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Conditions for increased cardiac output during occlusion of the descending thoracic aorta
Insights
Occluding the aorta increases stroke volume with intravenous isoproterenol but not with intracoronary infusion. This difference is due to greater increases in ventricular filling during intravenous administration, affecting both ventricles.
Area of Science:
- Cardiovascular Physiology
- Hemodynamics
- Pharmacology
Background:
- Descending thoracic aorta occlusion (AO) affects stroke volume differently based on isoproterenol administration route.
- Intravenous (i.v.) isoproterenol increases stroke volume during AO, while intracoronary (i.c.) isoproterenol does not.
Purpose of the Study:
- To investigate the hemodynamic mechanisms behind the differing stroke volume responses to AO during i.v. versus i.c. isoproterenol infusion.
- To compare the adjustments of both right and left ventricles to AO under these two conditions.
Main Methods:
- Anesthetized open-chest pigs were used to compare hemodynamic responses.
- Descending thoracic aorta occlusion was performed during continuous i.v. and i.c. isoproterenol infusions.
- Left ventricular systolic pressure, end-systolic and end-diastolic segment lengths, and inferior caval vein blood flow were measured.
Main Results:
- AO caused similar increases in left ventricular systolic pressure and end-systolic length with both i.v. and i.c. isoproterenol.
- Stroke volume increased significantly with i.v. (26.3%) but not i.c. (3.8%) isoproterenol.
- End-diastolic segment lengths increased more with i.v. than i.c. infusion in both ventricles, indicating greater preload augmentation.
Conclusions:
- The difference in stroke volume response to AO during i.v. versus i.c. isoproterenol is attributed to greater preload increase with i.v. administration.
- This preload augmentation, affecting both ventricles, is a key factor in the enhanced stroke volume response observed with systemic isoproterenol infusion.
Abstract:
Previous studies have demonstrated that occlusion of the descending thoracic aorta (AO) at constant heart rate induces a rise in stroke volume during a continuous intravenous (i.v.) isoproterenol infusion, but no change in stroke volume during a selective inotropic stimulation of the left ventricle as achieved by an intracoronary (i.c.) isoproterenol infusion. To determine the mechanism for this difference in stroke volume response, the haemodynamic adjustments of both the right and the left ventricle to AO during continuous i.v. and i.c. isoproterenol infusion in anesthetized open-chest pigs were compared. The AO induced a similar rise in left ventricular systolic pressure and end-systolic segment length (measured by an ultrasonic technique) in both ventricles whether isoproterenol was infused i.v. or i.c., but stroke volume rose by 26.3 (11.9-38.1%) (median and 95% confidence interval) (P less than 0.01) during i.v., compared with 3.8 (-7.4-14.7)% (n.s.) during i.c. isoproterenol infusion (difference in response: P less than 0.01). End-diastolic segment length increased more by AO during i.v. than i.c. isoproterenol infusion; 7.8 (5.1-16.9)% vs. 5.7 (3.1-8.5)% (difference in response: P less than 0.01) in the left ventricle, and 5.9 (3.5-8.1)% vs. 1.0 (-1.5-3.3)% (difference in response: P less than 0.01) in the right ventricle. Redistribution of blood through the inferior caval vein measured immediately after AO, amounted to 130 (110-172) ml during i.v. and to 77 (52-89) ml during i.c. isoproterenol infusion (n = 3).(ABSTRACT TRUNCATED AT 250 WORDS)