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Biomedical subjects

J F Spann

Publications and source records attributed to J F Spann.

At least 73 records · Page 4Linked to original sources
PubMed1979

Blood collection techniques, heparin and quinidine protein binding.

With the use of glass syringes without heparin and all glass equipment, the percent of unbound quinidine was measured by ultrafiltration and a double-extraction assay method after addition of 2 microgram/ml of quinidine sulfate. Compared to the all-glass method, collection of blood using Vacutainers resulted in an erroneous and variable decrease in quinidine binding related to blood to rubber-stopper contact. With glass, the unbound quinidine fraction was (mean +/- standard error) 10 +/- 1% in 10 normal volunteers, 8.5 +/- 1.5% in 10 patients with congestive heart failure, and 11 +/- 2% in 11 patients with chronic renal failure (although in 8 of the latter 11 patients the percent of unbound quinidine was 4 or more standard errors from the mean of the normal group). During cardiac catheterization, patients had markedly elevated unbound quinidine fractions: 24 +/- 2% (p less than 0.001). This abnormality coincided with the addition of heparin in vivo and was less apparent after the addition of up to 10 U/ml of heparin in vitro (120% and 29% increase in unbound quinidine fractions, respectively). Quinidine binding should be measured with all glass or equivalent equipment.

Blood Proteins↗
PubMed1979

Increased passive stiffness of short-term pressure-overload hypertrophied myocardium in cat.

The passive stress-strain relationship of right ventricular papillary muscles from 10 normal and 9 experimental cats with short-term pressure-overload right ventricular hypertrophy-failure was examined by plotting the logarithm of instantaneous stress (ln sigma) against the natural strain calculated as ln(l/l0) where l = instantaneous length and l0 = length at zero force. Such a stress-strain relationship was well approximated by a linear relationship. The slope K obtained from this linear relationship was higher in the hypertrophy-failure muscles (normal, 15.01 +/- 0.87 (SEM); hypertrophy-failure, 31.79 +/- 4.09; P less than 0.005). The value of the intercept, ln C was similar in the two groups (normal, -4.33 +/- 0.20; hypertrophy-failure, -4.71 +/- 0.10). This analysis indicates the the ln sigma-natural strain relationship is linear in the papillary muscle and the slope of this relationship, an index of stiffness, is increased in hypertrophy-failure muscles. Using a three-element muscle model, it is shown that increased diastolic stiffness may contribute to the decreased systolic performance.

Animals↗
PubMed1978

Quinidine pharmacokinetics in patients with cirrhosis or receiving propranolol.

Quinidine pharmacokinetics (half-life, volume of distribution, and clearance) as well as protein binding were evaluated following a single 200 mg. oral dose of quinidine sulfate in eight control patients, in eight patients with moderate to severe cirrhosis, and in seven patients receiving 40 to 400 mg./day of propranolol. Patients with cirrhosis had a significantly longer quinidine half-life (9 +/- 1 hr; p less than .01) when compared to control patients (6 +/- 0.5h). This was not related to a reduced quinidine clearance rate but rather to an increase in quinidine volume of distribution (4.1 +/- .4 L./Kg. in cirrhotic patients vs 2.6 +/- 1 L./Kg. in control patients; p less than .01). Abnormal quinidine binding (greater than 25 per cent unbound fraction) was noted in seven of the eight cirrhotic patients. In contrast, patients receiving propranolol had a normal quinidine half-life of 6 +/- 0.5 hr. However, these patients had a significantly reduced quinidine clearance (3.3 +/- .7 ml./min./Kg. vs. 5.3 +/- .5 ml./min./Kg. in controls; p less than .05) and higher peak concentrations (1.25 +/- .20 micrograms/ml. vs. .80 +/- .5 micrograms/ml. in controls; p less than .05). Therefore in patients receiving propranolol, quinidine levels may be higher than expected shortly after dosage, and therefore a potential for transient toxicity exists in these patients. Maintenance quinidine dosage may have to be reduced in patients with moderate to severe hepatic cirrhosis, but not in patients receiving propranolol. Total quinidine concentration measurement underestimate free quinidine concentrations in most cirrhotic patients.

Adult↗
PubMed1978

Computer analysis of left ventricular dynamic geometry in man.

Analysis of left ventricular performance in 20 normal patients was undertaken using biplane cineangiography and a semiautomatic computer image processing system. The analysis included evaluation of volumes, ejection fraction, regional shortening, patterns of ejection and filling and, when simultaneous left ventricular pressure was recorded stroke work, stroke power, wall stress and internal myocardial work. All of these data were calculated from digitized images stored permanently on digital magnetic tape, and can be reproduced without reanalysis of the cine film. Normal left ventricular function is described by an end-diastolic volume index of 82 +/- 3 ml, an ejection fraction of 60 +/- 2 percent, left ventricular mass index of 97 +/- 6 g/m2, peak first derivative of volume (dV/dt) of 485 +/- 28 ml/sec, anterior shortening of 48 +/- 2.3 percent, inferior shortening of 33 +/- 1.7 percent, lateral shortening of 29 +/- 1.5 percent, anterior mean shortening velocity (Vcf, in percent of end-diastolic length [L]/sec) of 1.5 +/- 0.1 L/sec, inferior Vcf of 1.1 +/- 0.06 L/sec and lateral Vcf of 0.94 +/- 0.2 L/sec, stroke work of 1.33 +/- 0.21 joules, mean stroke power of 3.7 +/- 0.62 joules/sec, integrated left ventricular pressure (tension-time index) of 2,866 +/- 340 mm Hg-sec, and integrated stress (stress-time index) of 7,260 +/- 765 (X 10(3)) dynes sec/cm2. Internal myocardial work was calculated from the strain energy. More internal work was expended in circumferential than logitudinal shortening (circumferential, 0.69 +/- 0.1 joules; longitudinal, 0.41 +/- 0.08, P less than 0.01), because hoop stress was greater than meridian stress (hoop, 201 +/- 20 dynes/cm3 X 10(3); meridian, 126 +/- 13, P less than 0.001). This analysis of left ventricular performance provides a reliable means for identifying abnormal ventricular function and may be more sensitive than any one measurement alone. The use of digital image processing makes this complex functional analysis of left ventricular performance feasible.

Adult↗
PubMed1978

Normal cardiac myosin ATPase and mechanics in pressure overload with digitalis treatment.

Cardiac muscle myosin ATPase activity is depressed and contractile function impaired when the heart is subjected to a chronic pressure overload. Administering digitalis in the presence of chronic pressure overload significantly attenuates the decline in mechanical function. The current study sought to determine if the cardiac muscle myosin ATPase activity of cats treated with digitalis in the presence of pressure overload remains normal in parallel with the mechanical function. Four groups of cats were studied: normal controls (C), animals with pressure-overload hypertrophy with or without failure (HF), normal cats that received treatment with digitalis (D), and animals that received digitalis prior to and together with pressure overload (DHF). Compared to C, the maximum myosin ATPase activity of HF was significantly (P less than 0.05) depressed, but the maximum ATPase activity of D and DHF was not altered significantly (P greater than 0.05) from C. In parallel with the enzyme maximum activity, the papillary muscle isometric rate of force development was significantly (P less than 0.005) depressed in HF compared to C; D and DHF were not significantly (P greater than 0.05) different from C. It is concluded that the depression of myosin ATPase observed in HF is not present when digitalis is administered concomitant with the pressure overload.

Adenosine Triphosphatases↗
PubMed1978

Effects of acute ethanol on the contractile state of normal and failing cat papillary muscles.

The direct effects of 100, 300 and 500 mg/100 ml ethanol on contractility of isolated, supported right ventricular papillary muscles were evaluated from 10 normal or failing cat hearts. In isometrically contracting muscles, 500 mg% ethanol decreased maximum tension in normal and failing hearts from 7.1 to 4.3 g/mm2 (P less than 0.001) and 3.4 to 2.3 (P less than 0.01) respectively, and lowered maximum tension rise from 30.4 to 20.2 g/mm2/sec (P less than 0.001) and 10.2 to 0.8 (P less than 0.01), without alterations of time to peak tension. In isotonically contracting muscles, 500 mg% ethanol reduced contractile element velocity at 0.5 g/mm2 load in normal and failing ventricles from 1.27 to 0.97 L/sec (P less than 0.001) and 0.59 to 0.39 (P less than 0.001) respectively. Thus, clinically meaningful doses of ethanol clearly, exerted dose-related negative inotropic actions on both normal and failing myocardium, thereby indicating that ethanol ingestion may exacerbate heart failure in diseased hearts.

Animals↗
PubMed1977

Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat.

This study examined the recuperative potential of cat hearts subjected to experimental right ventricular pressure overload (for a 10- to 14-day period) which provoked hypertrophy with and without congestive heart failure. Five groups of cats were studied: normal controls; one group with 70% pulmonary artery constriction which produced right ventricular hypertrophy (RVH); one group with an 87% constriction which also produced right ventricular hypertrophy but with congestive heart failure (CHF); and two groups which had been similarly subjected to pressure overload but which had been allowed a recovery period of 30 days after relief of the pressure overload. Both the 70% and 87% pulmonic constrictions were associated with extensive right ventricular hypertrophy, depression of myocardial contractile function, and severe redlction of cardiac norepinephrine stores (normal, 1.42 mug/g: RVH, 0.11 mug/g; CHF, 0.01 mug/g). After a 30-day period of relief from the pulmonic constriction normal hemodynamic function returned. In cats in which RVH had been relieved, right ventricular weight and contractile function were normal but catecholamine depletion persisted. Cats with relieved CHF showed depressed contractile function and depleted myocardial norepinephrine, and the right ventricular weight did not return to normal. Cardiac muscle of all pressure-overloaded nonrelieved hearts showed depressed velocity of shortening and depressed ability to sustain load. Cats with RVH alone regained normal muscle shortening velocity and load-bearing ability after relief. However, cardiac muscle from the CHF-relieved group recovered only unloaded shortening velocity while the ability to sustain load remained depressed. We conclude that the recuperative potential of myocardium damaged by pressure overload is adequate provided congestive heart failure has not occurred. Heart failure produces a persistent reduction in force-generating ability of the myocardium. Hypertrophy due to pressure overload, with or without CHF, leads to cardiac catecholamine depletion which is not readily reversed by relief of the overload.

Animals↗
PubMed1976

Retrograde coronary capillary perfusion for prevention and reversal of cardiogenic shock in experimental myocardial infarction.

The coronary sinus and coronary veins offer an access route for delivery of increased oxygen to ischemic myocardium surrounding the central dead zone of heart muscle in cardiogenic shock due to myocardial infarction. This investigation was conducted to determine if transvenous retrograde coronary capillary perfusion with oxygenated blood would prevent and reverse cardiogenic shock in experimental myocardial infarction produced by acute ligation of the circumflex and anterior descending left coronary artery in dogs. Cardiac output and systemic blood pressure were maintained near control values for up to 30 minutes when total left coronary ligation was accompanied by coronary retroperfusion. Conversely, both cariac output and systemic blood pressure fell to severe cardiogenic shocks levels within 2 minutes of total left cardiogenic shock levels within 2 minutes of total left coronary artery occlusion without retrograde flow or when retrograde flow was terminated 5 to 30 minutes following simultaneous coronary ligation and institution of retrograde flow.

Animals↗