(Hypertension. 1996;28:115-119.)
© 1996 American Heart Association, Inc.
Articles |
Reduced Distensibility of the Common Carotid Artery in Patients Treated With Ergotamine
the Departments of Medicine D (M.B., C.S., J.W., K.H.R., W.Z.) and Neurology (S.E.), University of Munster (Germany), and Cardiovascular Research Institute, University of Limburg (the Netherlands) (A.P.G.H.).
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
To investigate the effect of vascular smooth muscle contraction on mechanical vessel wall properties of proximal "elastic" arteries, we investigated the effect of the vasoconstrictor ergotamine on the distensibility of the common carotid artery in 10 migraine patients with ergotamine intake, in 10 control patients with migraine headache but no prior ergotamine intake, and in 10 healthy control subjects. The patients and control subjects were matched for age, blood pressure, and sex. In the ergotamine group, 2.2±1.4 mg ergotamine tartrate (0.25 to 6 mg) was taken within 12 hours before investigation. Differences in mean 24-hour blood pressure between the study groups were excluded by 24-hour blood pressure recording and differences in arterial wall thickness by high-resolution B-mode ultrasound. A multigate Doppler system was used for measurement of vessel wall movements by M-mode Doppler analysis. Blood pressure was determined by sphygmomanometry. The end-diastolic diameter of the common carotid artery was insignificantly reduced in the ergotamine group compared with the healthy control subjects and control patients (healthy control subjects, 6.6±0.4 mm; control patients, 6.7±0.5 mm; patients with ergotamine intake, 6.3±0.4 mm; P=NS). Arterial distensibility was significantly lower in the patients with ergotamine intake (17.4±4.0 10-3/kPa) than in the healthy control subjects (22.3±5.1 10-3/kPa) and control patients (22.8±3.6 10-3/kPa) (one-way ANOVA, P=.014). The results show that ergotamine reduces the distensibility of the common carotid artery. The data suggest that vascular smooth muscle contraction can modulate the buffering function of the arterial system independently of blood pressure changes.
Key Words: compliance • arteries • ergotamine • muscle, smooth, vascular
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Arterial compliance plays an important role in cardiovascular hemodynamics by damping down the fluctuation in arterial pressure and blood flow generated by the intermittent cardiac output.1 Stiffness of large arteries impairs the buffering function of the arterial system, leading to a disproportionate increase in systolic pressure and increase in pulse pressure at any given value of mean arterial pressure.2 3 Furthermore, the impaired buffering function contributes to the afterload imposed on the heart, leading to left ventricular hypertrophy.4
Several studies have shown that arterial compliance is decreased in patients with arterial hypertension.5 6 Reduced arterial compliance in hypertension has been related to increased distending blood pressure (BP) and to structural vessel wall changes. However, little is known about the role of vascular smooth muscle tone in the viscoelastic properties of large arteries. In the present study, we investigated the effect of the vasoconstrictor ergotamine on the vessel wall properties of the common carotid artery. Ergotamine can stimulate 
-adrenergic receptors in blood vessels and possesses a potent and long-lasting vasoconstrictive activity.7 8 The vasoconstrictive effect on arteries is relatively selective for the carotid arterial bed.7 In doses used in the treatment of migraine, ergotamine produces no or only little change in BP.9 Therefore, effects of vascular smooth muscle contraction on arterial distensibility independent of BP changes can be investigated in this model.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Vessel wall properties of the common carotid artery were determined in 10 migraine patients with regular ergotamine tartrate intake, in 10 migraine patients who had never taken ergotamine, and in 10 healthy control subjects. The study was performed in accordance with protocols approved by the local ethics committee, and the patients and subjects gave informed consent. In the ergotamine group, all patients had taken ergotamine tartrate within 12 hours before investigation. This protocol was chosen because despite a plasma half-life of about 2 hours, ergotamine produces vasoconstriction that endures for 24 hours or longer.9 10 The mean ergotamine dose taken within this period was 2.2±1.4 mg (range, 0.25 to 6 mg). The migraine patients with ergotamine intake were matched for age, BP, and sex with 10 migraine patients without prior ergotamine intake and with 10 healthy control subjects. In the group with ergotamine intake, all patients suffered from common migraine for an average of 12±8 years. In the group with no ergotamine intake, the patients had had headache attacks for 14±7 years. In this group, 9 patients suffered from common migraine and 1 from classic migraine with a visual aura. All patients included in the study were otherwise healthy. Arteriosclerotic disease or hypercholesterolemia, diabetes mellitus, renal failure, and heart failure were excluded by routine investigations. Asymptomatic arteriosclerotic plaques of the extracranial arteries were also excluded by ultrasound investigation. BP was determined by a mercury sphygmomanometer before enrollment into the study. BP measurements were based on three independent readings with subjects in a sitting position after a 10-minute rest. All individuals included had systolic BP below 140 mm Hg and diastolic BP below 90 mm Hg. Twenty-four-hour BP was recorded to exclude differences in mean 24-hour BP between the study groups. For this purpose, an automatic oscillometric BP recorder (SpaceLabs SL90207) was used. In the ergotamine group, all patients were on ergotamine at the time of 24-hour BP recording. BP was determined during the daytime (8 AM to 10 PM) at 15-minute intervals and during the nighttime (10 PM to 8 AM) at 30-minute intervals. The clinical characteristics of the study groups are shown in Table 1
.
|
Vessel wall properties of the common carotid artery were studied in the morning. After subjects had rested for 10 minutes in the supine position, the left common carotid artery was studied 2 cm below the bifurcation in a longitudinal projection with a multigate pulsed Doppler system (Cardiovascular Research Institute Maastricht).11 12 The probe was placed rectangularly on the vessel. In the multigate system, 64 sample volumes are spaced at 0.5-mm intervals. The observation range of 32 mm is sufficient for investigation of the carotid artery. Changes in vessel wall position can be monitored based on the low-frequency Doppler signals originating from the sample volumes coinciding with the anterior and posterior walls. The positions of the sample volumes are continuously adjusted according to the displacement of the wall. The Doppler signals in M-mode are temporarily stored and analyzed by a personal computer. The resolution for a 6.1-MHz Doppler system is equivalent to a displacement of 31.25 µm (assuming a speed of sound of 1525 m/s), which far exceeds the resolution capacity of a real-time scanner for static objects. Since both the recorded changes in diameter and the initial diameter similarly depend on the angle of observation, the ratio of both will be angle independent. The system allows the assessment of the relative change of major peripheral arteries as a continuous function of time, with an accuracy of about 0.5%. BP was determined on the brachial artery with a mercury sphygmomanometer before vessel wall movements were determined. With this noninvasive technique, the end-diastolic diameter (d [millimeters]) and systolic increase of vessel diameter (distension, 
d [micrometers]) were measured. From these data and from the systolic and diastolic BP (SBP, DBP), the relative systolic increase of vessel diameter (dxd-1 [%]) and the arterial wall distensibility coefficient (DC=2dxd-1x(SBP-DBP)-1 [10-3/kPa]) were calculated.13 The coefficients of variation were 3.4% for end-diastolic diameter, 7.4% for the relative systolic increase of vessel diameter, and 10.8% for the distensibility coefficient (n=15). For estimation of long-term variability, the distensibility coefficient of the common carotid artery was determined in 30 patients and the measurement was repeated after 2 years. Although arterial distensibility depends on the actual BP level, there is a close correlation between the distensibility coefficient after 2 years compared with the baseline value (n=30, r=.84, P<.001).
In 8 of 10 patients treated with ergotamine and the corresponding control subjects, intima-media thickness of the arterial wall was determined with an 8-MHz high-resolution B-mode ultrasound system (2000 II s.a., Biosound Inc). The ultrasound methods for carotid artery imaging are based on the technique described by Pignoli et al.14 Briefly, three arterial interfaces can be demonstrated by ultrasound scan. The first is the intima-lumen interface, the second the media-adventitia interface, and the third the adventitia interface. In a normal vessel, the combined thickness of the intima-media is approximately 0.8 mm. In the present study, intima-media thickness was measured at the far and near walls of the common carotid artery 2 cm below the carotid bifurcation. The arterial wall was scanned from anterior, lateral, and posterior angles, and mean intima-media thickness was calculated from six arterial segments.
Short-term variability of systolic and diastolic BPs and of heart frequency in the migraine group with ergotamine treatment and the group of healthy control subjects was estimated for evaluation of the influences of sympathetic tone on the vascular changes.15 For assessment of short-term BP and heart rate variation, the absolute (standard deviation) and percent (variation coefficient) variabilities of BP and heart rate recorded over a half-hour period were calculated.16 BP and heart frequency were therefore measured beat to beat by finger plethysmography (Finapres) for 30 minutes after subjects had rested supine for at least 10 minutes. The Finapres operates through a small finger cuff and has an infrared photoplethysmograph to measure arterial blood volume.17 Arterial blood volume is clamped at a set point value corresponding to two thirds of the maximal arterial blood volume. This volume-clamp set point is periodically adjusted at zero transmural pressure, and therefore, the cuff pressure continuously reflects the intra-arterial BP.17
Values are given as mean±SD. The parameters of vessel wall properties were tested for statistical significance by one-way ANOVA with a Bonferroni test as posttest. The t test was used for comparison of short-term BP and heart rate variation and the intima-media thickness of patients treated with ergotamine and healthy control subjects. Statistical significance was accepted at a value of P<.05.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The clinical characteristics of the different study groups are shown in Table 1
. Twenty-four-hour BP recording did not reveal different BP levels between the three study groups, with mean systolic and diastolic 24-hour BPs and mean BP during the daytime and nighttime being comparable between the groups (Table 1).
The BPs obtained by sphygmomanometer before registration of vessel wall movements and the vessel wall parameters for the different study groups are shown in Table 2. Systolic and diastolic BPs were similar between the groups with and without ergotamine intake and the control group. No significant BP difference was observed between the control group and the migraine group with no ergotamine intake. Vessel wall properties of the common carotid artery were also comparable between the control group and the migraine group with no ergotamine intake. There was no difference in end-diastolic diameter, absolute and relative distension, and distensibility coefficient of the common carotid artery between the groups (Table 2).
|
The end-diastolic diameter of the common carotid artery was slightly lower in the ergotamine group than in the control group. End-diastolic diameter was also reduced in the ergotamine group compared with the migraine group with no ergotamine intake. However, the differences in vessel diameter failed to reach statistical significance (Table 2).
The absolute distension of the common carotid artery was significantly lower in the ergotamine group than in the control group. A significant difference of the absolute distension was also found between the ergotamine group and the migraine group without ergotamine intake. (Table 2). The relative distension was also significantly reduced in the ergotamine group compared with the healthy control subjects or with the migraine group without ergotamine intake.
The distensibility coefficient of the common carotid artery was significantly reduced in the group with ergotamine intake compared with the control group. This was also true for the difference of the distensibility coefficient between the ergotamine group and the migraine group without ergotamine intake (P=.014, Table 2, Fig 1).
|
The intima-media thicknesses of the common carotid artery for the patients treated with ergotamine and the corresponding control subjects are shown in Fig 2. Intima-media thickness of the common carotid artery did not differ significantly between these groups. The ratio of diameter to intima-media thickness also was not significantly different between the ergotamine and control groups.
|
Short-term variabilities of systolic and diastolic BPs and of heart rate for the migraine group treated with ergotamine and the healthy control subjects are shown in Table 3. Absolute and percent variabilities of systolic and diastolic BPs and heart rate did not differ between these groups.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
In the present study, we investigated the effect of vascular smooth muscle contraction on the mechanical vessel wall properties of proximal "elastic" arteries. Ergotamine can stimulate
-adrenergic receptors and has a constrictive effect on arteries that is relatively selective for the external and also for the common carotid artery. Furthermore, in doses used for migraine therapy, ergotamine has no or only little effect on BP.7 8 9 The data of the present study demonstrate that ergotamine can induce a significant reduction of the distension of the common carotid artery. The decrease of arterial distensibility is probably not influenced by changes in distending pressure because BP levels were similar in the patients with ergotamine intake and the control patients compared with the healthy control subjects. The results therefore provide evidence that vascular smooth muscle activity can influence the mechanical properties of proximal "elastic" arteries. Modulators of vascular muscle tone, such as sympathetic stimulation, may thus influence the buffering function of large arteries independently of their BP effects. Alternatively, not only active contraction of vascular smooth muscle may explain the observed changes in arterial distensibility. Since the patients studied were under long-term treatment with ergotamine, structural changes in the vessel wall must be taken into account. Either an increase in connective tissue or hypertrophy of vascular smooth muscle could explain the decreased distensibility. However, the possibility that the observed decrease in distensibility is due to an increased wall thickness was excluded by high-resolution B-mode echography. Finally, alterations in shear stress due to changed blood flow in contracted vessels may be involved in the pathogenesis of decreased distensibility.18 19
In general, the viscoelastic properties of the arterial wall depend on a passive component due to elastic and collagenous connective tissue and on an active component due to smooth muscle activity.1 6 The aorta and other major branches such as the common carotid artery are from the "elastic type," with a higher proportion of elastic fibers and only a small quantity of vascular smooth muscle cells.1 Thus, an increased vascular smooth muscle tone should result in only minor changes of distensibility in "elastic" arteries. Nevertheless, animal studies have provided evidence that vascular smooth muscle tone can influence the vessel wall properties of larger arteries. Benetos et al20 used an experimental model of in situ isolated carotid arteries to investigate the role of adrenergic tone in common carotid artery compliance in younger and older rats. Stimulation of -adrenoceptors with phenylephrine decreased carotid artery compliance in older but not in younger rats. Blockade of adrenoceptors with prazosin or labetalol increased the compliance in younger and had no effect in older rats. ß-Adrenoceptor stimulation with isoproterenol had no effect on arterial compliance in both groups. Differences in basal adrenergic tone may explain these age-related responses. Several animal studies reported conflicting results regarding the effect of vascular smooth muscle contraction on vessel wall properties. Some studies demonstrated that in vitro vascular smooth muscle activation decreases vessel distensibility,21 22 and others showed that vascular smooth muscle activation increases vessel distensibility.23 24 These conflicting reports can be explained by the fact that the mechanical vessel wall properties of large arteries have to be defined at a given diameter and at distending pressure.25 At low pressures, mechanical properties of large arteries mostly depend on those of elastic fibers.26 As pressure increases, mechanical properties become strongly conditioned by the properties of elongated elastin and collagen fibers, which are being recruited to support the increasing load.26 27 On the other hand, vessel constriction may induce connective tissue retraction, resulting in a reduction in passive stiffness that may exceed the increase in stiffness induced by a higher vascular smooth muscle tone.28 However, the results of most animal studies are restricted to the fact that the data have been obtained from in vitro experiments or from in vivo investigations after surgical exposure of the vessel. It has been shown that even gentle dissection of an artery can reduce its compliance.29 30 In addition, the vascular response to vasoactive substances may be influenced by the preparation of the vessel. In vivo studies are therefore necessary for evaluation of the role of vascular smooth muscle function in the buffering function of the arterial system.
The mechanics of the arterial wall depend on the elastic, viscous, and intertial moduli, and a complete characterization of the vessel wall properties is difficult to achieve. Using a model by which viscous, intertial, and elastic moduli could be discriminated, Armentano et al31 could measure the different effect of vascular smooth muscle activation and of passive smooth muscle modulus on the aortic wall behavior in conscious dogs. Barra et al32 assessed the participation of vascular smooth muscle activation on the elastic modulus of the aortic wall. During activation of vascular smooth muscle, the elastic modulus decreased when plotted against internal pressure but increased when plotted against strain. These animal studies show that the effect of vascular smooth muscle activity on vessel wall properties is complex and depends on the type of analysis. Nevertheless, the data suggest that activation of vascular smooth muscle alters the stiffness of large arteries and support the view that vascular smooth muscle activation underlies the increased arterial stiffness in ergotamine-treated patients.
Only few data from in vivo studies suggest that vascular smooth muscle tone may affect arterial distensibility in humans. Discrepant data on the distensibility of radial arteries were reported after sympathetic stimulation by mental stress and cold pressor tests.33 34 35 Decreased as well as increased radial arterial distensibility has been demonstrated with these two tests. Apart from these conflicting results, it has to be pointed out that sympathetic activation may have different consequences on large arteries of the "elastic type" and on muscular medium-sized arteries. Smooth muscle activation in response to an increase in sympathetic drive should modify intrinsic viscoelastic properties of the radial arterial wall to a larger extent than in more elastic arteries such as the carotid artery. The unloading of the stiffer wall components during constriction is directly related to geometric changes associated with smooth muscle cell contraction.23 Moreover, differences in the ratio of arterial radius to wall thickness at a given level of BP change the mechanical properties of the arterial wall.36 The contributions of vessel geometry to mechanical properties are ignored by the distensibility coefficient. However, since the diameter and intima-media thickness of the common carotid artery were not different in the ergotamine and control groups, reduced arterial distensibility in patients treated with ergotamine cannot be explained by geometric changes of the arterial wall.
The effect of antihypertensive drugs on the vessel wall properties of larger arteries may be mediated by pressure-independent effects on vascular smooth muscle function. Antihypertensive drugs can induce vessel wall property changes that differ according to the mechanism of their action. Dihydralazine can decrease the diameter of the brachial artery, whereas diltiazem increased the diameter for a comparable BP reduction.37 Pressure changes alone thus cannot explain the effect of antihypertensive drugs on vessel diameter. A different influence of antihypertensive drugs on arterial distensibility also suggests the role of active changes of vascular smooth muscle tone. In a randomized double-blind study, the effects of lisinopril and metoprolol on the distensibility of the common carotid artery were compared.38 Despite the same reduction of BP during antihypertensive therapy, lisinopril improved arterial distensibility of the common carotid artery and metoprolol had no effect on arterial distensibility.
The present findings are subject to several methodological limitations: BP was measured at the site of the brachial and not the carotid artery, thereby introducing potential errors because of the different shape of the pressure curve at these sites. Generally, this methodological error should be similar in both groups and hence should not be relevant for the different distensibility coefficients in both groups. However, it can be argued that because of ergotamine-induced stimulation of the sympathetic nervous system, the pulse pressure amplification in peripheral vessels may be enhanced in the patients compared with the control subjects. Such an error of overestimation of the distensibility coefficient in the ergotamine patients may be unlikely because ergotamine in therapeutic doses is known to be ineffective in peripheral arteries.7 9 Given that there is indeed an effect of measurement site on the calculated data, the decrease of distension would nevertheless be uninfluenced by this methodological problem. The BP and heart rate variabilities recorded in the present study in both groups also argue against the role of a stimulated sympathetic nervous system, as these variabilities did not change between the groups. Short-term BP and heart rate variabilities are known to be measures of the level of sympathetic activity.15
In summary, the results of the present study demonstrate that the vasoconstrictor ergotamine can reduce the distensibility of the common carotid artery. Since ergotamine had no effect on BP and the decrease in distensibility was not associated with an increased wall thickness, reduced distensibility of the common carotid artery can be related to changes in vascular smooth muscle tone. The data therefore suggest that the cushioning function of the arterial system can be influenced by vascular smooth muscle contraction.
|
Footnotes |
|---|
Reprint requests to Dr Michael Barenbrock, Department of Medicine D, University of Munster, Albert-Schweitzer-Str 33, 48149 Munster, FRG.
Received November 7, 1995;
first decision November 24, 1995; first decision March 7, 1996;
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. O'Rourke MF. Arterial Function in Health and Disease. Edinburgh, UK: Churchill Livingstone; 1992.
2. Nicols WW, Nicolini FA, Pepine CJ. Determinants of isolated systolic hypertension in the elderly. J Hypertens. 1992;10(suppl 6):S73-S77.
3. Abbrams WB. Pathophysiology of hypertension in older patients. Am J Med. 1988;85(suppl 3B):7-12.
4. Bouthier JD, De Luca N, Safar ME, Simon AC. Cardiac hypertrophy and arterial distensibility in essential hypertension. Am Heart J. 1985;109:1345-1352.[Medline] [Order article via Infotrieve]
5. Laurent St, Caviezel B, Beck L, Girerd X, Billaud E, Boutouyrie P, Hoeks A, Safar M. Carotid artery distensibility and distending pressure in hypertensive humans. Hypertension. 1994;23(part 2):878-883.
6. Safar ME, Levy BI, Laurent St, London GM. Hypertension and the arterial system: clinical and therapeutic aspects. J Hypertens. 1990;8(suppl 7):S113-S119.
7. Saxena PR, Den Boer MO. Pharmacology of antimigraine drugs. J Neurol. 1991;238:S28-S35.
8. Hansen-Tfelt P. The effect of ergotamine on the arterial system in man. Acta Pharmacol Toxicol. 1986;59(suppl 3):1-30.
9. Bulow PM, Ibraheem JJ, Paalzow G, Hansen-Tfelt P. Comparison of pharmacodynamic effects and plasma levels of oral and rectal ergotamine. Cephalalgia. 1986;6:107-111.[Medline] [Order article via Infotrieve]
10. Perrin VL. Clinical pharmacokinetics of ergotamine in migraine and cluster headache. Clin Pharmacokinet. 1985;10:334-352.[Medline] [Order article via Infotrieve]
11. Hoeks APG, Brands PJ, Smeets FAM, Reneman RS. Assessment of local vessel wall elasticity of superficial arteries. Ultrasound Med Biol. 1990;16:121-128.[Medline] [Order article via Infotrieve]
12. Baumgart P, Laske V, Barenbrock M, Spieker C, Hoeks APG, Rahn KH. A novel method for noninvasive assessment of local vessel wall elasticity. Nieren- und Hochdruckkrankheiten. 1991;20:543-544.
13. Reneman RS, van Merode T, Hick P, Hoeks APG. Cardiovascular applications of multi-gate pulsed doppler systems. Ultrasound Med Biol. 1986;12:465-471.[Medline] [Order article via Infotrieve]
14.
Pignoli P, Tremoli E, Poli A, Oreste P, Paoletti R. Intimal plus medial thickness of the arterial wall: a direct measurement with ultrasound imaging. Circulation. 1986;74:1399-1406.
15.
Floras JS, Hassan MO, Vann Jones J, Osikowska BA, Sever PS, Sleight P. Factors influencing blood pressure and heart rate variability in hypertensive humans. Hypertension. 1988;11:273-281.
16.
Mancia G, Ferrari A, Gregorini L, Parati G, Pomidossi G, Bertinieri G, Grassi G, di Rienzo M, Pedotti A, Zanchetti A. Blood pressure and heart rate variabilities in normotensive and hypertensive human beings. Circ Res. 1983;53:96-104.
17.
Parati G, Casadei R, Groppelli A, Di Rienzo M, Mancia M. Comparison of finger and intra-arterial blood pressure monitoring at rest and during laboratory testing. Hypertension. 1989;13:647-655.
18. Stewart W, Werthgessen ND. Fluid mechanics of arterial flow. In: Wolf S, Werthessen NT, eds. Dynamics of Arterial Flow. New York, NY: Plenum Press; 1979:55-103.
19. Levenson J, Pithois-Merli I, Simon A. Mechanical factors in large artery disease and antihypertensive drugs. Am J Cardiol. 1990;66:39c-42c.
20.
Benetos A, Huguet P, Albaladejo P, Brisac AM, Pappo M, Safar ME, Levy BI. Role of adrenergic tone in mechanical and functional properties of carotid artery during aging. Am J Physiol. 1993;265:H1132-H1138.
21. O'Rourke MF, Avolio AP. Structural basis for increased distensibility of systemic muscular arteries with arterial dilator agents. J Mol Cell Cardiol. 1985;18(suppl 2):374-380.
22. Torrance HB, Schwatz S. The elastic behavior of the arterial wall. J R Coll Surg. 1961;7:55-60.
23. Dobrin PB, Rovick AA. Influence of vascular smooth muscle on contractile mechanics and elasticity of arteries. Am J Physiol. 1969;217:1644-1652.
24.
Gow BS, Taylor MG. Measurement of viscoelastic properties of arteries in the living dog. Circ Res. 1968;23:111-122.
25. O'Rourke MF. Therapeutic interventions. In: Nicols WW, O'Rourke MF, eds. McDonald's Blood Flow in Arteries. London, UK: Arnold; 1990:421-437.
26. Armentano RL, Levenson J, Barra JG, Cabrera BL, Fischer GJ, Breitbart GJ, Pichel RH, Simon A. Assessment of elastin and collagen contribution to aortic elasticity in conscious dogs. Am J Physiol. 1991;260:445-457.
27. Roach MR, Burton AC. The reason for the shape of the distensibility curves of arteries. Can J Biochem Physiol. 1957;35:681-690.
28. Dobrin PB. Vascular mechanics. In: Shepherd JT, Abboud FM, eds. Handbook of Physiology, Section 2: The Cardiovascular System, Volume III, Peripheral Circulation and Organ Blood Flow. New York, NY: American Physiological Society; 1983:65-102.
29.
Hasson JE, Megerman J, Abbot WM. Post-surgical changes in arterial compliance. Arch Surg. 1984;119:788-791.
30. Megerman J, Hasson JE, Warnock DF, L'Italien GJ, Abbot WM. Noninvasive measurements of nonlinear arterial elasticity. Am J Physiol. 1986;250:H181-H188.
31.
Armentano RL, Barra JG, Levenson J, Simon A, Pichel RH. Arterial wall mechanics in conscious dogs: assessment of viscous, intertial, and elastic moduli to characterize aortic wall behaviour. Circ Res. 1995;76:468-478.
32.
Barra JG, Armentano RL, Levenson J, Fischer EIC, Pichel RH, Simon A. Assessment of smooth muscle contribution to descending thoracic aortic elastic mechanics in conscious dogs. Circ Res. 1993;73:1040-1050.
33.
Boutouyrie P, Lacolley P, Girerd X, Beck L, Safar M, Laurent S. Sympathetic activation decreases medium-sized arterial compliance in humans. Am J Physiol. 1994;267:H1368-H1376.
34. Dobrin PB. Isometric and isobaric contraction of carotid arterial smooth muscle. Am J Physiol. 1973;225:664-670.
35.
Joannides R, Richard V, Moore N, Godin M, Thuillez C. Influence of sympathetic tone on mechanical properties of muscular arteries in humans. Am J Physiol. 1995;268:H794-H801.
36.
Bader H. Dependence of wall stress in the human thoracic aorta on age and pressure. Circ Res. 1967;20:354-361.
37. Safar ME, Simon AC, Levenson JA, Cazor JL. Hemodynamic effects of diltiazem in hypertension. Circ Res. 1983;52(suppl I):I-169-I-173.
38. Barenbrock M, Spieker C, Hoeks APG, Zidek W, Rahn KH. Effect of lisinopril and metoprolol on arterial distensibility. Hypertension. 1994;23(suppl I):I-161-I-163.
This article has been cited by other articles:
 |
|
 |
|
  M. Miyachi, H. Kawano, J. Sugawara, K. Takahashi, K. Hayashi, K. Yamazaki, I. Tabata, and H. Tanaka Unfavorable Effects of Resistance Training on Central Arterial Compliance: A Randomized Intervention Study Circulation, November 2, 2004; 110(18): 2858 - 2863. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. D. Monahan, F. A. Dinenno, D. R. Seals, C. M. Clevenger, C. A. Desouza, and H. Tanaka Age-associated changes in cardiovagal baroreflex sensitivity are related to central arterial compliance Am J Physiol Heart Circ Physiol, July 1, 2001; 281(1): H284 - H289. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Tanaka, F. A. Dinenno, K. D. Monahan, C. M. Clevenger, C. A. DeSouza, and D. R. Seals Aging, Habitual Exercise, and Dynamic Arterial Compliance Circulation, September 12, 2000; 102(11): 1270 - 1275. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||