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Altered diastolic [Ca 2+] i handling in human ventricular myocytes from patients with terminal heart failure

Beuckelmann, Dirk J. ; Näbauer, Michael ; Krüger, Carster ; Erdmann, Erland

The American heart journal, 1995-04, Vol.129 (4), p.684-689 [Periódico revisado por pares]

New York, NY: Mosby, Inc

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Título:
Altered diastolic [Ca 2+] i handling in human ventricular myocytes from patients with terminal heart failure
Autor: Beuckelmann, Dirk J. ; Näbauer, Michael ; Krüger, Carster ; Erdmann, Erland
Assuntos: Biological and medical sciences ; Calcium - metabolism ; Calcium-Transporting ATPases - physiology ; Cardiology. Vascular system ; Cells, Cultured ; Diastole - physiology ; Heart ; Heart Failure - metabolism ; Heart Failure - pathology ; Heart Failure - physiopathology ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Humans ; In Vitro Techniques ; Medical sciences ; Middle Aged ; Myocardium - metabolism ; Myocardium - pathology ; Patch-Clamp Techniques ; Sarcolemma - enzymology ; Sarcoplasmic Reticulum - metabolism
É parte de: The American heart journal, 1995-04, Vol.129 (4), p.684-689
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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Descrição: To investigate whether the slow diastolic decay of [Ca 2+] i in myocardium of patients with heart failure is a result of alterations of the Ca 2+ adenosine triphosphatase of the sarcoplasmic reticulum or the sarcolemma, [Ca 2+] i transients were recorded in voltage-clamped ventricular cells isolated from hearts of patients with terminal heart failure or from undiseased donor hearts. To isolate the [Ca 2+] i-reuptake function of the sarcoplasmic reticulum, myocytes were dialyzed via the patch pipette with Na +-free solution and incubated in Ca 2+-free and Na +-free solution to inhibit Na + Ca 2+ exchange. After superfusion with Ca 2+-containing, Na +-free medium, the sarcoplasmic reticulum was loaded with Ca 2+ through repetitive voltage-clamp pulses to +10 mV. Under these conditions, [Ca 2+] i decay was significantly slower in myocytes from patients with heart failure (538 ± 66 msec) than in controls (305 ± 16 msec; p < 0.05). After the addition of 10 mmol/L of caffeine, [Ca 2+] i levels did not show appreciable decay between two voltage-clamp pulses in diseased and undiseased myocytes. We conclude that diastolic decay of [Ca 2+] i in ventricular myocytes from patients with terminal heart failure is aprtially the result of a decreased rate of Ca 2+ reuptake by the sarcoplasmic reticulum. Sarcolemmal Ca 2+ adenosine triphosphatase does not contribute significantly to cytoplasmic [Ca 2+] i removal during an individual heartbeat.
Editor: New York, NY: Mosby, Inc
Idioma: Inglês

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Altered diastolic [Ca 2+] i handling in human ventricular myocytes from patients with terminal heart failure

Beuckelmann, Dirk J. ; Näbauer, Michael ; Krüger, Carster ; Erdmann, Erland

New York, NY: Mosby, Inc

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