Inotropic Effects of Isoflurane on Mechanics of Contraction in Isolated Cat Papillary Muscles from Normal and Failing Hearts

Kemmotsu, Osamu; Hashimoto, Yoshiaki; Shimosato, Shiro

doi:10.1097/00000542-197311000-00003

Cited by 83 publications

(9 citation statements)

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“…Although isoflurane depresses myocardial contractility in vitro (21), isoflurane is not a potent myocardial depressant in vivo. Awake values were not available for comparison in our patients but the cardiac outputs recorded during the normotensive anesthetized state were clearly adequate.…”

Section: Discussionmentioning

confidence: 94%

Cardiovascular Effects of Isoflurane-Induced Hypotension for Cerebral Aneurysm Surgery

Lam

Gelb

1983

Anesthesia & Analgesia

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A. M. LAM, A. W. GELB: Cardiovascular effects of isoflurane-induced hypotension for cerebral aneurysm surgery. Anesth Analg 1983;62:742-8. sion (4.6 rt 0.3 Llmin) was not significantly different from the control normotensive value (4.80 * 0.3 Umin). Gas tensions during hypotension and during normotension were;Pao, 116 * 6 and 111 * 8 mm Hx; Paco, 33 2 1 and 34 * 1 mm Hg; respectively. No complication could be attributed to the use of isoflurane. We conclude that isopurane can be employed safely and effectively as a hypotensiz)e agent in neurosurgery.Deliberate hypotension was induced with isoflurane in 13 patients undergoing craniotomy for clipping of aneurysms. Cardiovascular function and gas exchange were monitored before, durinx, and after hypotension. In all cases, the desired lezwl ofl hypotension -[40 -+ 1 ( S E M ) mm Hg] was achieved readily with prompt onset (5.7 2 1 .O min) and recovery (6.3 t 0.7 min). Cardiac output during hypoten-

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Section: Discussionmentioning

confidence: 94%

Cardiovascular Effects of Isoflurane-Induced Hypotension for Cerebral Aneurysm Surgery

Lam

Gelb

1983

Anesthesia & Analgesia

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“…Interestingly, inotropic state is greatly enhanced even in ␤1/␤2-AR double knockouts upon transition from anesthetized to awakening states. Depression of myocardial contractility while under isoflurane anesthesia can be due to indirect effects to reduce sympathetic outflow, as well as direct inhibitory effects on cardiac muscle (42)(43)(44). Despite the reduced positive and negative dP/dt values in ␤1/␤2-AR double knockouts, these mice develop equivalent peak left ventricular pressures in comparison to their wild type counterparts.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular and Metabolic Alterations in Mice Lacking Both β1- and β2-Adrenergic Receptors

Rohrer¹,

Chruscinski

Schauble

et al. 1999

Journal of Biological Chemistry

259

185

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The activation state of ␤-adrenergic receptors (␤-ARs) in vivo is an important determinant of hemodynamic status, cardiac performance, and metabolic rate. In order to achieve homeostasis in vivo, the cellular signals generated by ␤-AR activation are integrated with signals from a number of other distinct receptors and signaling pathways. We have utilized genetic knockout models to test directly the role of ␤1-and/or ␤2-AR expression on these homeostatic control mechanisms. Despite total absence of ␤1-and ␤2-ARs, the predominant cardiovascular ␤-adrenergic subtypes, basal heart rate, blood pressure, and metabolic rate do not differ from wild type controls. However, stimulation of ␤-AR function by ␤-AR agonists or exercise reveals significant impairments in chronotropic range, vascular reactivity, and metabolic rate. Surprisingly, the blunted chronotropic and metabolic response to exercise seen in ␤1/ ␤2-AR double knockouts fails to impact maximal exercise capacity. Integrating the results from single ␤1-and ␤2-AR knockouts as well as the ␤1-/␤2-AR double knockout suggest that in the mouse, ␤-AR stimulation of cardiac inotropy and chronotropy is mediated almost exclusively by the ␤1-AR, whereas vascular relaxation and metabolic rate are controlled by all three ␤-ARs (␤1-, ␤2-, and ␤3-AR). Compensatory alterations in cardiac muscarinic receptor density and vascular ␤3-AR responsiveness are also observed in ␤1-/␤2-AR double knockouts. In addition to its ability to define ␤-AR subtype-specific functions, this genetic approach is also useful in identifying adaptive alterations that serve to maintain critical physiological setpoints such as heart rate, blood pressure, and metabolic rate when cellular signaling mechanisms are perturbed.

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“…The decreases in maximal and submaximal Ca2+ -activated tension development of the contractile proteins and in Ca2+ uptake by the SR produced by isoflurane in skinned fibers of PM could be responsible in part for the isoflurane-induced decreases in myocardial contractility observed by others in isolated intact muscle preparations (2,18). The marked discrepancy between skinned myocardial fibers ( Table 1, Figs. 3,6) and isolated intact preparations (2,18) in the degree of depression by isoflurane, in contrast to that by halothane (3) or enflurane (4), could be due to a greater frequency-dependent effect (18). At the phys- iologic frequency of stimulation (>1 Hz), isoflurane causes much less depression of the peak development tension of isolated intact PM from guinea pigs (18) than at low frequencies.…”

Section: Discussionmentioning

confidence: 87%

Intracellular Mechanism of Action of Isoflurane and Halothane on Striated Muscle of the Rabbit

Bell

1986

Anesthesia & Analgesia

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SU JY, BELL JG. Intracellular mechanism of action of isoflurane and halothane on striated muscle of the rabbit. Anesth Analg 1986;65:457-62.Studies were conducted on the effects of isoflurane and halothane on intracellular mechanisms of striated muscle contraction: Caz+ activation of the contractile proteins and Ca2+ uptake and release from the sarcoplasmic reticulum. Functionally skinned muscle fibers (sarcolemma disrupted by homogenization) from isolated papilla y muscle (PM), soleus (SL) (slow-twitch skeletal muscle), and adductor magnus ( A M ) (fast-twitch skeletal muscle) of rabbits were mounted on a photodiode tension transducer. They were immersed in control solution (saturated with NJ, then in test solution (saturated with anesthetic-N, mixture), and in control solution again. The following two studies were carried out: I) in the study of Ca2+-activated tension development of the contractile proteins, free Ca2 + concentration in the bathing solution was controlled by the use of a high EGTA (7 mM), and 21 in the study of Ca" uptake and release from the sarcoplasmic reticulum (SR), Ca2+ was loaded into the SR and released with cafjeine and the resulting tension transients were measured. lsoflurane (1-4%) decreased (6-9%) the maximal Ca2 + -activated tension development in PM and SL but more in PM than in SL. In AM, howeuer, isoflurane and halothane (1-3%) produced no change. Isoflurane decreased submaximal Ca2 + -activated tension development in PM, but effected no change in it in SL. lsoflurane and halothane increased the tension development in AM to the extent of producing a shift to the left in the pCa-tension curves of 50.1 pCa unit. lsoflurane decreased by 16% Ca2+ uptake by the SR in PM at 3% concentration, increased uptake 110-143% in S L at 1-3%, and increased by 72-121 % and 15-73% Ca2+ release from the SR in S L and A M , respectively. With submaximal caffeine concentration at 2 mM, isoflurane (4% only) increased by 21% Ca" release from the sarcoplasmic reticulum in PM. Halothane (1-3%) decreased by 19-37% Ca2 + uptake and increased by 38-75% Ca2+ release from the SR in skinned fibers of AM. We conclude that isoflurane and halothane have similar infracellular mechanisms of action in striated muscle. lsoflurane-induced decreases in submaxima1 and maximal Ca2 + -activated tension development and in Ca2+ uptake by the sarcoplasmic reticulum in PM could partially contribute to decreased myocardial contractility. The increases in Ca2+ release from the SR produced by isoflurane and halothane in S L and AM could contribute to increased muscle contraction.

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Inotropic Effects of Isoflurane on Mechanics of Contraction in Isolated Cat Papillary Muscles from Normal and Failing Hearts

Cited by 83 publications

References 0 publications

Cardiovascular Effects of Isoflurane-Induced Hypotension for Cerebral Aneurysm Surgery

Cardiovascular Effects of Isoflurane-Induced Hypotension for Cerebral Aneurysm Surgery

Cardiovascular and Metabolic Alterations in Mice Lacking Both β1- and β2-Adrenergic Receptors

Intracellular Mechanism of Action of Isoflurane and Halothane on Striated Muscle of the Rabbit

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