Biomedical subjects

E VanBavel

Publications and source records attributed to E VanBavel.

23 records · Page 2Linked to original sources

PubMed1994

Compliance of isolated porcine coronary small arteries and coronary pressure-flow relations.

Compliance of small arteries is important for the interpretation of arterial pressure-flow relations. Six coronary small arteries (mean diameter 189 +/- 46 microns) were cannulated. Pressure-cross-sectional area (CSA) relations were obtained from isolated vessels by slowly varying pressure between 10 and 120 mmHg. Subsequently, small pressure variations were superimposed on constant mean pressures of 10, 30, and 50 mmHg with frequencies of 0.1-10 Hz. Normalized compliance (C0) was calculated as the compliance divided by the CSA at 50 mmHg. In vessels without tone, static C0 was 27.5 +/- 8.9, 6.4 +/- 1.1, and 3.8 +/- 1.0 x 10(-3) mmHg-1 at 10, 30, and 50 mmHg, respectively. At a frequency of 0.1 Hz, C0 decreased to one-third of static C0 at any pressure. Under these conditions, the phase shift between pressure and CSA was rather constant and ranged from -21 to -5 degrees. In four small arteries, smooth muscle tone was induced by the administration of acetylcholine. Activation decreased dynamic C0 by 60%. Two models of coronary input impedance were evaluated: the first model includes viscoelastic properties of the arterial wall and the second takes into account the blood inertia effect. The second model predicts much better the wall mechanics of single small arteries. The viscoelastic model overestimates the frequency dependence of compliance by a factor of 2 and the phase lag by a factor of 4. Moreover this model predicts a strong frequency dependence of induction of tone on compliance and phase lag, whereas this dependence is absent in the experimental results.

Animals↗

PubMed1992

Branching patterns in the porcine coronary arterial tree. Estimation of flow heterogeneity.

The aim of this study is to quantify the porcine coronary arterial branching pattern and to use this quantification for the interpretation of flow heterogeneity. Two casts of the coronary arterial tree were made at diastolic arrest and maximal dilation. The relation between length and diameter of arterial segments was quantified, as well as the area expansion ratio and diameter symmetry of vascular nodes. These relations were used to construct computer models of the coronary arterial tree, covering diameters between 10 and 500 microns. Topology of these simulated trees was analyzed using Strahler ordering: Bifurcation ratio, diameter ratio, and length ratio were constant along orders 2-8 and equal to 3.30, 1.51, and 1.63, respectively. In each order, the number of segments per Strahler vessel was almost geometrically distributed. For the lowest orders, these predictions were confirmed by direct observations. From the network model, local pressure and flow were also predicted: Pressure fell from 90 to 32 mm Hg at the 10-microns level. The coefficient of variation (CV) of flow in individual segments was dependent on the number of perfused terminal segments (Nt) according to the fractal relation CV(Nt) approximately Nt(1-D), where D is the fractal dimension (1.20). CV of flow in 1-g tissue units was predicted to be 18%. This study shows that the structure of the coronary arterial bed is an important determinant of the fractal nature of local flow heterogeneity.

Animals↗

PubMed1991

Influence of pressure alterations on tone and vasomotion of isolated mesenteric small arteries of the rat.

1. Myogenic responses may account for control of organ blood flow. The study of these responses without interference from the organ requires an isolation technique for vessels which contribute significantly to flow resistance. This study reports on experiments on isolated small mesenteric arteries. 2. Distal rat mesenteric arcade arteries and first-order branches (diameter range 145-365 microns, mean 293 microns) were manually dissected and cannulated using a double-barrelled micro-cannula. Luminal cross-sectional area of these vessels was continuously monitored by means of a fluorescence technique. 3. Nine out of eighteen vessels developed basal tone at 80 mmHg distending pressure, resulting in a 45.2 +/- 5.1% (mean +/- S.E.M) decrease of cross-sectional area. Tone was induced in the other vessels by 0.3-1 microM-noradrenaline, resulting in a 59.5 +/- 7.1% decrease in cross-sectional area. 4. In vessels with either spontaneous or induced tone, stepwise changes of pressure resulted in passive effects, followed by myogenic responses. 5. Steady-state pressure-cross-sectional area relations of vessels with basal tone showed a significant negative slope (-0.5% mmHg-1), while pressure-cross-sectional area relations of vessels with induced tone were essentially flat between 40 and 120 mmHg. 6. Five vessels with basal tone and eight vessels with induced tone developed vasomotion at 80 mmHg. Frequencies of spontaneous and induced vasomotion were 14 (range 4-31) and 21 (9-25) cycles min-1 respectively. Amplitudes were 5 (1-10) and 8 (3-17)% of the passive cross-sectional area. In both groups, frequency was positively, and amplitude negatively correlated with pressure. 7. These data show that myogenic responses are induced by wall stress, rather than by distension of the vascular wall. Basal tone is not a prerequisite for the appearance of myogenic responses.

Animals↗

PubMed1990

Cannulation and continuous cross-sectional area measurement of small blood vessels.

Techniques have been developed for the study of isolated small arteries. To pressurize and perfuse segments of these vessels, a cannula with a low resistance to flow was developed. This cannula consisted of two concentric micropipettes. The end of a vessel segment was sucked into the inner pipette and clamped by applying subatmospheric pressure on the outer pipette. Subsequently, the vessel was pressurized via the inner pipette. To enable perfusion, the segment was cannulated at both ends. Mean cross-sectional area (CSA) of the cannulated segments was continuously measured using a fluorescence technique. The emission of light by fluorescein isothiocyanate (FITC) labeled dextran in the vessel lumen was measured using a photomultiplier tube (PMT). PMT current was linearly related to the vessel CSA. Twenty-nine rat mesenteric vessels with inside diameters ranging from 110 to 350 microns (mean 226 microns) when maximally dilated at 80 mm Hg were cannulated. CSA was monitored during variations in perfusion pressure and addition of vasoactive agents.

Animals↗

PubMedDate not supplied

Voltage-operated calcium channels are essential for the myogenic responsiveness of cannulated rat mesenteric small arteries.

The role of L-type voltage-operated Ca2+ channels (VOCs) in myogenic responsiveness was studied in cannulated rat mesenteric small arteries [mean diameter at 100 mm Hg and full dilation was 329 +/- 9 (SE) micrometer]. Twenty-six arteries were cannulated and pressurized. The luminal cross-sectional area of these vessels was monitored continuously. To test for myogenic responsiveness, pressure was raised stepwise from 20 to 60 and from 60 to 100 mm Hg. Pressure elevation enhanced the vascular tone, reflecting spontaneous myogenic responsiveness. Nifedipine (1 and 10 microM) suppressed spontaneous myogenic responses. The alpha1-adrenoceptor agonist phenylephrine (1 and 10 microM), when administered at 20 mm Hg, elicited constriction and vasomotion, and potentiated myogenic constriction to subsequent pressure elevation. Nifedipine (1 and 10 microM) also suppressed phenylephrine-potentiated myogenic responsiveness. Stimulation of VOCs with BAY K 8644 (10-300 nM) had no effect at 20 mm Hg, but augmented myogenic responsiveness. K+ (16-46 mM) caused concentration-dependent constrictions when administered at 20 mm Hg, and potentiated myogenic responsiveness when the pressure was raised from 20 to 60 mm Hg. Thus, any intervention that blocked the VOCs also blocked myogenic responses. Therefore, we conclude that VOCs are essential for the myogenic responsiveness of cannulated rat mesenteric small arteries.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗