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Can Humeral Flow Response
After Isometric Contraction
(Hand Grip) be Standardized?

Ramos, Miguel H.; Gómez Rinesi, Juan F.;
Marecos, Edgardo A.; Marecos, Edgardo M.

Cardiocentro S.R.L., Corrientes, Argentina

SUMMARY
Introduction: With the publication of Cellermajer´s works have been demonstrated that humeral artery endothelial function is representative of all arteries function. Increasing the studied endothelial surface, by means of the quantification of flow variations, sensitivity could be improved.
Objectives: To quantify variations in humeral flow after isometric contraction.
Materials and Methods: In 30 individuals (13 women and 17 men) ranging from 20 to 30 years-old, with no evidence of hypertension, hypercholesterolemia, diabetes or coronary disease, flow spectrograms from the humeral artery were taken before (basal), during and after isometric contraction (hand grip).
Isometric contraction (IC) was considered as the individual´s manual compression against the inflated cuff of an sphygmomanometer during 2 minutes without presence of diastolic flow during procedure. [resistance index (RI) = 1]
Under basal conditions (BC) and after isometric contraction (AIC), peak systolic velocity (PSV), and peak diastolic velocity (PDV) were measured and RI was calculated; during isometric contraction, just PSV(PSVDIC). Increments in flow after IC was calculated with respect to flow under BC and during contraction. Confidence intervals (95%), standard deviation and medium were also calculated.
Results: Differences in PSV after IC (PSVAIC) and under BC (PSVUBC), PSVAIC and PSVDIC, between PDV after contraction (PDVAIC) and under BC (PDVUBC), PDVAIC and PSVDIC, RI of flow after contraction (RIAIC) and RI under BC (RIUBC), and between RIAIC and during contraction (RIDIC) were significant (p-value less than 0.0000001). Table 1 shows these results.

Discussion: We observed statistically significative increment of PSV and PDV after IC in comparison with the measurements taken under BC and during the IC. RIAIC was lower than RIUBC and RIDIC. The RIDIC-RIAIC difference is a reliable quantifier due to its low dispersion and narrow CI (95%).
Conclusion: The RIDIC-RIAIC difference is the best quantifier of vasomotor response to isometric contraction. Clinical studies are needed to validate its diagnostic usefulness.

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INTRODUCTION
   In the early 80's, Furchgott et al. started a new field in the study of coronary diseases when describing the active role of the endothelium as modulators of the arterial function (1), with the discovery of endothelium derived relaxation factor (EDRF). Later studies advanced the first discoveries of these authors with the description of new factors and functions of the endothelium (2,3,4,5 ) even on the vasomotor behavior as on other arterial processes (proliferation, inflammation, immunity, etc.) and in the interface blood-endothelium (thrombolytic inhibition, antithrombocytic effect) (6).

   The demonstrated role of the endothelium in the genesis of vascular damage has stimulated the development of techniques for the clinical detection of their dysfunction and has risen the interest about the vasomotor response by proposing invasive and non invasive techniques for their evaluation.

   In the 90's, Celermajer et al. (7) developed a non invasive method to evaluate arterial vasodilatation by friction, mediated by the endothelium, in the humeral and femoral arteries, as an expression of endothelial function, utilizing the reactive hyperemia that follows ischemia as a modifier of flow and measuring then, the arterial diameter by high resolution ultrasonography before and after the ischemia provocated by the expansion of the sphygmomanometer cuff in the arm or leg homolateral to the studied artery. Also, flow peaks were compared, calculated as the product of the section of the artery and flow velocity, in both circumstances. They realized that in normal individuals, there was a statistically significant increment in the femoral (4%) y humeral (11%) diameter, and in the flow after decompression of the cuff, while in patients with coronary disease and in smokers it was substantially lesser and the flow increments were not different to those of normal individuals.

   Similar results were reported by Esper et al. (8) when studying the behavior of the humeral artery using similar method.

   Several studies reported the close correlation between the presence of risk factor and endothelial dysfunction in the preclinical period (9,10,11,12). Furthermore, the behavior of the peripheral vascular tree reflects very closely the one of the coronary arteries endothelium (13).

   The vasodilator response mediated by the endothelium respond to two types of stimulus: mechanical (flow friction) yand chemical (acetylcholina, bradyquinin, P substance, drop in PO2, increment in CO2, etc.) most of which are produced se during tisular oxygen demand and there are also evidences that in resistance arterioles that participate in the local regulation of perfusion certain changes of vasodilatation endothelium mediated similar to those produced in conductance arteries and that the inhibition of NO synthesis produces a drop in the maximal flow drop (14).

   Conformed to this observations, during the development of oxygen demand it is produced in the vascular territory a drop in the peripheral resistance, and its highest expression would be the post ischemia reactive hyperemia where endothelium independent vasodilator factors such as acidosis, natriuretic factor histamine can operate or, like in the case of coronary circulation, adenosine (15). In Celermajer and similar studies, has been demonstrated that there is a significant increment in post ischemia flow but not a different behavior among individuals with endothelial dysfunction respect to normal individuals.

   We assume that these results can not demonstrate the modulator effect of normal endothelium flow, as it was previously demonstrated due to one or more of the following reasons:

1) Release of endothelium-non dependent vasodilators by prolonged and intense hypoxia.
2) Measurements took in count flow in absolute values and were indirectly determined by the section af each vessel and the speed
3) Not necessarily the metabolic rate was the same in all individuals nor the basal resistance before occlusion.

   For these reasons we think that it is possible to improve the flow evaluation conditions by taking in count the absolute values of velocity and the change in behavior of resistance vessels (arterioles) through the resistance index of Pourcelot.

   Moreover, being flow an expression of vasomotor behavior of a more extended surface that covers the adjacent territory of the studied artery, an amplification of the effects of endothelial response can occur, respect to the one evaluated by arterial width measurement, that can facilitate its reading and sensitivity.

   The objective of these work is to determine the standards of humeral flow variation that it is mediated by endothelium dependant arteriolar vasodilatation in response to the oxygen deprivation controlled by isometric contraction.

MATERIALS AND METHODS
Population
   In the study were included 30 individuals (13 women and 17 men) with ages between 20-30 years (23.06 ± 1.8 a.), asymptomatic, with LDL-Cholesterol < 160 mg/dl, non smokers, arterial tension (TA) systolic < 140 mmHg y TA diastolic < 90 mmHg., corporal mass index less than 30, glycemia between 70 and 110 mg/dl, an ECG with normal rhythm, cardiac frequency above 65 and below 95 bpm, with no evidence of hypertrophy or cardiac dilation, ST normal and no signs of ischemia, blocks or repolarization problems.

Procedure
   All individuals were examined in morning hours, after overnight fasting, in supine decubitus, after a five minute rest humeral artery was localized in the dominant arm at 1 or 2 cm proximally to the elbow fold with an ATL3500 using a 7,5 MHz transducer.

   Arterial flow speed spectrograms were registered during 5 beats in basal conditions, during contraction and after isometric contraction, with correction of the isoniation angle in all cases (60º).

   The isometric contraction was done using an semi-inflated cuff of a sphygmomanometer that each individual had to compress with his hand (of the dominant arm) until reaching a pressure that could suppress the diastolic flow on the spectrogram during two minutes. The registration of each contraction was immediately done after decompression. In basal flow spectrograms (BF) and post isometric contraction flow (FPA) systolic peak velocity (SPV) was measured at the zenith of the diastolic peak, diastolic peak velocity (DPV) at the end of diastole and were calculated, the resistance index (RI) of Pourcelot [(SPV-DPV)/SPV] (16). In the during contraction spectrogram flow (AF) was only necessary the measurement of the SPV due to the design of the study, DPV in all cases was zero and resistance index 1. All measurements were done by three independent operators and these were considered consistent if the maximal deviations were below 5 % of the mean of three observations (fig 1).

   Differences between SPV, DPV and RI of the spectrogram del of the FPA were compared with the ones of the spectrograms of BF and AF and medium standard deviation and confidence intervals 0.05 [CI(95%)] were obtained for each one of the variables and for the increments in SPV, DPV and RI of APF with respect to BF (PICSPV - BSPV; PICDPV - DICDPV; PICRI - BRI) and AF (PICSPV - DICSPV; PICDPV - DICDVP; PICRI - DICRI).

   In all cases, the meaning of these differences was calculated with the t student test.

   This data was recopilated and analyzed using Microsoft Excel and SPSS 9.0 statistical package.

RESULTS
   In all cases an adequated registration of the flow speed spectrogram was reached and measurement was consisted.

   The observed differences between SPV, DPV and RI between FPIC (PICSPB, PICDPV and PICRI) and the ones that correspond to BF (BSPV, BDPV and BRI) and AF (DICSPV, DICDPV and DICRI) were always statistically significant (p< 0.001). Mean values, standard deviation and confidence intervals of the observed increments in the APF and mean an standard deviation of SPV, DPV and RI are shown in table 1. Porcentual increments in PICSPV respect to BSPB and DICSPV were of 62% y 37%, respectively.

DISCUSSION
   Even though statistically significant differences were observed among the values of the studied variables, with an increment in speed and reduction of the resistance index in the post contraction flow in relation to the one during the contraction and at resting; in the particular case of the peak diastolic velocity this extreme difference can be due to: being the humeral artery a high resistance artery with a diastolic velocity of practically zero, little changes after contraction due to the drop in resistance , may not be a proportional expression of the change in the vasomotor response. Postcontraction systolic increment with respect to the basal and the registered during the contraction; however, in this work was not estimated the total flow in all phases, having in mind that we assumed that absolute values can bring up errors due to technical difficulties that intervene in this calculations. This does not occur with the resistance indexes because these are not determined by indirect calculations such as the arterial section area or the isonacion angle correction. Being these differences, in fact, the ones with less dispersion (D.E.) and confidence intervals that were demonstrated in this study. Specially the difference PAICRI-DCRI, seemed to be the best indicator of the vasomotor behavior among the studied variables.

   The discoveries of Age et al (17) stating that the exercise with handgrip during the arterial occlusion increments the vasodilatation by hyperemic flow with no modification, helps to demonstrate our belief about the participation in all mechanisms of local regulation (endothelium dependent or not dependent) in response to the ischemia due to prolonged occlusion (5 min), having in mind, that besides the endothelium non dependent vasodilatation mediators (histamine, local increment in local potassium) have a role before tisular injury. In our study, the persistence of the systolic component of the spectrogram during the contraction suggests that no significant restriction in tisular flow is produced and that instead an increment in local oxygen demand of short duration that produces the release of local factors, endothelium non dependent, of autoregulation. Even though a certain participation of factors related to tisular hypoxia can not be ruled out, there are some evidences like the ones on the cited studies (16) or the one by Shoemaker et al. (18) that the vasomotor resonse mediated by flow can be influenced by metabolic components on this sort. Also, as Correti, Plotnick and Vogel (19) reported, the hyperemic vasodilation mediated by the endothelium in conduction arteries are evidenced with occlusion periods of 5 minutes but not in shorter periods (1 and 3 min) even when the flow increment is the same at one minute, at three and at five.

   In this study the hemodinamic response best quantifiable to the oxygen demand generated distally to the humeral and attributable to the endothelial mediation in normal individuals is the drop of the peripheral resistance, and can be objetivized as an increment of - 0.32 ± 0.08 in the resistance index after isometric contraction compared to during the contraction, although we can not establish the cut off point due to the study characteristics. Comparative clinical studies are missing between normal individuals and those with endothelial dysfunction to determined the behavior of this variable and to validate this method.

   Also, there are technical reasons that encourage research in this matter. The possibility of doing it, without sophisticated machinery, like the use of continuous Doppler as in arterial fluxometry, at low cost and of simple use, can facilitate its application at higher scale for the early detection of endothelial dysfunction.

CONCLUSIONS
   The difference PICRI - DICRI is the best quantifier of the vasomotor response to hand grip in the muscular territory of the humeral artery in normal individuals and can be used as an standard indicator of the flow response to isometric contraction.

REFERENCES

1. Furchgott RF, The discovery of endothelium-dependent relaxation. Circulation 1993;87[Suppl V] V-3 - V-8.

2. Balton TB, Lang RJ, Takewaky T,. Mechanism of action of noradrenaline and carbadiol on smooth muscle of guinea-pig anterior mesenteric artery. J Physiol 1984; 351: 549-572

3. Lüscher TF, Vanhouette PM. The endotelium: modulator of cardiovascular function. Boca Ratón, Flda.CRC Press.Inc. 1990.pp 1-228

4. Rubanyi GM, Vanhouette PM. Hypoxia releases a vasoconstrictor substance from the canine vascular endothelium. J. Physiol. 1985;364: 45-56.

5. Vanhouette PM. Other Endothelium-derived vasoactive factors. Circulation 1993; 87(Suppl V): V9 - V17.

6. Rubanyi GM. The role of endothelium in cardiovascular homeostasis and disease. J. Cardiovasc. Pharmacol. 1993. Vol 2 (suppl 4): S1 - S14.

7. Celermajer DS, Soerensen KE, Gooch VM, Spiegelhalter DJ, Miller OI, Sullivan ID, Lloyd JK, Deanfield JE. Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis. Lancet 1992, 340:1111-15

8. Vilariño JL, Cacharon JL, Suarez DH, Kura M, Machado R, Bolaño AL, Esper RJ. Evaluación de la función endotelial por eco doppler. Influencia de la edad, sexo y factores de riesgo. Rev. Argent Cardiol 1998; 66 (5):523-532.

9. Celermajer DS, Soerensen KE, Bull C, Robinson J, Deanfield JE. Endothelium-dependent dilatation in the systemic arteries of asymptomatic subjects relates to coronary risk factor and their interaction .J Am Coll Cardiol 1994,24:1468-74.

10. Clarkson P, Celermajer DS, Powe A, Donald AE, Henry MA, Deanfield JE. Endothelium dependent dilatation is impaired in young healthy subjects with family history of premature coronary disease. Circulation 1997;96:3378-3383.

11. Panza JA, Quyyumi AA, Brush JE, Epstein SE. Abnormal endothelium dependent vascular relaxation in patients with essential hypertension. N Engl J Med 1990; 323: 22-27.

12. Kimura Y, Matsumoto M, Den YB, Iwai K, Munheyra J,Hattori H, Hocino T,Yamada K, Kawanishi K, Tsuchiya H. Impaired Endothelial function in hypertensive elderly patients evaluated by high resolution ultrasonography. Can J Cardiol 1999 May; 15(5): 563-8

13. Schoders S, Weisner C, Bumbach A, Herderg C, Oberoff M, Ossen R, Pfohl M, Karsh Kr. The ultrasonic measurement of the endothelial function of the brachial artery in suspected coronary heart disease. Dtsh Med Wochenschr 1999 Jul30; 124(30): 886-90.

14. Joannides R, Haefeli WE, Linder L, Richard V, Bakkali EH, Thuillez C, Lüscher TF. Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in vivo.

15. Ganong WF. Fisiología Médica. Decimotercera Edición. Editorial El manual moderno, S.A. de C.V. México, DF.1992.pag.538.

16. Pourcelot L. L'examen doppler des vaisseaux périphériques.ACD.Paris.1982

17. Age W, Walley GA, Doughty RN, Sharpe SN. Handgrip exercise increases postoclusion Hyperaemic brachial artery dilatation. Heart 1999 Jul,82(1):93-5

18. Shoemaker JK, Mac Donald MJ, Hughson RL. Time course of brachial artery diameter responses to rhythmic handgrip exercises in humans.

19. Corretti MC, Plotnick GD, Vogel RA. Technical aspects of evaluating brachial artery vasodilatation using high-frequency ultrasound. Am. J. Physiol. 268(Heart Circ. Physiol. 37): H1397- H1404,1995.

 

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2nd Virtual Congress of Cardiology

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