Mechanism of Adenosine-Induced Elevation of Pulmonary Capillary Wedge Pressure in Humans

Nussbacher, Amit; Ariê, Sigemituzo; Kalil, Roberto; Horta, Pedro; Feldman, Marc D.; Bellotti, Giovanni; Pileggi, F; Ellis, Mark; Johnson, William H.; Camarano, Gustavo; Kass, David A.

doi:10.1161/01.cir.92.3.371

Cited by 32 publications

(11 citation statements)

References 48 publications

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“…23,24 The latter parameter (slope of relations between cardiac stroke work [ie, pressure ⅐ volume] and end-diastolic volume) is particularly useful since it has force (pressure) units and is chamber scaling-size independent. This parameter was measured in C3H/HeJ control mice under ␣-chloralose/urethane anesthesia and yielded values in the range of 80 to 100 mm Hg, very similar to values reported in conscious humans 19 and dogs.…”

Section: What Is Normal For the Restingsupporting

confidence: 76%

Murine Cardiac Function

Kass¹,

Hare²,

Georgakopoulos³

1998

Circulation Research

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158

104

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Section: What Is Normal For the Restingsupporting

confidence: 76%

Murine Cardiac Function

Kass¹,

Hare²,

Georgakopoulos³

1998

Circulation Research

Self Cite

158

104

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“…Right atrial pressure (P RA ) was not directly measured. This influences the calculation of absolute values of pressure indexes, but because P RA does not considerably change during adenosine infusion, 22,34 it would not decisively affect the assessment of the intraindividual response to adenosine.…”

Section: Study Limitationsmentioning

confidence: 99%

Direct Assessment of Coronary Steal and Associated Changes of Collateral Hemodynamics in Chronic Total Coronary Occlusions

Werner

Figulla

2002

Circulation

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Background-Coronary steal can occur in collateral-dependent myocardium during pharmacologically induced vasodilation. This study assessed coronary steal invasively in chronic total coronary occlusions (TCOs). Methods and Results-In 35 consecutive patients with a percutaneous transluminal coronary angioplasty of a TCO (duration Ͼ4 weeks), coronary flow velocity (APV) by a Doppler wire and distal pressure (P D ) by a pressure wire were assessed in the collateral-dependent vascular bed before dilatation. Indexes of peripheral resistance (R P ) and for the collateral pathway, including the donor artery segment (R CP ), were calculated. Changes of these parameters were assessed during intravenous adenosine (140 g · kg Ϫ1 · min Ϫ1 ). Adenosine caused a decrease of APV, ie, coronary steal, in 13 patients (37%; group S), an increase in 11 patients (group R), and no change in 11 patients (group N). Angiographic analysis of collateral pathways showed no difference between the groups, except that in group S all collateral connections were continuously visible but no large collaterals (Ͼ0.5 mm) were found. In group N, collaterals were least developed. The increase of APV in group R was associated with a decrease of R P , whereas R CP remained unchanged. In contrast, group S showed no change in R P but a significant increase of R CP , indicating an increased resistance of the donor segment. Conclusions-Coronary

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“…The hemodynamic response to intravenous adenosine in humans has been studied in considerable detail. Adenosine induces a dose-dependent increase in heart rate and stroke vol ume and reduces diastolic blood pressure and total peripheral resistance, mainly by vasodilation of skin and splanchnic vascular beds (Biaggioni et al, 1991a;Edlund et a l 1990;Nussbacher et al 1995;Smits et al 1987a). The other inter vention, LBNP of-15 mmHg, reduces central venous pressure and stroke volume, and to a lesser extent increases peripheral resistance, resulting in modest hypotension (Floras 1990).…”

Section: Discussionmentioning

confidence: 99%

Comparison of hemodynamic and sympathoneural responses to adenosine and lower body negative pressure in man

Rongen¹,

Senn²,

Ando³

et al. 1997

Rev. can. physiol. pharmacol.

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Adenosine increases heart rate and sympathetic nerve activity reflexively in conscious humans through several mechanisms. The purpose of this study was to assess the relative contributions of arterial baroreceptor unloading, carotid chemoreceptor stimulation, and other adenosine-sensitive afferent nerves to these responses. In 12 healthy men, the effect on blood pressure, heart rate (HR), and muscle sympathetic nerve activity (MSNA; peroneal nerve) of lower body negative pressure (LBNP; -15 mmHg (1 mmHg =133.3 Pa)) was compared with the effect of intravenous adenosine (35, 70, and 140 |ag*kg"1*min_1). In eight subjects, the highest dose was reinfused during 100% oxygen to suppress arterial chemoreceptors. Blood pressure reductions during LBNP and adenosine (140 jxg-kg'^min"1) were similar. HR did not change significantly during LBNP (+2 ± 2 beats/min; mean ± SE) but increased at the highest adenosine dose (+25 ± 3 beats/min; p < 0.05). MSNA increased significantly (p < 0.05) during both interventions (+255 ± 82 and +247 ± 5 8 units/100 beats for adenosine and LBNP, respectively), and there was no difference in the MSNA response to these two stimuli (p > 0.1). Oxygen inhibited adenosine-induced increases in HR and MSNA (from +305 ± 99 to +198 ± 75 units/100 beats and from +26 ± 4 to +18 ± 3 beats/min;p < 0.05 for both comparisons). The MSNA response to these combined stimuli was similar to that observed during LBNP. In contrast, the residual HR response (+18 ± 3 beats/min) was significantly greater than the response to LBNP (+2 ± 2 beats/min; p < 0.05). These data indicate that arterial baroreceptor unloading cannot account for the marked adenosine-induced increase in HR, but may be sufficient to explain its effect on MSNA. The effect of 100% oxygen confirms that stimulation of carotid chemoreceptors accounts for approximately one-third of the HR and MSNA response to adenosine. However, other mechanisms, such as stimulation of adenosine-sensitive afferent nerves in other vascular beds, are involved in the HR and possibly the MSNA response.Key words: adenosine, human, heart rate, sympathetic nervous system, baroreflex.Résumé : L 'adénosine augmente la fréquence cardiaque et l'activité nerveuse sympathique de manière réflexe chez les humains conscients et ce, par 1*intermédiaire de divers mécanismes. Le but de la présente étude a été d'évaluer l'influence sur ces réponses d'une décharge des barorécepteurs artériels, d'une stimulation des chémorécepteurs carotidiens, ainsi que d'autres nerfs afférents sensibles à Padénosine. Chez 12 hommes sains, on a comparé l'effet d 'une pression négative des membres inférieurs (PNMI; -15 mmHg (1 mmHg = 133,3 Pa)) avec celui de Padénosine intraveineuse (35, 70 et 140 jig-kg^-m ür1) sur la pression artérielle, la fréquence cardiaque (FC) et l'activité nerveuse sympathique musculaire (ANSM; nerf périonnier). Chez huit sujets, on a réinjecté la plus forte dose d'adénosine en présence de 100% d'oxygène afin de supprimer les chémorécepteurs artériels. Les réductions de press...

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Mechanism of Adenosine-Induced Elevation of Pulmonary Capillary Wedge Pressure in Humans

Abstract: PCWP elevation in response to adenosine primarily results from changes in vascular loading rather than from direct effects on cardiac diastolic or systolic function.

Cited by 32 publications

References 48 publications

Murine Cardiac Function

Murine Cardiac Function

Direct Assessment of Coronary Steal and Associated Changes of Collateral Hemodynamics in Chronic Total Coronary Occlusions

Comparison of hemodynamic and sympathoneural responses to adenosine and lower body negative pressure in man

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