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Effect of severe, nonhypotensive hypovolemia on heart rate in rats
Author(s) -
Stedenfeld Kristen A,
Hoffmann Myriam L,
Sved Alan F,
Stricker Edward M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.738.21
Subject(s) - hypovolemia , heart rate , bradycardia , tachycardia , medicine , blood volume , mean arterial pressure , blood pressure , anesthesia , cardiology , sympathetic nervous system
The present experiments evaluated the effects of progressive, severe hypovolemia on heart rate (HR) and mean arterial blood pressure (MAP) in adult rats. HR and MAP were continuously monitored with telemetry. Subcutaneous injection of a 30% polyethylene glycol (PEG) solution was used to produce a volume loss of 4–5% per hour for 5–6 h, a rate that subsequently slowed with volume deficits asymptoting at ~40% during hours12–24 post‐injection. In all animals, MAP was stable at ~110 mm Hg throughout the 24‐h test period. In contrast, HR increased gradually by ~50 bpm during the first 4 h from basal values of 370–400 bpm, and then it fell by 150–200 bpm during the next 4 h before gradually rebounding during the next 12 h. These results allow the hypotheses that the initial tachycardia reflected excitation of the sympathoadrenal system, the subsequent fall in HR reflected an inhibition of the sympathetic nervous system associated with a large and sustained drop in plasma volume unrelated to changes in MAP, and the later restoration of HR reflected a return of sympathetic activity when the rate of volume loss slowed. Similar to these findings, previous studies have shown that bradycardia follows tachycardia after severe hemorrhage; consequently, the present results suggest that this pattern results from the induced change in blood volume. Ongoing experiments are evaluating these hypotheses.