Abstract
Enflurane, at clinical concentrations, decreases the contractility of isolated intact cardiac muscle. The authors investigated the intracellular mechanism(s) of this depression by examining the Ca2+ activation of the contractile proteins and Ca2+ uptake and release from the sarcoplasmic reticulum (SR) using functionally skinned fibers from right ventricular papillary muscle of rabbits. This preparation permits control of intracellular ionic composition (pH 7.0, 20°C). The [Ca2+]-tension relationship and caffeine-induced tension transient (as a measure of the amount of Ca2+ release) were analyzed. Enflurane significantly but only slightly depressed the maximum Ca2+-activated tension (10% decrease at 5% enflurane) and did not change the [Ca2+] required for half-maximal activation of the fibers. In contrast, enflurane markedly inhibited the Ca2+ uptake by the SR (30-85% decrease at 2.5-7.5% enflurane). The inhibition was dose-dependent. Ca2+ release from the SR with 25 mM caffeine was not changed at low concentrations of enflurane (1-5%), but was decreased at high concentration (25% decrease at 7.5% enflurane). Enflurane (1-7.5%), however, increased (13-44%) the submaximum caffine (2 mM)-induced Ca2+ release from the SR, and the effect was not dose-dependent. The aforementioned effects were reversible. These results are similar to those previously reported for halothane. It is concluded that enflurane may induce myocardial depression mainly by inhibiting Ca2+ uptake by the SR.
| Original language | English |
|---|---|
| Pages (from-to) | 385-389 |
| Number of pages | 5 |
| Journal | Anesthesiology |
| Volume | 52 |
| Issue number | 5 |
| State | Published - Jan 1 1980 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Anesthesiology and Pain Medicine
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Effects of enflurane on functionally skinned myocardial fibers from rabbits. / Su, J. Y.; Kerrick, W. Glenn.
In: Anesthesiology, Vol. 52, No. 5, 01.01.1980, p. 385-389.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of enflurane on functionally skinned myocardial fibers from rabbits
AU - Su, J. Y.
AU - Kerrick, W. Glenn
PY - 1980/1/1
Y1 - 1980/1/1
N2 - Enflurane, at clinical concentrations, decreases the contractility of isolated intact cardiac muscle. The authors investigated the intracellular mechanism(s) of this depression by examining the Ca2+ activation of the contractile proteins and Ca2+ uptake and release from the sarcoplasmic reticulum (SR) using functionally skinned fibers from right ventricular papillary muscle of rabbits. This preparation permits control of intracellular ionic composition (pH 7.0, 20°C). The [Ca2+]-tension relationship and caffeine-induced tension transient (as a measure of the amount of Ca2+ release) were analyzed. Enflurane significantly but only slightly depressed the maximum Ca2+-activated tension (10% decrease at 5% enflurane) and did not change the [Ca2+] required for half-maximal activation of the fibers. In contrast, enflurane markedly inhibited the Ca2+ uptake by the SR (30-85% decrease at 2.5-7.5% enflurane). The inhibition was dose-dependent. Ca2+ release from the SR with 25 mM caffeine was not changed at low concentrations of enflurane (1-5%), but was decreased at high concentration (25% decrease at 7.5% enflurane). Enflurane (1-7.5%), however, increased (13-44%) the submaximum caffine (2 mM)-induced Ca2+ release from the SR, and the effect was not dose-dependent. The aforementioned effects were reversible. These results are similar to those previously reported for halothane. It is concluded that enflurane may induce myocardial depression mainly by inhibiting Ca2+ uptake by the SR.
AB - Enflurane, at clinical concentrations, decreases the contractility of isolated intact cardiac muscle. The authors investigated the intracellular mechanism(s) of this depression by examining the Ca2+ activation of the contractile proteins and Ca2+ uptake and release from the sarcoplasmic reticulum (SR) using functionally skinned fibers from right ventricular papillary muscle of rabbits. This preparation permits control of intracellular ionic composition (pH 7.0, 20°C). The [Ca2+]-tension relationship and caffeine-induced tension transient (as a measure of the amount of Ca2+ release) were analyzed. Enflurane significantly but only slightly depressed the maximum Ca2+-activated tension (10% decrease at 5% enflurane) and did not change the [Ca2+] required for half-maximal activation of the fibers. In contrast, enflurane markedly inhibited the Ca2+ uptake by the SR (30-85% decrease at 2.5-7.5% enflurane). The inhibition was dose-dependent. Ca2+ release from the SR with 25 mM caffeine was not changed at low concentrations of enflurane (1-5%), but was decreased at high concentration (25% decrease at 7.5% enflurane). Enflurane (1-7.5%), however, increased (13-44%) the submaximum caffine (2 mM)-induced Ca2+ release from the SR, and the effect was not dose-dependent. The aforementioned effects were reversible. These results are similar to those previously reported for halothane. It is concluded that enflurane may induce myocardial depression mainly by inhibiting Ca2+ uptake by the SR.
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UR - http://www.scopus.com/inward/citedby.url?scp=0018832605&partnerID=8YFLogxK
M3 - Article
C2 - 7377571
AN - SCOPUS:0018832605
VL - 52
SP - 385
EP - 389
JO - Anesthesiology
JF - Anesthesiology
SN - 0003-3022
IS - 5
ER -