TY - JOUR
T1 - Influence of the pericardium on ventricular loading during respiration
AU - Takata, M.
AU - Mitzner, W.
AU - Robotham, J. L.
PY - 1990
Y1 - 1990
N2 - The influence of the pericardium on ventricular loading during respiration was studied in 17 acutely instrumented anesthetized dogs. Changes in intrapericardial surface pressures (Ppe) on the ventricles were measured by use of air-filled flat latex balloons during acute changes in ventricular loading with the chest open or during negative intrathoracic pressure (NITP) produced by phrenic nerve stimulation with the chest closed. Ppe always demonstrated a phasic change within a cardiac cycle, with its maximum near end diastole and minimum near end systole, and a waveform similar to ventricular dimensions measured by sonomicrometer crystals. With the chest open we found that 1) inferior vena caval constriction decreased Ppe on both ventricles at end diastole (P < 0.01), 2) aortic constriction increased Ppe on both ventricles at end systole and end diastole (P < 0.05), and 3) pulmonary artery constriction increased Ppe on the right ventricle (RV) (P < 0.01) while decreasing Ppe on the left ventricle (LV) at end diastole (P < 0.05). Thus regional Ppe over a ventricle is influenced by changes in ventricular loading conditions. During NITP with lung volume either constant or increased, Ppe over the anterolateral LV decreased less than two independent extrapericardial measures of intrathoracic pressure, and this resulted in an increased transpericardial pressure at end systole (P < 0.05) and end diastole (P < 0.01). During NITP with increased transpericardial pressure, Ppe over the anterior LV, lateral LV, and RV inflow showed small regional differences, but all decreased less than esophageal pressure (P < 0.01). These results suggest that the increase in transpericardial pressure during late diastole to early systole, produced by increases in ventricular volume during NITP, could effectively attenuate the increases in ventricular preload and afterload caused by respiration, analogous to a negative feedback loop.
AB - The influence of the pericardium on ventricular loading during respiration was studied in 17 acutely instrumented anesthetized dogs. Changes in intrapericardial surface pressures (Ppe) on the ventricles were measured by use of air-filled flat latex balloons during acute changes in ventricular loading with the chest open or during negative intrathoracic pressure (NITP) produced by phrenic nerve stimulation with the chest closed. Ppe always demonstrated a phasic change within a cardiac cycle, with its maximum near end diastole and minimum near end systole, and a waveform similar to ventricular dimensions measured by sonomicrometer crystals. With the chest open we found that 1) inferior vena caval constriction decreased Ppe on both ventricles at end diastole (P < 0.01), 2) aortic constriction increased Ppe on both ventricles at end systole and end diastole (P < 0.05), and 3) pulmonary artery constriction increased Ppe on the right ventricle (RV) (P < 0.01) while decreasing Ppe on the left ventricle (LV) at end diastole (P < 0.05). Thus regional Ppe over a ventricle is influenced by changes in ventricular loading conditions. During NITP with lung volume either constant or increased, Ppe over the anterolateral LV decreased less than two independent extrapericardial measures of intrathoracic pressure, and this resulted in an increased transpericardial pressure at end systole (P < 0.05) and end diastole (P < 0.01). During NITP with increased transpericardial pressure, Ppe over the anterior LV, lateral LV, and RV inflow showed small regional differences, but all decreased less than esophageal pressure (P < 0.01). These results suggest that the increase in transpericardial pressure during late diastole to early systole, produced by increases in ventricular volume during NITP, could effectively attenuate the increases in ventricular preload and afterload caused by respiration, analogous to a negative feedback loop.
KW - cardiorespiratory
KW - dog
KW - ventricular interdependence
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U2 - 10.1152/jappl.1990.68.4.1640
DO - 10.1152/jappl.1990.68.4.1640
M3 - Article
C2 - 2347803
AN - SCOPUS:0025337787
SN - 0161-7567
VL - 68
SP - 1640
EP - 1650
JO - Journal of applied physiology
JF - Journal of applied physiology
IS - 4
ER -