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[During experimental coronary occlusion dobutamine further slows down the time constant of isovolumetric relaxation]
S Perlini1, T E Meyer, L Bernardi
1Clinica Medica I, Università degli Studi, Pavia.
Insights
Beta-adrenergic stimulation improves left ventricular (LV) relaxation during ischemia, but acute regional ischemia itself slows LV pressure fall. Dobutamine infusion counteracted ischemia-induced slowing of LV relaxation.
Area of Science:
- Cardiology
- Physiology
- Pharmacology
Background:
- Beta-adrenergic stimulation enhances myocardial relaxation and LV pressure fall.
- Acute regional ischemia slows LV relaxation due to mechanical nonuniformity.
Purpose of the Study:
- To assess the effect of inotropic stimulation on LV pressure fall during acute regional ischemia.
- To investigate how dobutamine influences LV relaxation dynamics under ischemic conditions.
Main Methods:
- 7 anesthetized dogs were instrumented with LV and aortic micromanometers.
- Sonomicrometers monitored subendocardial segment length during regional ischemia induced by circumflex artery occlusion.
- Left ventricular (LV) pressure fall time constant (tau) was derived during dobutamine infusion and compared to baseline and ischemic states.
Main Results:
- Acute regional ischemia increased tau (36 +/- 2 ms vs. 32 +/- 2 ms, p < 0.01), indicating slower LV relaxation.
- Dobutamine infusion reduced tau (27 +/- 2 ms vs. 32 +/- 2 ms, p < 0.01), improving LV relaxation.
- Ischemia-induced slowing of tau was partially counteracted by dobutamine infusion.
Conclusions:
- Beta-adrenergic stimulation, exemplified by dobutamine, can improve myocardial relaxation even during acute regional ischemia.
- LV mechanical nonuniformity during ischemia significantly impairs relaxation dynamics.
- Inotropic agents may mitigate the negative effects of ischemia on LV diastolic function.
Abstract:
It has been shown that the time constant (tau) of isovolumic left ventricular (LV) pressure fall is shortened by beta-adrenergic stimulation, possibly reflecting enhanced myocardial relaxation and improved uniformity within the LV wall. Conversely, acute regional ischaemia , slows tau due to mechanical nonuniformity between the nonischaemic and the ischaemic regions. In order to assess the effect of inotropic stimulation on LV pressure fall during acute regional ischaemia, 7 anaesthetized dogs (16 +/- 2 kg) were instrumented with LV and aortic micromanometers. Sonomicrometers were implanted in the areas supplied by the left circumflex and anterior descending arteries to monitor subendocardial segment length (L). After baseline recordings, acute regional ischaemia was induced by 60 s occlusion of the proximal circumflex artery. After a 30 min recovery, the same was repeated during dobutamine infusion (5 micrograms/kg/min). In order to derive tau from heart beats with comparable end-systolic pressures, a caval occlusion run was performed at each stage. The % systolic bulging of the ischaemic zone was defined as: (maximal L--end-diastolic L)/end-diastolic L x 100. The fitting of the exponential model used to derive tau was always good (r > or = 0.99). At comparable end-systolic pressures, tau was increased by acute regional ischaemia (36 +/- 2 versus 32 +/- 2 ms, p < 0.01) and reduced by dobutamine infusion (27 +/- 2 versus 32 +/- 2 ms, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)