Premium
Left ventricular pressure‐volume relationship following rewarming from experimental hypothermia in rat
Author(s) -
Tveita Torkjel,
Han Young Soo,
Zhan WenZhi,
Sieck Gary C
Publication year - 2006
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.20.5.a1197-c
Subject(s) - preload , isovolumetric contraction , medicine , cardiology , diastole , hypothermia , stroke volume , pulse pressure , ventricular pressure , blood pressure , anesthesia , chemistry , heart rate , hemodynamics
This study was aimed at investigating whether left ventricular (LV) hypothermia‐induced dysfunction persisting after rewarming rat heart in situ could be characterized as systolic, diastolic, or combined disturbance using the Millar pressure‐volume (P‐V) conductance catheter system. Core temperature of 7 Sprague Dawley rats was lowered to 15°C, maintained at 15°C for 3h and finally rewarmed to 37°C. We evaluated systolic and diastolic function before cooling and after rewarming including preload recruitable stroke work (PRSW), maximum rate of increase in LV pressure (dP/dtmax), and its relation to end‐diastolic volume (dP/dtmax‐EDV) as well as the time constant of LV pressure decay, as an index of relaxation. The slope of the end‐diastolic P‐V relation (EDPVR), an index of LV stiffness, was also calculated. Rewarming from 15°C was associated with decrease in LV systolic pressure, dP/dtmax, maximal slope of diastolic pressure decrement, dP/dtmax‐EDV, PRSW, cardiac output (CO) and stroke volume (SV). Taken together, these observations indicate that cooling and rewarming induce long‐lasting effects on the excitation‐contraction coupling, the actin‐myosin interaction, as well as sarcoplasmic reticulum (SR) Ca2+ handling, leading posthypothermic LV dysfunction into a combined systolic and diastolic perturbation.