Premium
Effects of Formaldehyde on Cardiovascular System in In Situ Rat Hearts
Author(s) -
Takeshita Daisuke,
NakajimaTakenaka Chikako,
Shimizu Juichiro,
Hattori Hiroshi,
Nakashima Tamiji,
Kikuta Akio,
Matsuyoshi Hiroko,
Takaki Miyako
Publication year - 2009
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2009.00442.x
Subject(s) - ventricle , medicine , ryanodine receptor , heart failure , metabolic acidosis , cardiology , acidosis , myofibril , sarcoplasm , calcium , chemistry , anesthesia
The aim of the present study was to examine the effects of formaldehyde solution on rat left ventricular function and compare it with those in hypertrophic hearts treated with isoproterenol by pressure–volume measurements with the catheter method. After 20–30 min. of intravenous infusion of 3.7% formaldehyde solution (FA) at 10 μl (3.7 mg)/kg/min, normal and hypertrophic hearts showed significant decreases in left ventricle end‐systolic pressure (ESP), heart rate and cardiac output per minute, indicating an acute pumping failure. Hypertrophic hearts showed significantly smaller ESP, stroke volumes and cardiac output than those in normal hearts. Systolic pressure–volume area at midrange left ventricular volume (PVA mLVV : a mechanical work capability index) was significantly smaller than that in normal hearts and per cent of mean PVA mLVV versus pre‐infusion mean value in hypertrophic hearts was significantly decreased compared to normal hearts 30 min. after FA infusion. The marked decrease in pH, base excess and no changes in PaO 2 and PaCO 2 suggest metabolic acidosis. The correction of metabolic acidosis with 9% NaHCO 3 did not influence on the acute pumping failure, indicating that metabolic acidosis did not cause it. Ultrastructural observations revealed marked dilation of the sarcoplasmic reticulum with intact sarcolemmal membranes and no disintegration of muscle myofibrils. Ryanodine receptors and calcium (Ca 2+ ) pumps (SERCA2A) located in the sarcoplasmic reticulum have major roles in the cytosolic Ca 2+ handling. Taken together, acute pumping failure by FA may derive from the impairment of Ca 2+ handling in the cardiac excitation–contraction coupling.