Key result
Endotoxin lowers mean arterial pressure by ~20 mm Hg and suppresses heart rate variability in rabbits.
Why the study?
Gram-negative septic shock causes severe hypotension and autonomic cardiovascular dysfunction, but the changes in autonomic modulation of cardiac activity during endotoxin shock are unclear.
Does Escherichia coli endotoxin-induced shock alter autonomic modulation of heart rate variability in anesthetized rabbits?
Does Escherichia coli endotoxin-induced shock alter autonomic modulation of heart rate variability in anesthetized rabbits?
Endotoxin shock in a rabbit model is associated with decreased sympathetic modulation of cardiac activity (low-frequency HR power) despite unchanged plasma catecholamines, suggesting HR variability could serve as an early marker for impending shock.
Answers are grounded in this paper and cite their sources.
Endotoxin shock reduces LF HR power without catecholamine change in rabbits; hypothesis-generating for HRV as early sepsis marker pending human validation.
Objective Gram-negative septic shock is associated with severe hypotension and autonomic cardiovascular dysfunction. We hypothesized that in an anesthetized rabbit model of endotoxin shock, autonomic modulation of cardiac activity, as measured by power spectral analysis of heart rate (HR) variability, would be decreased compared with the anesthetized control rabbits. Design Experimental, comparative study. Setting Laboratory of a university hospital. Subjects Fourteen adult male New Zealand white rabbits (2.7 to 3.1 kg body weight) were studied under anesthesia. Interventions None. Measurements and main results We studied the absolute and temporal changes in HR power spectra and plasma catecholamine concentrations in eight experimental and six control New Zealand white rabbits during Escherichia coli endotoxin-induced shock. HR, respirations, arterial blood pressure (BP), HR power spectra, and plasma catecholamine concentrations were measured at 5- to 10-min intervals for 60 mins in control rabbits or until the mean arterial pressure (MAP) decreased by > or = 20 mm Hg in experimental rabbits. There were no differences in basal HR, respiratory rate, BP, HR power spectra, or catecholamine concentrations between groups. After endotoxin administration, MAP decreased (82 +/- 7 vs. 62 +/- 5 mm Hg; p < .05) as did log low-frequency HR power (-2.14 +/- 2.46 vs. -2.20 +/- 2.48 beats/min2; p < .05). Low-frequency HR power and MAP remained unchanged in control animals. Log high-frequency HR power decreased in control and experimental rabbits (-1.02 +/- 1.34 vs. -1.69 +/- 2.12 [control], p < .05; -1.53 +/- 2.19 vs. -2.19 +/- 2.85 beats/min2 [experimental], p < .05). While there was an inverse relationship between low- and high-frequency HR power and MAP, the direction of change was opposite in six of six rabbits in the control group and in six of eight rabbits in the experimental group. Plasma catecholamine concentrations did not change during the experiment in either group. Conclusions Sympathetic modulation of cardiac activity decreased, while the sympathomedullary response remained unchanged during endotoxin shock. We speculate that a concomitant decrease in low-frequency HR power as MAP decreases may prove to be an early marker for impending shock.
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Goldstein et al. (1995) studied Gram-negative septic shock / Endotoxin shock (n=14). Escherichia coli endotoxin vs. Anesthetized control rabbits (no endotoxin) was evaluated on Absolute and temporal changes in heart rate power spectra (log low-frequency heart rate power) and mean arterial pressure (p=<.05). Escherichia coli endotoxin decreased mean arterial pressure (82 vs 62 mm Hg; p<0.05) and log low-frequency heart rate power (-2.14 vs -2.20 beats/min2; p<0.05) in anesthetized rabbits.
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