Effects of age and hypertension on cardiac responses to the α1-agonist phenylephrine in humans

White, Michel; Fourney, Adam; Mikes, Etel; Leenen, Frans H. H.

doi:10.1016/s0895-7061(98)00220-9

Cited by 25 publications

(19 citation statements)

References 27 publications

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“…4). We concluded (18) that decreased responsiveness was offset by diminished blunting by the arterial baroreflex in the hypertensive subjects (5,16). In contrast, in the present study, we show that young normotensive and hypertensive subjects show similar cardiac responses to epinephrine not only when infused alone but also when infused combined with ganglion blocker.…”

Section: Discussioncontrasting

confidence: 73%

“…aging; arterial baroflex; neuronal uptake; ␤-receptor responsiveness; heart HYPERTENSION IS GENERALLY considered to cause a decrease in cardiac ␤-adrenergic responsiveness. Hypertension also leads to blunting of counterregulatory mechanisms such as the arterial baroreflex (5,16), which also influences cardiac responses to a ␤-agonist in vivo (16). Combined with autonomic blockade, chronotropic responses to the ␤-agonist isoproterenol were not different in young normotensive and hypertensive subjects (7,18), whereas left ventricular (LV) responses showed blunting in the hypertensive subjects (18).…”

Section: Effects Of Hypertension On Cardiovascular Responses To Epinementioning

confidence: 99%

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Effects of hypertension on cardiovascular responses to epinephrine in humans

Leenen¹,

Fourney²,

Coletta³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Cardiac beta-receptor responsiveness is diminished by both aging and hypertension. However, concomitant decreases in the activity of counterregulatory mechanisms, such as the arterial baroreflex and neuronal catecholamine uptake, influence the ultimate cardiac responses to adrenergic agents in vivo. In the present study, we evaluated by echocardiography cardiac responses to intravenous infusion of epinephrine in 14 young and 18 older normotensive men and women and in 10 young and 17 older hypertensive men and women. To assess the relative contribution of intrinsic cardiac and counterregulatory components to the overall response, infusions were repeated combined with a ganglionic blocker in the young groups. Epinephrine-induced increases in heart rate were similar in the four groups. Increases in stroke volume, ejection fraction, and cardiac index were similar in the two hypertensive and two young normotensive groups. In contrast, they were attenuated in the older normotensive group, resulting in higher left ventricular responses in older hypertensive than in normotensive subjects. Heart rate and left ventricular responses to epinephrine in the presence of ganglionic blockade did not differ between the two young groups. Increases in plasma norepinephrine due to epinephrine infusion were larger in hypertensive than in normotensive subjects. One may conclude that compared with young normotensive subjects, in hypertensive subjects mechanisms increasing versus decreasing cardiac responses to epinephrine may remain in balance, and, compared with older normotensive subjects, older hypertensive subjects exhibit enhanced cardiac responses to sympathetic stimulation.

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Section: Discussioncontrasting

confidence: 73%

Section: Effects Of Hypertension On Cardiovascular Responses To Epinementioning

confidence: 99%

Effects of hypertension on cardiovascular responses to epinephrine in humans

Leenen¹,

Fourney²,

Coletta³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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show abstract

“…There are conflicting reports with regards to the effect of age on pressor responsiveness to phenylephrine. One small study (n=6 per group) that failed to rigorously screen subjects showed reduced responsiveness with aging [19], but two larger studies showed an increased blood pressure response with age, as we also demonstrated [10,20].…”

Section: Discussionsupporting

confidence: 50%

The effect of aging on phenylephrine response in normal subjects

Madden

Levy

Jacobson

et al. 2003

AGE

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“…33 The phenylephrine infusion was started at 0.4 mg/kg/min and increased to 0.8, 1.6 and 2.4 mg/kg/min at 6 min intervals. The infusion was discontinued if SBP increased .40 mm Hg, diastolic BP increased .20 mm Hg, or the patient developed intolerable symptoms or ventricular arrhythmias.…”

Section: Phenylephrine Protocolmentioning

confidence: 99%

Impact of blood pressure on the Doppler echocardiographic assessment of severity of aortic stenosis

Little

Chan

Burwash

2006

Heart

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Objective: To investigate the impact of blood pressure (BP) on the Doppler echocardiographic (Doppler-echo) evaluation of severity of aortic stenosis (AS). Methods: Handgrip exercise or phenylephrine infusion was used to increase BP in 22 patients with AS. Indices of AS severity (mean pressure gradient (DP mean ), aortic valve area (AVA), valve resistance, percentage left ventricular stroke work loss (% LVSW loss) and the energy loss coefficient (ELCo)) were measured at baseline, peak BP intervention and recovery. Results: From baseline to peak intervention, mean (SD) BP increased (99 (8) (6) vs 16.5 (6)%, p,0.001), suggesting a less severe valve stenosis. There was an inverse relationship between the change in mean BP and AVA (r = -0.34, p = 0.02); however, only the change in Q mean was an independent predictor of the change in AVA (r = 0.81, p,0.001). Conclusions: Acute BP elevation due to increased SVR can affect the Doppler-echo evaluation of AS severity. However, the impact of BP on the assessment of AS severity depends primarily on the associated change in Q mean , rather than on an independent effect of SVR or arterial compliance, and can result in a valve appearing either more or less stenotic depending on the direction and magnitude of the change in Q mean .T ransvalvular pressure gradient and aortic valve area (AVA) are the standard indices to determine the haemodynamic severity of aortic stenosis (AS).1 2 However, a patient's physiological state can affect these indices and therefore the assessment of AS severity. Pressure gradients and AVA vary with transvalvular flow and flow-mediated forces.3-10 Valve resistance, % left ventricular stroke work loss (% LVSW loss) and the energy loss coefficient (ELCo) have been proposed as alternative indices of AS severity that may be less sensitive to transvalvular flow.7 11-21 However, this has not been corroborated in individual patients when transvalvular flow was altered using exercise or inotropic infusion. The impact of blood pressure (BP) on the assessment of AS severity has received less attention.2 Traditionally, low systolic BP (SBP) and a decreased pulse pressure have been considered signs of severe AS, whereas the presence of hypertension excluded severe AS. 22 However, recent data demonstrate that hypertension commonly coexists with and is a risk factor for AS. [23][24][25][26][27] Hypertension can lead to an underestimation of AS severity on physical examination. 22Furthermore, BP and systemic vascular resistance may influence the assessment of the haemodynamic severity.2 In a catheterisation study, Laskey et al 28 observed a decrease in transvalvular pressure gradient and a potential underestimation of AS severity when peripheral resistance was increased. Similarly, induction of hypertension in an animal model of supravalvular AS resulted in a decrease in pressure gradient and an increase in the area of the supravalvular stenosis. 29In contrast, pressure gradient increased and valve area decreased when systemic vascular resistance was increased in a...

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Effects of age and hypertension on cardiac responses to the α1-agonist phenylephrine in humans

Cited by 25 publications

References 27 publications

Effects of hypertension on cardiovascular responses to epinephrine in humans

Effects of hypertension on cardiovascular responses to epinephrine in humans

The effect of aging on phenylephrine response in normal subjects

Impact of blood pressure on the Doppler echocardiographic assessment of severity of aortic stenosis

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