PMID- 1309621
OWN - NLM
STAT- MEDLINE
DCOM- 19920211
LR  - 20190626
IS  - 0002-8703 (Print)
IS  - 0002-8703 (Linking)
VI  - 123
IP  - 1
DP  - 1992 Jan
TI  - Inotropic and lusitropic dysfunction in myocardium from patients with dilated 
      cardiomyopathy.
PG  - 116-28
AB  - Isometric force of contraction (DT), peak rate of tension increase (+T), peak 
      rate of tension decrease (-T), time to peak tension (TPT), and time to 
      half-relaxation (T 1/2 T) were measured in electrically driven human papillary 
      muscle strips (New York Heart Association [NYHA] class IV heart transplants, 
      dilated cardiomyopathy; nonfailing (NF) donor hearts, brain dead) (1 Hz, 37 
      degrees C) under basal conditions (1.8 mmol/L Ca2+) and after stimulation with 
      isoprenaline, ouabain, and Ca2+. There was no difference in the isometric 
      contraction (+T, -T, TPT, and T 1/2 T) between NYHA IV hearts and NF hearts under 
      basal conditions. Inotropic stimulation above 300% of basal DT increased -T 
      significantly more in NF hearts (p less than 0.05) compared with NYHA IV hearts. 
      The effectiveness of ouabain and Ca2+ to increase DT was not significantly 
      changed in NYHA IV hearts compared with NF hearts. The isoprenaline-mediated 
      increase in DT was reduced (p less than 0.05) in NYHA IV hearts to a similar 
      extent (70%) as beta-adrenoceptors were downregulated. When the rate of 
      stimulation was increased to 3 Hz (force-frequency relationship), force of 
      contraction increased only in NF preparations, whereas it decreased in NYHA IV 
      myocardium (p less than 0.05). It was concluded that the contractile apparatus in 
      terminally failing human myocardium is sufficient to maximally increase DT. 
      During inotropic stimulation, abnormalities in diastolic rather than systolic 
      contraction become evident. This may indicate abnormal intracellular Ca2+ 
      handling.
FAU - Schwinger, R H
AU  - Schwinger RH
AD  - Medizinische Klinik I, Universitat Munchen, Germany.
FAU - Bohm, M
AU  - Bohm M
FAU - Erdmann, E
AU  - Erdmann E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am Heart J
JT  - American heart journal
JID - 0370465
RN  - 0 (Receptors, Adrenergic, beta)
RN  - 5ACL011P69 (Ouabain)
RN  - L628TT009W (Isoproterenol)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Calcium/metabolism/pharmacology
MH  - Cardiomyopathy, Dilated/*physiopathology
MH  - Heart/drug effects/physiology/*physiopathology
MH  - Humans
MH  - In Vitro Techniques
MH  - Isometric Contraction/drug effects/physiology
MH  - Isoproterenol/pharmacology
MH  - Myocardial Contraction/drug effects/*physiology
MH  - Myocardium/chemistry/metabolism
MH  - Ouabain/pharmacology
MH  - Papillary Muscles/physiopathology
MH  - Receptors, Adrenergic, beta/analysis
EDAT- 1992/01/01 00:00
MHDA- 1992/01/01 00:01
CRDT- 1992/01/01 00:00
PHST- 1992/01/01 00:00 [pubmed]
PHST- 1992/01/01 00:01 [medline]
PHST- 1992/01/01 00:00 [entrez]
AID - 0002-8703(92)90755-K [pii]
AID - 10.1016/0002-8703(92)90755-k [doi]
PST - ppublish
SO  - Am Heart J. 1992 Jan;123(1):116-28. doi: 10.1016/0002-8703(92)90755-k.