity of attacks. Side-effects were uncommon. It is concluded that nisoldipine is a promising agent for the symptomatic treatment of idiopathic Raynaud's phenomenon.

Adult↗
PubMed1986

Controlled double-blind trial of the clinical effect of nifedipine in the treatment of idiopathic Raynaud's phenomenon.

Twenty-six patients with idiopathic Raynaud's phenomenon participated in a double-blind, crossover clinical trial comparing the clinical effect of nifedipine with that of placebo. Four patients discontinued the study because of side effects and one patient defaulted at the return visit. Nifedipine significantly reduced frequency and severity of attacks (p less than 0.01). In an overall evaluation of drug effectiveness, 19 of 21 patients preferred nifedipine to placebo (p less than 0.01). Nifedipine proved to be effective in the treatment of idiopathic Raynaud's phenomenon, but side effects should be expected in some 30%.

Adult↗
PubMed1986

Metabolism of exercising skeletal muscle during beta 1-selective adrenoceptor blockade.

Concentrations of glycogen, glucose, glucose-6-phosphate and lactate in the lateral vastus muscle were measured in seven subjects before and after dynamic muscle exercise at a work load of 75% of each subject's maximal working capacity, and with and without intravenous administration of the beta 1-selective beta-adrenoceptor blocking agent, atenolol. Pulmonary oxygen uptake was measured during exercise. Heart rate and arterial blood pressure were measured throughout the study. Arterial concentrations of glucose, lactate and free fatty acids were measured at rest and during exercise. The muscle concentration of glycogen and the extent of glycogen depletion with exercise were not influenced by the beta 1-adrenoceptor blocker. Similarly, there was no change in the muscle concentrations of glucose, glucose-6-phosphate and lactate. Heart rate decreased at rest and during exercise. Arterial blood pressure was not influenced by beta-blockade. Pulmonary oxygen uptake decreased by 6.5%. The exercise induced rise in arterial blood concentration of free fatty acids was abolished by beta 1-selective beta-blockade. It is concluded that the decrease in lactate release from exercising muscles during beta 1-adrenoceptor blockade seen in other studies cannot be explained by an impaired breakdown of muscle glycogen. It may be inferred, however, that a reduced availability of free fatty acids in the exercising muscles during beta 1-selective (and non-selective) beta-blockade may enhance the combustion of pyruvic acid and thereby decrease the production of lactate.

Adult↗
PubMed1986

Lack of effect of nifedipine on counterregulatory mechanisms in essential hypertension.

The influence of long-term nifedipine treatment on body fluid compartments, renal function, the renin-angiotensin system, and the adrenergic system was studied in 18 patients with essential hypertension. A placebo period of 4 weeks was followed by a 6-week dose-titration period. Thereafter, the dose was kept constant for an additional 6 weeks (mean dose, 51 mg/day). As compared with placebo values, diastolic blood pressure decreased approximately 12% during nifedipine treatment. Plasma volume, extracellular fluid volume, and the ratio of plasma to interstitial fluid volume did not change significantly, either in the group as a whole or in a subgroup in which pedal edema developed. Plasma concentrations of epinephrine and norepinephrine increased slightly after 2 weeks of treatment, but they returned to control values after 6 weeks of therapy. Plasma concentrations of renin, angiotensin II, and aldosterone did not change significantly. Glomerular filtration rate and renal clearances of sodium and potassium were unchanged as well. These results indicate that long-term nifedipine treatment does not lead to activation of counterregulatory mechanisms, such as fluid retention or the renin-angiotensin or adrenergic systems. This may well be of importance for the antihypertensive efficacy of nifedipine treatment.

Adult↗
PubMed1986

The influence of a background correction that considers the heart volume on radionuclide left ventricular ejection fraction determination.

A correction of background activity that considers the heart volume is introduced in radionuclide equilibrium cardiography. Left ventricular ejection fraction (LVEF) was determined in 19 patients with ischaemic heart disease by multigated equilibrium scan with 99Tcm-labelled red blood cells (99Tcm-RBC). Assuming that the majority of background activity in the ventricular and periventricular regions of interest arises from 99Tcm-RBC in lung tissue, a ventricular/periventricular background ratio was calculated from the distribution of 99Tcm-labelled macroaggregated albumin. The mean relative distribution of pulmonary 99Tcm-RBC activity in the ventricular region of interest was 0.590 (range 0.279-1.061) compared with the periventricular region. The modified background correction resulted in a mean LVEF of 43.0% (range 12.9-67.6%) compared with 46.8% (range 10.9-67.8%) with the standard correction, p less than 0.005. Since no attempt was made to calculate the proportion of 99Tcm-RBC activity arising from the myocardium and thoracic wall, this difference represents an upper limit of the general overestimation of LVEF obtained by the standard calculation. A further decrease in LVEF was seen when no background correction was applied. The present results suggest that standard LVEF calculation, by neglecting the background volume displaced by the cardiac blood pool, results in a slight overestimation of LVEF.

Background Radiation↗
PubMed1985

Bilateral subdural haematoma demonstrated at scintigraphy of the brain.

Bilateral subdural haematoma is not a rare disorder, but only a few cases diagnosed at brain scintigraphy have been reported. Bilateral subdural haematoma was demonstrated at scintigraphy in a 66-year-old man. Subsequent computerized-tomography scanning of the brain also demonstrated the lesion. After bilateral burr-hole aspiration, the patient made a good recovery.

Aged↗
PubMed1985

The influence of nifedipine treatment on counter-regulatory mechanisms in essential hypertension.

The influence of nifedipine treatment on plasma (PV) and extracellular fluid volume (ECV), the ratio of plasma volume to interstitial fluid volume (PV:IF), glomerular filtration rate (GFR), renal clearances of Na+ and K+, plasma concentrations of renin (PRC), angiotensin II (pANG II), aldosterone (pAldo), adrenaline (PA) and noradrenaline (PNA) were studied in 18 consecutive patients with essential hypertension. A 4-week placebo period was followed by a 6-week dose-titration period (period A). Thereafter the dose was kept constant for an additional 6 weeks (period B), the mean dose being 51 mg/day. As compared with placebo, diastolic blood pressure (DBP) decreased from 105 +/- 7 to 93 +/- 9 mmHg at the end of period B. Extracellular fluid volume, PV, and PV:IF were not significantly changed at the end of period A or B, neither in the group as a whole nor in a subgroup, who developed pedal oedema. After 2 weeks on nifedipine, PA as well as PNA increased slightly but returned to control values after 6 weeks of therapy. Plasma renin concentration, pANG II, pAldo and GFR did not change significantly. Renal sodium handling was also unchanged. It is concluded that long-term nifedipine therapy (exceeding 6 weeks) does not lead to activation of counter-regulatory mechanisms such as fluid retention, activation of the renin-angiotensin system and the adrenergic system. Renal function is unaffected by nifedipine.

Adult↗
PubMed1985

Changes in blood pressure, fluid volumes and glomerular filtration rate during long-term treatment with prizidilol, an antihypertensive drug with combined vasodilatator and beta-adrenoceptor blocking actions.

The long term effects on blood pressure, body fluid volumes, glomerular filtration rate and plasma renin concentration were studied in 11 patients with essential hypertension during treatment with prizidilol, which is an antihypertensive compound with combined vasodilatator and beta-adrenoceptor blocking actions. After the patients had been treated for four weeks with placebo, the active treatment was given for 12 weeks. Prizidilol reduced both supine and erect blood pressure by 26/14 mmHg (p less than 0.01) and 24/16 mmHg (p less than 0.01) respectively, without inducing significant changes in heart rate. Plasma volume increased significantly by eight percent (p less than 0.02), whereas the increase in extracellular fluid volume was insignificant. Glomerular filtration rate decreased by 4 ml/min./1.73 m2 (p less than 0.02). Plasma renin concentration was unchanged. Prizidilol was tolerated well, but six patients developed oedema and gained weight, which necessitated addition of diuretics in three patients.

Adrenergic beta-Antagonists↗
PubMed1984

Dose-response relationship in normal subjects of prenalterol, a beta-adrenergic agonist with positive inotropic and resistance lowering effects.

The acute haemodynamic effects of increasing doses of parenterally administered prenalterol-a beta-adrenergic stimulating drug-were assessed in normal subjects by means of radionuclide ventriculography. Prenalterol induced dose-related increases in the left ventricular ejection fraction and the systolic pressure end-systolic volume ratio. Left ventricular end-systolic and end-diastolic volumes decreased to the same extent accounting for an unchanged stroke volume. Cardiac output increased due to a rise in the heart rate. Systolic blood pressure increased, whereas diastolic and mean blood pressure remained unchanged. Calculated total peripheral resistance decreased significantly. The maximum effect of prenalterol on cardiac performance occurred with a dose of 18 to 36 micrograms/kg. Plasma concentrations of prenalterol showed large interindividual variations. In conclusion, prenalterol improves the pump function of the normal heart and causes a fall in peripheral vascular resistance, implying a reduction of the load on the heart. These effects may prove beneficial in the treatment of acute heart failure.

Adrenergic beta-Agonists↗
PubMed1984

Evaluation of intravenous radionuclide angiography in detection of occlusive disease of the iliac arteries.

Radionuclide angiography (angioscintigraphy) of the iliac arteries was performed in 173 patients consecutively referred for arterial insufficiency of the legs. In 83 of the patients femoral angiography was also performed. The interobserver variation was evaluated by the agreement indices, kappa (K) and weighted kappa (Kw). For angiography the interobserver agreement was high (K and Kw 0.65 and 0.77 respectively). For angioscintigraphy the agreement between observers was fair (K = 0.52, Kw = 0.68), and equal to the intraobserver agreement (K = 0.55, Kw = 0.65). The comparison between angioscintigraphy and angiography gave K-values of 0.22-0.31 and Kw-values of 0.37-0.48. The nosographic sensitivity of angioscintigraphy was 61%, the nosographic specificity was 93%, and the predictive value for both a positive and a negative test was 83%. The prevalence of occlusion or severe stenosis was 34%. Inguinal pulse palpation detected 48% of iliac occlusions. It is concluded that the reliability of angioscintigraphy in the diagnosis of iliac arterial occlusive disease is acceptable for a non-invasive, rapid, inexpensive and widely available screening procedure. Although anatomical details are not visualized the information obtained is useful for the detailed planning and choice of subsequent diagnostic and therapeutic procedures. The method is well suited for repeat studies and may be modified to include the femoral arteries.

Adult↗
PubMed1983

Haemodynamic and metabolic effects of alpha-adrenoceptor blockade with phentolamine at rest and during forearm exercise.

The pre- and post-junctional alpha-adrenoceptor blocking agent, phentolamine, was given by intravenous infusion to eight healthy volunteers during rest, forearm exercise and post-exercise. Phentolamine produced a sustained increase in heart rate. The diastolic blood pressure decreased slightly whereas systolic and mean blood pressures remained unchanged. Phentolamine caused a marked increase in the forearm blood flow and a decrease in vascular resistance at rest and post-exercise, but did not influence the blood flow or vascular resistance in the exercising forearm. There was a small increase in arterial blood glucose concentration, and a decrease in blood alanine concentration during drug infusion. Blood lactate was not affected by phentolamine. The arterial concentrations of free fatty acids and glycerol increased, and the concentration of triglycerides decreased during phentolamine infusion. Forearm exchange of glucose, lactate, alanine, glycerol, free fatty acids, triglycerides and forearm oxygen consumption were not changed significantly. These findings corroborate the concept that alpha-adrenoceptor induced vasoconstriction plays a subordinate role in exercising skeletal muscle. All of the metabolic findings might be explained as secondary to an increased noradrenaline release during phentolamine infusion.

Adult↗