Use of a Short-Acting β1 Blocker During Endotoxemia May Reduce Cerebral Tissue Oxygenation if Hemodynamics are Depressed by a Decrease in Heart Rate

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Abstract

Background:

A decrease in heart rate (HR) using a short-acting β blocker has potential benefits in sepsis; however, depression of hemodynamics and reduction of cerebral oxygenation may also occur in endotoxemia.

Methods:

Seventeen swine were allocated to landiolol or control groups. In the landiolol group, the dose was sequentially changed from 0 to 40 to 200 μg kg−1 min−1, and stopped. Hemodynamics, blood variables, and the cerebral tissue oxygenation index (TOI) were recorded by near infrared spectroscopy at each dose. Lipopolysaccharide (LPS) was then administered continuously at 1 μg kg−1 h−1 after a 100 μg bolus administration. After 30 and 150 min, as two severity stages of endotoxemia (endotoxemia 1 and 2), landiolol was administered as above and measurements were made. In the control group, landiolol was not administered, but measurements were made.

Results:

LPS increased HR and landiolol decreased HR, with similar effects in each endotoxemia stage. In endotoxemia 1, LPS decreased stroke volume (SV), but landiolol restored SV to a value similar to that before endotoxemia, and did not decrease cardiac output (CO), even at 200 μg kg−1 min−1. In contrast, landiolol did not restore SV in endotoxemia 2, resulting in a decrease in CO and mean arterial pressure, accompanied with a dose-dependent decrease in TOI.

Conclusions:

A short-acting β blocker has various hemodynamic effects in endotoxemia. Use of a short-acting β blocker during endotoxemia may reduce cerebral tissue oxygenation if hemodynamics are depressed by a decrease in HR.

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