SUMMARY. Biphasic contractions were produced in dog trabeculae by replacing 90-95% of the calcium in the bathing solution with strontium. These conditions produced prolonged action potentials accompanied by contractions with two distinct phasic components. The early component disappeared slowly when the remaining Ca ++ was removed, whereas the late component was eliminated quickly when Sr ++ was removed. Manganese ion (0.25 ITIM) preferentially decreased the late component without changing the action potential, whereas caffeine and ryanodine decreased or eliminated the early component. Ryanodine did not alter the action potential. Isoproterenol rapidly increased the early component and, more slowly and to a lesser degree, increased the late component. The results suggest that the early component is caused by intracellular release of activator cation, probably from the sarcoplasmic reticulum, whereas the late component is the result of Sr ++ entry across the sarcolemma, possibly by way of the slow inward current. TWO distinct components of contraction, one fast and one slow, have been shown to exist in mammalian ventricular myocardium under certain conditions. They can be seen in rested state contractions, after a 10-to 15-minute stimulation-free period, in the absense (Allen et al., 1976) or in the presence of an adrenergic agonist (Berescewicz and Reuter, 1977;Seibel et al., 1978), in low-temperature, constant frequency contractions under the influence of noradrenaline (Bogdanov et al., 1979), and after 90% replacement of Ca ++ with Sr ++ (Braveny and Sumbera, 1972). The common characteristic of these conditions is an increase in the duration of the action potential, and, in fact, biphasic contractions can be produced when the plateau of the action potential is lengthened by voltage clamp techniques (Morad and Trautwein, 1968;Braveny and Sumbera, 1970) or by toxins (Coraboeuf et al., 1975;Honerjager and Reiter, 1975). Although it is generally agreed that each component of contraction is due to a specific type of cation release, the site of the cation pools is the subject of some controversy.A number of proposals of the origin of the two cation release sites have been published, one visualizing Ca release from the same site but by different mechanisms (Allen et al., 1976) and the others hypothesizing contractile activation by two morphologically distinct pools (Braveny and Sumbera, 1972; Berescewicz and Reuter, 1977;Seibel et al., 1978;Bogdanov et al., 1979). The present study was designed to try to resolve the question of the origin of biphasic contractions by using specific pharmacological interventions. Strontium-induced resolution of the two components was used because it allows constant, relatively high frequency (0.5 Hz) stimulation while enabling a quantitative comparison of the effects of adrenergic agonists on the separate components to be made. The results are discussed in relation to the other models of two-component contractions. Methods Mechanical ExperimentsMongrel dogs (3-10 kg) of either sex wer...
Accepted for publication 8th April, 1993 widely implemented, particularly in young women for idiopathic scoliosis. As this generation of women approaches child-bearing age, it is not uncommon for them to present to the obstetric anaesthesia team. Indeed, the need for anaesthesia for operative delivery is even more likely in these patients than in normal parturients.Previous reports on this subject have focused on considerations in achieving successful epidural anaesthesia. 2-5 At our institution, spinal anaesthesia is more often employed for both elective and urgent operative delivery. We describe the successful use of and advantages of this technique in a patient with Harrington fusion. Case reportA 33-yr-old G2P1 patient presented for elective repeat Caesarean delivery at 38 wk gestation. She had received a uneventful epidural anaesthetic for her first operative delivery. Subsequently, she had undergone Harrington rod placement and iliac bone grafting for worsening idiopathic scoliosis while in her teens. The course of her pregnancy had been uneventful. Aside from her surgical history her preoperative anaesthetic review revealed a 165 cm, 85 kg woman with a normal airway. Her only symptom was occasional back pain during her pregnancy. She could not recall the extent of her spinal fusion and old x-rays were not available. However, she had a midline back scar extending down to the level of L 5 and another scar over her left iliac crest.She consented to spinal anaesthesia after explanation of its advantages and potential difficulties. After intravenous hydration with one L warmed Ringer's lactate, she was placed in the right lateral decubitus position and her back was prepared aseptically. After multiple unsuccessful attempts via both the midline and paramedian approaches at the L3_ 4 level with a 25 g Whitacre needle and 21 g introducer, a successful dural puncture was made on the first attempt at the rnidline of the Ls-S 1 interspace.Clear CSF was obtained and 15 mg bupivacaine 0.75% in aqueous dextrose 8.25% was injected. With the patient turned immediately supine and placed in 15 ~ Trendelenburg, a T 6 level of anaesthesia was obtained within CAN J ANAESTH 1993 / 40:7 / pp 667-9
1 The mechanism of post-extrasystolic, rest and frequency potentiation was studied in canine isolated ventricular muscle. 2 Ryanodine, which impairs Ca availability from the sarcoplasmic reticulum (SR), reduced the amplitude of the extrasystole less than that of the steady state contraction. Ryanodine also inhibited post-extrasystolic potentiation and converted rest-potentiation into rest depression. Restpotentiation was blocked preferentially by ryanodine compared to post-extrasystolic potentiation. An increase in the contribution of extracellular Ca to the extrasystolic contraction could not entirely account for the post-extrasystolic potentiation. 3 Prolonged rest, by itself, also caused depression of the first post-rest contraction. During restpotentiation, SR Ca seemed to play a greater role in contraction than transmembrane Ca influx. However, the ability of the 'release pool' of Ca in the SR to be reprimed after a contraction was reduced. This was seen as a decrease in post-extrasystolic potentiation elicited immediately after rest.4 A decrease in stimulus interval was associated with a transient decrease in contraction amplitude followed by an increase. An abrupt increase in stimulus interval had the opposite effect. Ryanodine blocked the initial transient changes and accelerated the delayed changes. These results suggest that the transient changes in contraction after sudden changes in drive interval are dependent on the SR. 5 Transmembrane Ca entry and the rate of recovery of the Ca release process (repriming) in the SR after a contraction seem to be interval-dependent. The data also indicate that different mechanisms are involved in post-extrasystolic and rest-potentiation. 6 The results are consistent with a model which proposes 'recirculation' of activator Ca within the SR after a contraction or of the presence of an appreciable amount of inactivation of the SR Ca release process during normal stimulation. An increased pool of releasable Ca due to longer recirculation time or a time-dependent decay in the level of inactivation of Ca release from the SR may give rise to rest-potentiation.
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