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Biomedical subjects

F L Abel

Publications and source records attributed to F L Abel.

At least 19 recordsLinked to original sources
PubMed2001

Pmax, end systolic elastance, and Starling's law of the heart.

Starling's law is a description relating the energy released by the contracting ventricle to the end diastolic fiber length. The peak systolic pressure during isovolumic contraction is an example of this relationship; Sunagawa and coworkers (12) termed that pressure Pmax. It may also be estimated during ejecting beats. Here we compare the variable Pmax at a given end diastolic volume with that of end systolic elastance as an indicator of ventricular function, changes in either being indicative of changes in the inotropic state of the heart. We specifically investigate 2 points on the end systolic pressure-volume relationship (ESPVR) plot: 1) the Pmax, EDV point, obtained from the concept of the maximum pressure, Pmax, the pressure an isovolumically contracting ventricle would produce at a given end diastolic volume (EDV); and 2) the end systolic pressure, end systolic volume point. Both points would be expected to shift proportionally with changes in the slope of ESPVR. Data were obtained from 2 published reports in humans in the literature and from a group of 5 dogs subjected to a wide range of preloads and afterloads. High correlations (>0.9) were obtained for changes in the slope of ESPVR and the Pmax, EDV points. The latter, a more readily obtainable variable from single ejecting beats, is proposed as a version of Starling's law, the changes in which are directly comparable with the changes in end systolic elastance. The changes in the end systolic pressure, end systolic volume points, were not as reliable (<0.7).

Animals↗
PubMed2001

Beat-to-beat evaluation of cardiac function in low-dose endotoxemia using a conscious sheep model.

The effects of very low doses of endotoxin (20 ng/kg/h for 8 h) were evaluated in a conscious sheep model in which introducers for catheters for monitoring pressure and ventricular dimensions had been previously inserted so that the studies could be performed without anesthesia and without a previous thoracotomy. Analog data was obtained at hourly intervals for 10 h and again at 24 h and was used to construct a beat-to-beat analysis of left ventricular performance. Only minimal effects were observed on heart rate, end diastolic pressure, arterial pressure, cardiac output, or cardiac work, although there was a significant rise in pulmonary artery pressure at 1 h of infusion. Despite the absence of changes in heart rate, preload, or afterload, maximal dp/dt decreased significantly by 4 h and remained decreased for the 10-h observation period; it returned to normal at 24 h. End systolic elastance decreased at 6 h and Pmax/EDV, a new indicator of performance, also decreased at 6 and 9 h. Thus, systolic performance decreased. Negative dp/dt did not change, but time for relaxation from 80% to 20% of peak ventricular pressure increased significantly at 5, 6, and 8 h. Plasma TNF-alpha was also measured and showed a significant rise at 2 h, but rapidly decreased thereafter. These results indicate an early depression of myocardial contractility and distensibility at doses of endotoxin insufficient to produce measurable effects on arterial pressure or cardiac output.

Animals↗
PubMed2000

Effects of hyperbaric oxygen on ventricular performance, pulmonary blood volume, and systemic and pulmonary vascular resistance.

The cardiovascular effects of hyperbaric (3 atm abs) air, 100% oxygen, and hyperbaric oxygen (HBO2) at 3 atm abs were investigated in 13 pentobarbital-anesthetized dogs. We measured heart rate, arterial pressure, pulmonary artery pressure, right atrial pressure, left and right ventricular pressure, and cardiac output. From these we determined end diastolic pressure, +/-maximal dp/dt, maximal (dp/p), end systolic elastance, cardiac work, and systemic (SVR) and pulmonary vascular resistance (PVR). Pulmonary blood volume was obtained from the mean transit time of ascorbic acid. The significant results with HBO2 were a decrease in heart rate, cardiac output, and cardiac work. All left ventricular performance indices decreased, without a change in preload or afterload. In contrast, only right ventricular -dp/dt decreased. SVR increased but PVR did not change; 100% O2 produced similar but less pronounced responses. Hyperbaric air had only mild effects. Pulmonary blood volume and lung wet/dry ratio did not change. Our data suggest that HBO2 may act by a differential effect on the autonomic innervation of the right and left ventricles. The resultant ventricular imbalance may be of clinical importance in the mechanism of pulmonary edema in patients in congestive heart failure undergoing hyperbaric therapy.

Animals↗
PubMed1998

Problems with use of the end systolic pressure-volume slope as an indicator of left ventricular contractility: an alternate method.

The use of end-systolic elastance as a parameter of left ventricular contractility is based on a theory put forward by Sagawa and is limited by an assumed linearity of the model for a time varying compliance. A major problem is the contractility-dependent curvilinearity of the end-systolic pressure-volume relationship (ESPVR), which may result in intercept volumes that are below a passive unstretched volume. Based on the experimental data of Burkhoff et al., we demonstrate the reasons for the lack of correlation of the slope (k) of the end-systolic pressure (P(es))-volume (V(es)) relationship with ventricular contractility. A parabolic relation, P(es) = a x V(es)2 + b x V(es) + c, was used for approximation of the ESPVRs, as proposed by Burkhoff et al., and the slope (k = 2 x a x V(es) + b), together with the volume axis intercepts (V0), calculated for the tangents for all P(es)/V(es) points of the ESPVRs. The results demonstrate the volume range dependence of the slope and V0 of linear regression lines. However, intercepts of the ESPVRs tangents with a midrange constant pressure line (e.g., 80 mmHg or 100 mmHg) justify the use of the shift of the end-systolic pressure-volume relationship as a parameter of left ventricular contractility. This method appears to be valid over a much wider range of end-systolic volumes than is the use of the slope alone.

Animals↗
PubMed1998

Left ventricular potential energy is represented in the ejecting left ventricular pressure curve.

Sunagawa and coworkers have proposed an ejecting, single beat, cosine curve matching method for the estimation of the maximum potential left ventricular pressure during an isovolumic contraction. We tested the hypothesis that this same information could be obtained from maximum dp/dt and the length of the ventricular contraction curve using a simple formula. The method was tested using Sunagawa's reported data as well as on data obtained from five dogs over a wide range of afterloads, and from three rabbits, four pigs, and four sheep. A high correlation coefficient between the two methods (.85 to .97), based on a linear model, was obtained in all the experiments. The formula method gave slightly higher values than the cosine curve matching procedure, was much simpler, and involved few of the curve matching assumptions. The maximum left ventricular pressure was also highly correlated with stroke work. These results imply that the maximum potential left ventricular pressure or energy is represented in, and can be predicted from, the ventricular pressure during normal ejection at a given end diastolic volume. When combined with measurements of end systolic pressure and stroke volume, reliable beat-to-beat estimates of the slope of the end systolic pressure-volume relationship (end systolic elastance) might be obtainable from single, left ventricular beats.

Algorithms↗
PubMed1998

Distribution of coronary arterial capacitance in a canine model.

The capacitative properties of the major left coronary arteries, left main (LM), left anterior descending (LAD), and left circumflex (LCX), were studied in 19 open-chest isolated dog hearts. Capacitance was determined by using ramp perfusion and a left ventricular-to-coronary shunt diastolic decay method; both methods gave similar results, indicating a minimal systolic capacitative component. Increased pericardial pressure (PCP), 25 mmHg, was used to experimentally alter transmural wall pressure. The response to increased PCP was different in the LAD vs. LCX; increasing PCP decreased capacitance in the LCX but increased capacitance in the LAD. This may have been due to the different intramural vs. epicardial volume distribution of these vessels and a decrease in intramural tension during increased PCP. Increased PCP decreased LCX capacitance by approximately 13%, but no changes in conductance or zero flow pressure intercept occurred in any of the three vessels, i. e., evidence against the waterfall theory of vascular collapse at these levels of PCP. Coronary arterial capacitance was also linearly related to perfusion pressure.

Animals↗
PubMed1996

Exercise- and hypertension-induced collagen changes are related to left ventricular function in rat hearts.

Chronic hypertension, known to affect the collagen profile of the heart, and exercise result in impaired or improved heart function, respectively. Collagen types I [alpha 1(I)2 and alpha 2(I)] and III [alpha 1(III)3] are the predominant interstitial collagens thought to influence cardiac function, and the ratio of type III to I (collagen III/I) is thought to be a significant factor in the altered relaxation observed in hypertrophy. The present study tested the hypothesis that the myocardial structure and function are different in chronically exercise-trained vs. hypertensive rat hearts. Male rats were either chronically exercised (XTr) or submitted to experimental hypertension by coarctation of the abdominal aorta (Hyp) for 10 wks. Heart rate, blood pressure, and maximal rate of fall of the left ventricular pressure (-dp/dt) were recorded during isoproterenol stimulation. Results showed that both Hyp and XTr had higher heart weight and left ventricular weight-to-body weight ratios (P < 0.05). Mean arterial pressure (MAP) was higher in Hyp and lower in XTr (P < 0.05), whereas (-dP/dt)/MAP was diminished in Hyp but enhanced in XTr. Left ventricular collagen was higher in Hyp than XTr, whereas collagen III/I was reduced in Hyp compared with XTr (P < 0.05). Scanning and transmission electron microscopy also supported an accumulation of left ventricular collagen in Hyp compared with XTr. A negative correlation was observed between collagen III/I and (-dP/dt)/ MAP (r = -0.91; P < 0.05). These results suggest an important relationship between adaptations in left ventricular collagen and the changes in diastolic function observed in both chronic hypertension and exercise cardiac stress.

Animals↗
PubMed1995

Macro- and microcirculatory effects of IL-15.

The recently isolated and cloned cytokine interleukin (IL)-15 was studied to ascertain its systemic and local cardiovascular effects. IL-15 was studied in rats anesthetized with 50 mg/kg sodium pentobarbital. In Group I, 10-50 micrograms of IL-15 were administered intravenously. Heart rate and arterial pressure decreased significantly for the duration of the study. In Group II, IL-15 was administered topically to the exposed cremaster muscle in four doses of 10 ng each. Heart rate and arterial pressure decreased significantly for the duration of the study. A1 and A2 arteriolar diameters decreased, but A3 diameters remained unchanged as determined by videomicroscopy. Vasodilation induced by either topical acetylcholine or nitroprusside was abolished by IL-15. Reduced heart rate and arterial pressure suggest reduced cardiac output. Arteriolar constriction due to abolished smooth muscle dilation was caused by IL-15.

Administration, Topical↗
PubMed1995

Effects of pericardial pressure on systemic and coronary hemodynamics in dogs.

The effects of pericardial tamponade on coronary capacitance and coronary systemic hemodynamics were calculated in two groups of animals subjected to increases in pericardial pressure (PCP) up to approximately 20 mmHg. In one group (A), flow in the left circumflex artery was measured in the intact animal under conditions of increased PCP. In the second group (B), coronary artery perfusion pressure was maintained constant with a pump while PCP was increased. In group A increased PCP was accompanied by a decrease in arterial pressure. This resulted in a marked decrease in coronary blood flow after vasodilation but without a change in coronary vascular resistance. In group B there was no change in coronary flow or coronary vascular resistance with increased PCP. Microsphere distribution to the left ventricular wall showed less endocardial than epicardial flow but no change in going from low to high PCP. Characteristic impedance was altered in the group B animals after vasodilation at medium and high PCP, indicating a loss of reflection sites and probably increased vessel tethering. The coronary artery in a subgroup of group B animals was also perfused by left ventricular pressure, the time constants for coronary backflow showing an 8-12% decrease in capacitance with low and high PCP; these values represent minimal epicardial capacitances vs. total bed capacitance. A diastolic model for the values for resistance and capacitance in the coronary bed is suggested. As expected, most of the capacitance is in the venous bed and most of the resistance is in the arterial bed.

Animals↗
PubMed1995

Direct action of endotoxin on cardiac muscle.

While the cardiovascular effects of endotoxin include myocardial depression, presumably due to circulating myocardial depressant substances, endotoxin itself is supposed to have no direct effect on the heart. In these experiments, we compared the direct effects of endotoxin on the contractile response of feline papillary muscle to calcium with that seen after administration to the intact animal. The contractile state of the muscle was assessed from developed tension as extracellular calcium concentrations were varied from .5 to 8.0 mM. When endotoxin was administered to the intact animal as well as given to the muscle directly in the bathing solution, endotoxin- exposed muscles showed smaller increases in contractile tension with increasing calcium concentrations than control muscles after 70-85 min. NaOH-inactivated endotoxin produced results similar to the control experiments. Previous experimenters have reported myocardial depression only after endotoxin had circulated in the intact animal for 1-2h; these experiments show a direct depressant effect of endotoxin on cardiac muscle without the release of a substance elsewhere in the body.

Animals↗
PubMed1994

Effects of cardiac work on the threshold for ventricular fibrillation.

Ventricular fibrillation threshold (VFT) was measured in anesthetized dogs, while cardiac work was altered by changing arterial pressure (pressure work) or by opening an aorta to left atrial shunt (flow work). When VFT during pressure work was compared with that during flow work, at a constant heart rate, it was found that there was a negative correlation (a lower threshold for fibrillation) between VFT and flow work but not pressure work. VFT also had negative correlations with the rate of contraction and relaxation indexes; maximal +/- dp/dt and negative dp/dt were the most significant variables. On the other hand, coronary flow, oxygen consumption, end diastolic pressure, and tension time index were not correlated with VFTs. Thus, VFT depended on mechanical factors not necessarily correlated to alterations in myocardial perfusion.

Animals↗
PubMed1994

Intramyocardial pressure gradients in working and nonworking isolated cat hearts.

This study presents an improved method for the measurement of intramyocardial pressure (IMP) using the servo-nulling mechanism. Glass micropipettes (20-24 microns OD) were used as transducers, coated to increase their mechanical resistance to breakage, and placed inside the left ventricular wall with a micropipette holder and manipulator. IMP was measured at the base of the left ventricle in working and nonworking isolated cat hearts that were perfused with Krebs-Henseleit buffer. In working hearts a transmural gradient of systolic IMP oriented from endocardium toward the epicardium was found; the endocardial values for systolic IMP were slightly higher than systolic left ventricular pressure (LVP), by 11-18%. Increases in afterload induced increases in IMP, without changing the systolic IMP-to-LVP ratio. In nonworking hearts with drained left ventricles, the systolic transmural gradient for IMP described for working hearts persisted, but at lower values, and was directly dependent on coronary perfusion pressure. Systolic IMP-to-LVP ratios were always > 1. The diastolic IMP of both working and nonworking hearts exhibited irregular transmural gradients. Our results support the view that generated systolic IMP is largely independent of LVP development.

Animals↗
PubMed1993

Use of fluorescent latex microspheres to measure coronary blood flow distribution.

Radioactive microspheres have long been in use to measure blood flow distribution to various vascular beds. Their drawbacks are the short half-lives of the radioactive material, the need for appropriate care in handling and disposing of such material, and their relative expensiveness. We investigated the use of fluorescent microspheres as indicators of coronary blood flow distribution in a canine model. Radioactive (125I) microspheres were used as a comparison standard. Four colors of fluorescent microspheres were used: blue, yellow-green, orange, and red, having emission frequencies ranging from 385 to 605 nM. The experiments were carried out in dogs under pentobarbital anesthesia, in which the microspheres were given during pump perfusion of the left circumflex artery with the animal's own blood. The hearts were removed, fixed for 3 days in 10% formalin, and sectioned. Samples from the endocardial, myocardial, and epicardial layers were read on a gamma counter. The fluorescent microspheres were extracted from the same tissues into ethyl acetate, and read in a fluorescence spectrophotometer at the appropriate excitation/emission frequencies. Comparable results were obtained from the two methods, with good sensitivity and resolution of dye colors, using the fluorescent microspheres.

Animals↗
PubMed1993

Hemodynamic responses to changes in carotid sinus pressure after endotoxin and ibuprofen.

The hemodynamic responses to changes in carotid sinus pressure (CSP) were evaluated in nine pentobarbital-anesthetized dogs during control, endotoxin-treatment, and ibuprofen (after endotoxin) treatment periods. Both carotid sinuses were isolated and perfused at varying pressures with oxygenated blood in the vagotomized animal. Alterations in carotid sinus pressure and the resultant responses were measured at 15-min intervals during a 30-min control period, for 60 min after 1 mg/kg endotoxin, and for 60 min after 10 mg/kg ibuprofen given after endotoxin. The results showed a reduction in calculated gain for mean arterial pressure (MAP) (change in arterial pressure/change in CSP), heart rate, and peripheral resistance (TPR) after endotoxin, without a corresponding reduction in cardiac output (CO) gain. These gain changes were accompanied by a decrease in absolute MAP, CO, and TPR. An indicator for cardiac performance gain also increased. Relatively, arterial pressure was partially maintained by an increase in CO despite a loss in ability to vasoconstrict. Ibuprofen failed to correct the MAP gain, and only partially restored MAP, but shifted a greater relative response to peripheral resistance. To test if TPR would also decrease if the decrease in CO was prevented, three additional animals were studied with a pump in series with the heart to maintain CO; TPR again dropped after endotoxin. The results indicate a loss of peripheral arterial tone after endotoxin, partially restored by ibuprofen. The CO response indicates a peripheral vascular failure rather than a central or carotid sinus failure mechanism.

Animals↗