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

Ovid Technologies (Wolters Kluwer Health) - Tập 92 Số 3 - Trang 371-379 - 1995
Amit Nussbacher1,2, Sigemituzo Ariê1,2, Roberto Kalil Filho1,2, Pedro Horta1,2, Marc D. Feldman1,2, Giovanni Bellotti1,2, Fúlvio Pileggi1,2, Mark Ellis1,2, William H. Johnson1,2, Gustavo B. Camarano1,2, David A. Kass1,2
1Department of Medicine (D.A.K.), Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Md.
2From Instituto do Coraçao (A.N., S.A., R.K., P.H., G.B., F.P.), University of Sáo Paulo, Brazil; Division of Cardiology (M.D.F., M.E., W.H.J., G.B.C.), University of Virginia (Charlottesville); and Department of Medicine (D.A.K.), Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Md.

Tóm tắt

Background Continuous intravenous administration of adenosine to humans often results in a paradoxical rise in pulmonary capillary wedge pressure (PCWP), whereas arterial resistance is lowered and cardiac output and heart rate increase. This is believed to be due to diastolic stiffening of the ventricle or to a negative inotropic effect. In the present study, we tested these and other mechanisms by using pressure–volume (PV) analysis and echocardiography. Methods and Results Fifteen patients with normal rest left ventricular function underwent cardiac catheterization and received adenosine at a rate of 140 μg/kg per minute IV for 6 to 10 minutes. PV relations were measured in 9 patients (without coronary artery disease) using the conductance catheter method. In 6 additional patients with coronary artery disease, echocardiograms were used to assess wall thickness and function, and aortic and coronary sinus blood, lactate, oxygen, and adenosine levels were measured. Adenosine increased PCWP by 19% (+2.6 mm Hg) in both patient groups while lowering arterial load by 30% and increasing cardiac output by 45% (all P <.001). There was no significant effect of adenosine on mean linear chamber compliance or monoexponential elastic stiffness, as the diastolic PV relation was unchanged in most patients. Diastolic wall thickness also was unaltered. Thus, the PCWP rise did not appear to be due to diastolic stiffening. Adenosine induced a rightward shift of the end-systolic PV relation (ESPVR) (+12.7±3.7 mL) without a slope change. This shift likely reflected effects of afterload reduction, as other indexes (stroke work–end-diastolic volume relation and dP/dt max at matched preload) were either unchanged or increased. Furthermore, this modest shift in ESPVR was more than compensated for by vasodilation and tachycardia, so reduced systolic function could not explain the increase in PCWP. There also was no net lactate production to suggest ischemia. Rather than arising from direct myocardial effects, PCWP elevation was most easily explained by a change in vascular loading, as both left ventricular end-diastolic volume and right atrial pressure increased ( P <.05). This suggests that adenosine induced a redistribution of blood volume toward the central thorax. Conclusions PCWP elevation in response to adenosine primarily results from changes in vascular loading rather than from direct effects on cardiac diastolic or systolic function.

Từ khóa


Tài liệu tham khảo

10.1016/0033-0620(89)90015-7

10.7326/0003-4819-113-2-104

10.1016/0301-0082(86)90005-5

10.1097/00000542-198410000-00007

10.1042/cs0790131

10.1111/j.1365-2125.1987.tb03227.x

10.1161/circ.82.5.2225364

10.1016/0735-1097(91)90604-8

10.1161/circ.86.3.1516201

10.1161/circ.86.3.1516202

10.1093/oxfordjournals.eurheartj.a059629

10.1161/circ.82.1.2364527

10.1161/circ.86.3.1516176

Sutton FJ. Vasodilator therapy. Am J Med. 1986;80(suppl 2B):54-58.

10.1016/0002-8703(93)90069-L

10.1161/circ.57.1.618383

10.1161/circ.65.7.6280890

10.1161/01.RES.51.4.465

10.1016/0002-9149(85)91169-5

10.1016/0735-1097(91)90795-B

10.1002/ccd.1810150314

10.1161/circ.81.2.2297855

10.1161/circ.85.4.1555285

Steendijk P, Van der Velde ET, Baan J. Left ventricular stroke volume by single and dual excitation of conductance catheter in dogs. Am J Physiol. 1993;264:H2198-H2207.

Sunagawa K Maughan WL Burkhoff D Sagawa K. Left ventricular interaction with arterial load studied in isolated canine ventricle. Am J Physiol. 1983;215(Heart Circ Physiol 14):H773-H780.

10.1161/01.CIR.86.2.513

10.1161/circ.71.5.3986986

10.1161/01.RES.56.6.808

Touchstone DA, Beller GA, Nygaard TW, Tedesco C, Kaul S. Effects of successful intravenous reperfusion therapy on regional myocardial function and geometry in humans: a tomographic assessment using two-dimensional echocardiography. J Am Coll Cardiol. 1998;13:1506-1513.

10.1093/clinchem/38.2.256

Linden J, Taylor H, Feldman MD, Woodward EB, Ayers CR, Ripley ML, Patel A. The precise radioimmunoassay of adenosine: minimization of sample collection artifacts and immunocrossreactivity. Anal Biochem. 1992;210:246-254.

10.1093/clinchem/13.4.314

10.1172/JCI112976

10.1016/S0735-1097(10)80216-5

10.1161/res.70.6.1374299

10.1113/jphysiol.1989.sp017698

10.1161/res.63.4.3168181

10.1093/cvr/27.3.403

10.1007/BF00582203

10.1002/j.1875-9114.1990.tb02573.x

10.1016/0022-2828(91)90106-V

10.1161/res.61.6.3677336

10.1161/circ.76.6.3454658

10.1161/01.CIR.74.5.1107

10.1152/ajpcell.1990.259.4.C619

10.1161/circ.87.4.8462143

10.1111/j.1365-2125.1992.tb04004.x

10.1097/00000542-198406000-00005

10.1161/res.68.3.1683822

Thông tin
Thông tin xuất bản

Ovid Technologies (Wolters Kluwer Health)

Tập 92 Số 3

371-379

Thông tin tác giả