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Biomedical subjects

N Westerhof

Publications and source records attributed to N Westerhof.

At least 55 records · Page 3Linked to original sources
PubMed1996

Effect of length and contraction on coronary perfusion in isolated perfused papillary muscle of rat heart.

We studied the impeding effect of cardiac muscle contraction on coronary arterial inflow in six isolated, perfused papillary muscles of the rat. Special attention was given to the effect of changes in muscle length and contractility on flow impediment in systole. Contractility was changed by resumption of pacing after a quiescent period of 60-100 s or by doubling the calcium concentration in the perfusate and the superfusion fluid from 1 to 2 mM. The vascular bed was maximally dilated with adenosine, and perfusion pressure was kept constant at 69 +/- 3 cmH2O. We found that contractions impede arterial inflow by 29% [from 17.3 +/- 2.2 ml.min-1.g-1 during diastole to 12.4 +/- 1.8 (SE) ml.min-1.g-1 at peak systole, P < 0.001] while the muscle was kept at 90% of maximum muscle length (MLmax). When the muscle was stretched from 80 to 97% of MLmax, diastolic force increased from 0.5 +/- 0.3 to 11.1 +/- 1.2 mN/mm2, systolic force increased from 11.1 +/- 1.5 to 44.6 +/- 4.0 mN/mm2, diastolic flow decreased by 12% (from 18.2 +/- 2.3 to 15.9 +/- 1.9 ml.min-1.g-1, P < 0.05), and systolic flow decreased by 3% (12.4 +/- 2.3 to 12.0 +/- 1.6 ml.min-1.g-1, P = NS). Increased contractility by elevated [Ca2+] did not affect diastolic flow but increased systolic flow impediment from 29 to 39% (systolic flow decreased from 12.4 +/- 1.8 to 10.3 +/- 1.4 ml.min-1.g-1, P < 0.01). The results are qualitatively similar to findings in the intact heart. Limitations on quantitative comparison due to differences in muscle architecture and differences in force vectors in the papillary muscle and the left ventricle are discussed. The results show that ventricular pressure is not essential in systolic coronary arterial flow impediment. The findings are in agreement with the varying elastance concept where the flow impediment is predicted to depend on myocardial elastic properties.

Animals↗
PubMed1996

Perfusion-induced changes in cardiac O2 consumption and contractility are based on different mechanisms.

Increased cardiac perfusion results in increased oxygen consumption (VO2) and increased contractility (Gregg phenomenon) in the isolated heart. We investigated whether these two aspects of the Gregg phenomenon are related to coronary flow or arterial pressure. Coronary flow and, thus, arterial pressure were changed in the reference state and during vasoconstriction (3 nM vasopressin) in the Langendorff-perfused rat heart contracting isovolumically (ventricular balloon) at 27 degrees C (n = 5). All hearts showed an increase in developed isovolumic left ventricular pressure (measure of contractility) and in VO2 with increased perfusion. Developed left ventricular pressure depended primarily on arterial pressure, so its relationship with coronary flow was shifted by vasoconstriction. Conversely, VO2 primarily depended on coronary flow, so its relationship with arterial pressure was shifted with vasoconstriction. By use of vasoconstriction (decreased vascular radii), the effects of arterial pressure and wall shear stress (proportional to arterial pressure x radius) should be separable, but the results did not reach significance. Thus contractility is related to arterial pressure or shear stress, whereas VO2 is related to coronary flow. We conclude that the two aspects of the Gregg phenomenon are based on different mechanisms.

Animals↗
PubMed1996

Method for determining distribution of reflection sites in the arterial system.

We developed a new method to determine the location and importance of reflection sites in the arterial system. The method is based on the decomposition of the aortic pressure wave into its forward and backward components, and it provides the reflection profile of the arterial system as a wave reflection site amplitude versus distance from the heart. The reflection profile can be seen as the response of the arterial system to a pressure delta pulse where reflections upstream from the measurement location have been eliminated. The method was successfully tested on a simple model loaded with a pure resistor, a two-element windkessel, and a bifurcating tube system. It was then applied to the aortic pressure and flow signals measured in six mongrel dogs whose aorta was occluded at different levels. The profiles obtained from measurements at control showed two main reflection regions, one located in the vicinity (0.1-0.2 m) of the heart and the other located in the region of the iliac bifurcation. All occlusions, even the most distant one at the iliac bifurcation, could be identified in both amplitude (amount of reflections) and distance from the heart. The spatial resolution of the profiles was approximately 0.1 m as a result of the limited power spectrum contained in the arterial pulse, and the identification of reflection sites decreased rapidly with the distance.

Animals↗
PubMed1996

Bisferiens peaks in the radial artery pressure wave during patent ductus arteriosus in newborn infants: relationship with ascending aortic flow.

Previously, we found evidence that bisferiens peaks in the radial artery pressure wave in the newborn infant may suggest the presence of a left-to-right shunt through a patent ductus arteriosus (PDA). The purpose of the present study was to analyze the origin of this pulsus bisferiens. Starting from the assumption that the radial artery pressure wave form is similar to the aortic pressure wave form, as described previously, we attempted to explain the bisferiens peaks on the basis of echocardiographically obtained ascending aortic flow. We studied 11 preterm mechanically ventilated infants with a left-to-right shunt through a PDA and 7 without. Aortic volume flow was established echocardiographically, and radial artery blood pressure measurement was performed with a high fidelity cathetermanometer system. Ascending aortic peak flow during PDA was significantly higher in the case of PDA, compared with the case without PDA. An augmented peak flow with an abrupt decline after the high peak in PDA, resulting in a sharp pressure peak with a steep decline after the peak, was thought to explain the first sharp peak of pulsus bisferiens. An abrupt decline of flow after peak flow is thought to be due to the fast runoff of blood through the ductus. According to the pulsatile pressure dynamics theories, which state that pressure wave forms consist of forward and backward wave forms, the second peak of the pulsus bisferiens can be explained by the return of the reflected (backward) wave form when the forward wave form has already considerably decreased. We conclude that the bisferiens peaks found in PDA result from a combination of large stroke volume (augmented first peak) and large runoff (quick decline of the forward wave) before the return of the reflected wave.

Aorta↗
PubMed1995

In vivo validation of magnetic resonance blood volume flow measurements with limited spatial resolution in small vessels.

The accuracy of magnetic resonance phase contrast volume flow measurements in small blood vessels is expected to be smaller than in large vessels, because of partial volume effects at the vessel boundary. Accuracy was validated in the dog femoral artery, diameter 3.5 +/- 0.7 mm, using an ultrasonic transit-time flowmeter (TT). The number of pixels per vessel diameter (ND) ranged from 1.6 to 4.8. The vessel cross-section was determined using a threshold in the magnitude image. Between the two methods the correlation coefficient was 0.95 (range 10-200 ml/min). The proportional difference (PD), (QTT-QMR)/1/2(QTT+QMR), was 0.8%, showing no systematic difference between the methods. The PDs standard deviation was 27%, and 19% for flow rates above 30 ml/min. Only a significant decrease of the PDs variance was found at the highest ND values, suggesting other sources of error than partial volume effects. It is concluded that with an ND value of about 3, accurate blood volume flow rates can be determined.

Animals↗
PubMed1995

Haemodynamic basis for the development of left ventricular failure in systolic hypertension and for its logical therapy.

In youth, properties of the human arterial system are such that pulse pressure generated by ventricular ejection is low, and the major component of wave reflection returns to the heart after the aortic valve has shut, so making no contribution to ventricular load, but boosting pressure throughout diastole and so aiding coronary perfusion. That constitutes optimal arterial function and optimal vascular/ventricular interaction. With ageing, the aorta and elastic arteries stiffen, so that aortic pulse pressure is markedly increased. This is a consequence of a direct stiffening effect on the aorta itself, and of an indirect effect caused by early return of wave reflection consequent upon stiffening of the whole arterial system with an increase in its pulse wave velocity. There is a change in contour of the aorta pressure wave with wave generation of a late systolic peak and disappearance of the diastolic wave; the reflected wave moves from diastole and systole. Because the lowest diastolic pressure remains relatively constant [1,10], increased pulse pressure causes a substantial increase in aortic systolic pressure. Increased aortic systolic pressure is associated with increased left ventricular pressure and leads to left ventricular hypertrophy. Sustained elevation in systolic pressure and persistent left ventricular hypertrophy are associated with progressive degenerative changes in the hypertrophied myocytes such that these weaken, developing less force with each contraction. The weakened, hypertrophied fibres lengthen and the ventricle dilates, with force and cardiac output initally being maintained at greater muscle length and ventricular volume through the Frank-Starling mechanism. Ultimately compensation is lost. The hypertrophied ventricle normally functions as a flow source, which is capable of generating flow even against very high pressure. With the development of cardiac failure through muscle weakening, the ventricle comes to act as a pressure source, with ventricular output very sensitive to pressure and to changes in pressure. The normal ventricle functions in an intermediate position, even though it is closer in behaviour to a flow than to a pressure source. Wave reflection adds to pressure but subtracts from flow. In youth, wave reflection returns to the heart during diastole when the aortic valve is shut. Negative flow is not possible, so wave reflection is apparent only as a secondary pressure wave in the ascending aorta. In older subjects, when the left ventricle is beating powerfully, return of wave reflection during systole has less obvious an effect on the ascending aortic flow wave, but causes an obvious secondary boost to pressure in the ascending aorta and left ventricle. Hence, under normal circumstances, wave reflection at the heart is apparent as a positive secondary pressure wave, either because the aortic valve is shut when this wave returns, or because the ventricle possesses enough power that it virtually overcomes any negative influence on flow when reflection returns during systole. When the myocardium weakens and the heart fails, the heart starts to behave like a pressure source, and wave reflection starts to have a far greater effect on flow; wave reflection is manifested more as a negative influence on flow than as a positive influence on pressure. As heart failure develops, there is a progressive change in flow wave contour, with early deceleration of aortic flow and ultimately, abbreviation of systolic ejection duration with fall in stroke volume. Early wave reflection is the major factor in the genesis of systolic hypertension. Early wave reflection remains a major factor when heart failure develops, although its effect is apparent in reduction of late systolic flow rather than as a boost to late systolic pressure. Reduction in wave reflection through use of vasodilatory agents is a logical strategy in treatment of systolic hypertension. That type of therapy is equally logical in treatment

Animals↗
PubMed1995

Effect of perfusion pressure on diastolic stress-strain relations of isolated rat papillary muscle.

The effect of perfusion on diastolic muscle properties was investigated in six isolated right ventricular papillary muscles from rat hearts perfused with a crystalloid solution via the septal artery. Stress-strain relations were obtained at different perfusion pressures. Increased perfusion pressure caused an increase of stress at large strains but a decrease of stress at low strains. Thus stress-free strain increased with increasing perfusion pressure. Stress-strain relations of a given muscle at different perfusion pressures (range 12-122 cmH2O) intersected at a single "crossover" strain. Muscle stiffness, defined as the slope of the stress-strain relation, increased at all strains. Muscle diameter measurements indicated that the observed changes of the stress-strain relation occurred in association with vascular filling rather than with formation of edema. To explain the findings, the papillary muscle was modeled by two parallel compartments: muscle cells (together with the extracellular matrix) and vasculature. Perfusion was assumed to have an effect on the axial vascular properties but not on muscle cells. Combination of the stress-strain data of the muscle compartment and the vascular compartment (taken from literature) predicted stress-strain relations similar to those obtained in our perfused papillary muscles. We conclude that increased muscle stiffness at increased perfusion pressure is mainly caused by pressure-dependent changes in mechanical behavior of the vascular compartment.

Animals↗
PubMed1995

Evaluation of methods for estimation of total arterial compliance.

Seven classic and recently proposed methods used for the estimation of total arterial compliance have been evaluated for their accuracy and applicability in different physiological conditions. The pressure and flow data are taken from a computer model that provides realistic simulations of the nonlinear-distributed systemic arterial tree. Besides the great flexibility in simulating different physiological or pathological cases, the major advantage of the computer model is that it allows precise knowledge of the pressure-dependent total arterial compliance, which is the variable of interest. The results show that the methods based on the two-element windkessel (WK) model are more accurate than those based on the three-element WK model. The classic exponential decay and the diastolic area method yield essentially similar results, and their compliance estimates are accurate within 10% except at high heart rates. The later part of diastole, i.e., from the time that the systolic pressure wave has reached all peripheral beds, gives the best results. The newly proposed two-area and pulse pressure methods, both based on the two-element WK model, are accurate (errors in general < 10%) and can be applied to other locations in the arterial tree where the decay time and area method cannot. Methods based on the three-element WK model consistently overestimate total arterial compliance (> or = 25%). The errors in the methods based on the three-element WK model arise from the fact that the input impedance in that model deviates significantly from the true input impedance at low frequencies. The strong dependence of compliance on pressure (elastic nonlinearity) does not invalidate the compliance estimates.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Modeling pressure-area relations of coronary blood vessels embedded in cardiac muscle in diastole and systole.

Pressure-cross-sectional area (P-A) relations of a (thick-walled) arteriole and (thin-walled) small vein (both maximally dilated), embedded in cardiac muscle in both static systole and diastole at slack length and at 90% of maximal length (Lmax), were calculated. The elastic properties of cardiac muscle and vessel wall per se were taken into account. Muscle fibers and vessels were assumed to run in parallel. The muscle tissue (fibers + collagen) was assumed to be incompressible, homogeneous, nonlinearly elastic, and transversely isotropic. Cross-fiber stress-strain relations were assumed to be proportional to those in fiber direction. It is predicted that cardiac muscle in diastole has little effect on the P-A relation of the arteriole but strongly affects that of the small vein. In systole, the myocardium strongly affects the P-A relations of both vessels. Isometric transition from static diastole to static systole (isometric "contraction") was found to reduce arteriolar and venous area (at constant pressures of 35 and 7 mmHg, respectively) by approximately 50 and 40, respectively. Contraction with a 14% shortening was found to reduce these areas by 48 and 32%, respectively. The differences in the results for the two vessels were found to be determined mainly by their difference in the ratio of outer to inner radius. Furthermore, it was found that the area reductions are much larger for contractions (with or without shortening) than for muscle stretch per se. It is concluded that the change in elastic properties and, more specifically, development of stress in cross-fiber direction of the cardiac muscle during contraction causes the area reductions of coronary vessels.

Animals↗
PubMed1995

Scatter in input impedance spectrum may result from the elastic nonlinearity of the arterial wall.

We have examined the role of the nonlinear elastic properties of the arterial wall on the human aortic input impedance obtained at different heart rates and different pressure and flow wave shapes. Pressure and flow were taken from a computer model that provides realistic simulations of the nonlinear distributed systemic arterial tree. Different wave shapes of ascending aorta pressure and flow and different heart rates were used to derive input impedance moduli and phase angles via Fourier analysis. The results show that the nonlinear elastic properties of the arterial wall are responsible for significant variations in the input impedance spectrum when changes in heart rate and aortic flow wave shape take place. This finding may explain the scatter often observed in experimentally determined input impedance data using different heart rates obtained by pacing.

Arteries↗
PubMed1995

Bisferiens peaks in the radial artery pressure wave in newborn infants: a sign of patent ductus arteriosus.

Previously, we found evidence that radial artery pressure wave forms in newborns represent central aortic wave forms, provided that pressure is measured with adequate accuracy. Therefore, we postulated that the neonatal radial artery wave form, like the adult aortic wave form, may contribute to cardiovascular diagnosis. We investigated whether radial artery wave forms in infants suffering from patent ductus arteriosus (PDA) are different from the wave forms as seen without the presence of PDA. We studied 34 newborn infants with a radial artery line and with the possible clinical diagnosis of PDA with left-to-right shunt. On the basis of echocardiographic examination to assess PDA, these infants were divided in two groups: infants with PDA (n = 24) and without PDA (n = 10). In 15 out of 24 infants with PDA, recordings were repeated after ductal closure. Blood pressure measurement was performed with a high fidelity cathetermanometer system using a tip-transducer (natural frequency 95 Hz, damping coefficient 0.15). Contour analysis was performed by describing morphology of the waves during PDA and without PDA. In 23 out of 24 infants with PDA, a pulsus bisferiens was present: two peaks separated by a deep cleft. The average pressure difference between the first pressure peak and the cleft [delta Ppeak1] was 0.35 +/- 0.19 kPa, and the average difference between the cleft and the second pressure peak [delta Ppeak2] was 0.44 +/- 0.23 kPa. the ratio of mean magnitude of delta Ppeak1 and delta Ppeak2 was 0.81 +/- 0.26. None of the 10 infants without PDA showed pulsus bisferiens.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1994

Local mitochondrial enzyme activity correlates with myocardial blood flow at basal workloads.

To study whether heterogeneous myocardial blood flow relates to the local oxidative capacity of cardiac muscle, local blood flow at resting cardiac workloads and the activity of the mitochondrial enzyme succinate dehydrogenase (SDH) were determined in small regions of the left ventricle of seven anaesthetized, mechanically ventilated, open-chest pigs (25-35 kg). Following injection of radioactive microspheres (15 microns phi) into the left atrium, the heart was rapidly excised and cut into five transverse slices, which were simultaneously freeze-clamped between two aluminum blocks precooled at -80 degrees C. The left ventricle was then subdivided into 84 samples of about 0.9 g. Myocardial blood flow was 0.88 +/- 0.34 ml/min/g wet weight (ww), and SDH activity 1.46 +/- 0.33 mumol/min/g ww (mean +/- S.D., n = 7). Local data were normalized to their respective mean values in each pig, and then pooled. Local blood flow ranged from 0.32 to 1.63 of the mean, and blood flow heterogeneity characterized by the coefficient of variation (CV = S.D./mean) was 18.4%. Normalized local SDH activity ranged from 0.16 to 1.94, with a CV of 21.8%, significantly exceeding measurement error (CV = 4.5%). Local blood flows and SDH activities did not vary among transmural sublayers of the left ventricle, but variation within each sublayer was considerable. In six of the seven pigs, local blood flow correlated (P < 0.05) with SDH activity, with correlation coefficients (r) ranging from 0.26 to 0.54 (for pooled data: r = 0.27, P < 0.0001). When expressed per gram dry weight, heterogeneity of SDH activity increased (P < 0.05), and here also local blood flow correlated with SDH activity in all pigs (for pooled data: r = 0.45, P < 0.0001). Hence, heterogeneity of mitochondrial capacity within cardiac muscle partly explains the heterogeneity of myocardial blood flow, even though myocardial perfusion at rest was studied in relation with a maximal enzyme rate. The low correlation coefficient clearly indicates that at resting workloads other factors also play a role.

Animals↗
PubMed1994

The microvascular unit size for fractal flow heterogeneity relevant for oxygen transport.

In this study we used a computer model for oxygen transport in heterogeneously perfused tissue to define the microvascular unit size of relevance to oxygen transport. Flow within this unit is presumably heterogeneous, but this internal heterogeneity is by definition of negligible importance for the oxygen tension distribution. In saline-perfused heart the linear dimension of the thus defined unit is 500 microns, in blood-perfused heart it is 100 microns.

Animals↗
PubMed1994

Function of isolated rabbit hearts perfused with erythrocyte suspension is not stable but improvement may be feasible with hemoglobin solution.

In the present study isolated rabbit hearts were perfused with erythrocyte suspensions (hematocrit 21.5 +/- 0.5%) or hemoglobin solutions according to Langendorff with a constant flow at 37 degrees C. In preliminary experiments three types of stroma-free hemoglobin were used: unmodified, but carefully purified, stroma-free hemoglobin (SFHb), HbNFPLP which is a chemically modified Hb molecule and polyHbNFPLP which is a polymer of HbNFPLP. In hearts perfused with erythrocyte suspensions left ventricular developed pressure and oxygen consumption decreased and perfusion pressure increased steadily from the beginning of the perfusion. Dark spots appeared on the surfaces of these hearts, which were the result of extravasation of erythrocytes. As a consequence capillaries probably became obstructed, leading to reduced cardiac function. Hearts perfused with stroma-free hemoglobin solutions showed an initial increase in left ventricular developed pressure after switching from Tyrode perfusion to perfusion with hemoglobin solutions. Left ventricular developed pressure and perfusion pressure were stable for about 2 hours in hearts perfused with SFHb and were reasonable for 2 hours when the heart was perfused with HbNFPLP or more than 4 hours with polyHbNFPLP. More extensive experiments with stroma-free hemoglobin solutions when these become available in sufficient quantities have, according to the results from preliminary experiments, the potential of showing good oxygen supply resulting in reasonable cardiac function.

Animals↗
PubMed1994

Vasomotor tone affects diastolic coronary flow and flow impediment by cardiac contraction similarly.

We studied the effect of cardiac contraction on coronary arterial flow with vasomotor tone (control) and during maximal vasodilation with adenosine in the isolated blood-perfused rat heart at constant perfusion pressure (105 mmHg) with a left ventricular balloon (n = 6). Ventricular pressure was changed by volume changes and contractility via postextrasystolic potentiation. Contractility was expressed as the slope of the end-systolic pressure-volume ratio, elastance. Constant vasomotor tone was judged from stable diastolic flow. Coronary flow reduction (diastolic minus systolic flow, delta CBF, ml.min-1.g-1) due to contraction was related to developed ventricular pressure (devPLV) and developed elastance (devELV, systolic minus diastolic elastance) by multiple regression: delta CBF = SP.devPLV+SE.devELV+I, where SP and SE represent changes in coronary blood flow due to changes in devPLV and devELV, respectively, and I is intercept. In control, delta CBF = (0.016 +/- 0.008).devPLV + (0.0022 +/- 0.0009).devELV + (0.29 +/- 0.77); during vasodilation, delta CBF = (0.046 +/- 0.011).devPLV + (0.009 +/- 0.0053).devELV + (2.50 +/- 2.56). Diastolic flow increased by a factor of 4.06 +/- 1.57 (SD) during vasodilation. The increases in diastolic flow, SP, and SE were not different. We conclude that vasodilation has similar effects on diastolic flow and flow amplitude without affecting the relative contributions of ventricular pressure and contractility.

Animals↗
PubMed1994

Measurement of aortic input impedance in rats.

Measurement of aortic input impedance in the rat is complicated by a high basal heart rate but is possible if appropriate compensation is made for frequency-dependent errors in modulus and phase resulting from analog filters in the equipment and from nonalignment of pressure and flow sensors. Because input impedance is a complex quantity, accurate values for both phase and modulus are required before meaningful interpretation of the data can be made. We measured aortic pressure and electromagnetic ascending aortic blood flow in mature, ether-anesthetized, open-chest male Wistar rats. Pressure and flow waveforms were averaged in the time domain and converted to Fourier series. Flow moduli were corrected for the measured frequency response of the flowmeter. Phase spectra were corrected by the classic frequency-domain and two new time-domain methods. Compensation for instrumentation errors was assessed at two different flowmeter filter settings in five animals. Reproducibility, variability, and the effects of vasoconstriction were assessed in 43 animals. Three methods of estimating characteristic impedance from the impedance spectra were evaluated and found to produce comparable results at baseline and following pharmacological elevation of blood pressure with graded methoxamine infusion. Physiologically equivalent values for phase, as assessed by comparing oscillatory power calculated from the impedance spectra, were obtained with each of the phase-correction techniques. The new time-domain methods facilitate the assessment of aortic input impedance in this small animal model because they do not require measurement of the spatial separation between pressure and flow transducers and pulse wave velocity in the proximal aorta.

Analysis of Variance↗
PubMed1994

Relationship between strength of short-term systemic autoregulation and initial resistance.

The relationship between strength of short-term whole body autoregulation and peripheral resistance in the reference state (initial resistance) was investigated in 9 anesthetized closed-chest dogs and 18 anesthetized open-chest cats. Baroreflex regulation was abolished in one of three ways: barodenervation, ganglionic blockade, or setting pressure constant in the isolated carotid sinuses after vagotomy. Ascending aortic pressure and flow and venous pressure were measured in the reference state and 1-3 min after partial occlusions of the inferior vena cava. Cardiac output and peripheral resistance (ratio between arteriovenous pressure difference and cardiac output) were normalized for body weight. Strength of autoregulation was quantified by a resistance gain (Gra), defined as the ratio between change in normalized peripheral resistance and corresponding change in normalized cardiac output. A broad range of values for peripheral resistance in the reference state (Ro) was obtained as a result of the different interventions used to abolish baroreflex regulation. Arteriovenous pressure difference and normalized cardiac output during multiple vena cava occlusions in the 9 dogs and in 8 of the cats were fitted with a parabola convex to the flow axis. From the best fit, Gra was estimated. In the remaining 10 cats Gra was estimated from a single occlusion of vena cava. When data of all dogs and cats were taken together, we found a linear relationship between Gra and Ro: Gra = K1.Ro + K2. The constants K1 and K2 were 17.9 x 10(-3) min.kg.ml-1 and -14.5 x 10(-3) mmHg.min2.kg2.ml-2, respectively. The correlation coefficient was 0.9.

Animals↗