Pulmonary capillary wedge pressure and pulmonary arterial pressure in heart failure patients with sleep-disordered breathing

2009 ◽  
Vol 10 (7) ◽  
pp. 726-730 ◽  
Author(s):  
Olaf Oldenburg ◽  
Thomas Bitter ◽  
Marcus Wiemer ◽  
Christoph Langer ◽  
Dieter Horstkotte ◽  
...  
1987 ◽  
Vol 63 (1) ◽  
pp. 145-151 ◽  
Author(s):  
D. P. Nyhan ◽  
P. W. Clougherty ◽  
H. M. Goll ◽  
P. A. Murray

Our objectives were to investigate the pulmonary vascular effects of exogenously administered bradykinin at normal and reduced levels of cardiac index in intact conscious dogs and to assess the extent to which the pulmonary vascular response to bradykinin is the result of either cyclooxygenase pathway activation or reflex activation of sympathetic beta-adrenergic and -cholinergic receptors. Multipoint pulmonary vascular pressure-cardiac index (P/Q) plots were constructed during normoxia in conscious dogs by step-wise constriction of the thoracic inferior vena cava to reduce Q. In intact dogs, bradykinin (2 micrograms X kg-1 X min-1 iv) caused systemic vasodilation, i.e., systemic arterial pressure was slightly decreased (P less than 0.05), Q was markedly increased (P less than 0.01), and mixed venous PO2 and oxygen saturation (SO2) were increased (P less than 0.01). Bradykinin decreased (P less than 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure) over the entire range of Q studied (140–60 ml X min-1 X kg-1) in intact dogs. During cyclooxygenase pathway inhibition with indomethacin, bradykinin again decreased (P less than 0.05) pulmonary arterial pressure-pulmonary capillary wedge pressure at every level of Q, although the magnitude of the vasodilator response was diminished at lower levels of Q (60 ml X min-1 X kg-1). Following combined administration of sympathetic beta-adrenergic and -cholinergic receptor antagonists, bradykinin still decreased (P less than 0.01) pulmonary arterial pressure-pulmonary capillary wedge pressure over the range of Q from 160 to 60 ml X min-1 X kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)


1988 ◽  
Vol 118 (2) ◽  
pp. 168-172 ◽  
Author(s):  
Niels Keller ◽  
John Larsen ◽  
Roman Sykulski ◽  
Tommy Storm ◽  
Gorm Thamsborg

Abstract. In order to evaluate the potential relationship between atrial pressure development and release of atrial natriuretic factor (ANF), 33 patients with congestive heart failure were investigated with rightsided heart catheterization during supine graded bicycle exercise. Resting plasma ANF levels were higher in patients with heart failure as compared with normal controls, 75.1 ± 45.6 pmol/l vs 12.3 ± 6.2 pmol/l (mean ± sd, N = 33 and N = 42, respectively) and correlated with right atrial, pulmonary arterial and pulmonary capillary wedge pressures. During exercise, central pressures rose steeply with a simultaneous increase in plasma ANF in all patients. Plasma ANF levels correlated with heart rate at a workload of 25 w, to pulmonary arterial and pulmonary capillary wedge pressure at 50 w, and to pulmonary capillary wedge pressure at 75 w. The increments in ANF levels between the different workloads during exercise did not correlate with the corresponding increments in pressure values. In congestive heart failure, the capability of ANF secretion in consequence to pressure stimuli is preserved, and left atrial pressure seems to be the major stimulus for ANF release during exercise.


2012 ◽  
Vol 28 (6) ◽  
pp. 728-734 ◽  
Author(s):  
Akiomi Yoshihisa ◽  
Satoshi Suzuki ◽  
Takashi Owada ◽  
Shoji Iwaya ◽  
Hiroyuki Yamauchi ◽  
...  

1992 ◽  
Vol 123 (2) ◽  
pp. 427-432 ◽  
Author(s):  
Eulogio E. Martinez ◽  
Steven F. Horowitz ◽  
Helio J. Castello ◽  
Mario L.V. Castiglioni ◽  
Antonio C.C. Carvalho ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document