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1. Mild hypothermia induces incomplete left ventricular relaxation despite spontaneous bradycardia in pigs.

Author

Schwarzl, M., Alogna, A., Zirngast, B., Steendijk, P., Verderber, J., Zweiker, D., Huber, S., Maechler, H., Pieske, B. M., and Post, H.

Subjects
*DIASTOLE (Cardiac cycle), *BRADYCARDIA, *HYPOTHERMIA, *LEFT heart ventricle, *LABORATORY swine, *PHYSIOLOGY
Abstract

Aim Mild hypothermia ( MH) decreases left ventricular ( LV) end-diastolic capacitance. We sought to clarify whether this results from incomplete relaxation. Methods Ten anaesthetized pigs were cooled from normothermia ( NT, 38 °C) to MH (33 °C). LV end-diastolic pressure ( LVPed), volume ( LVVed) and pressure-volume relationships ( EDPVRs) were determined during stepwise right atrial pacing. LV capacitance (i.e. LVVed at LVPed of 10 mmHg, LV VPed10) was derived from the EDPVR. Pacing-induced changes of diastolic indices ( LVPed, LVVed and LV VPed10) were analysed as a function of (i) heart rate and (ii) the ratio between diastolic time interval (t-dia) and LV isovolumic relaxation constant τ, which was calculated using a logistic fit ( τL) and monoexponential fit with zero asymptote ( τZ) and nonzero asymptote ( τ NZ). Results Mild hypothermia decreased heart rate (85 ± 4 to 68 ± 3 bpm), increased τL (22 ± 1 to 57 ± 4 ms), τZ (26 ± 2 to 56 ± 5 ms) and τ NZ (41 ± 1 to 96 ± 5 ms), decreased t-dia/ τ ratios, and shifted the EDPVR leftwards compared to NT (all P < 0.05). During NT, pacing at ≥140 bpm shifted the EDPVR progressively leftwards. During MH, relationships between diastolic indices and heart rate were shifted towards lower heart rates compared to NT. However, relationships between diastolic indices and t-dia/ τ during NT and MH were superimposable. Conclusion We conclude that the loss of LV end-diastolic capacitance during MH can be explained at least in part by slowed LV relaxation. MH thereby is an example of incomplete LV relaxation at a spontaneous low heart rate. Caution may be advised, when heart rate is increased in patients treated with MH. [ABSTRACT FROM AUTHOR]

Published
2015
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2. The induction of mild hypothermia improves systolic function of the resuscitated porcine heart at no further sympathetic activation.

Author

Schwarzl, M., Steendijk, P., Huber, S., Truschnig-Wilders, M., Obermayer-Pietsch, B., Maechler, H., Pieske, B., and Post, H.

Subjects
*HYPOTHERMIA, *LABORATORY swine, *CATECHOLAMINES, *ELECTROPHYSIOLOGY, *HEART beat, ANIMAL models of cardiac arrest
Abstract

Aim: Mild hypothermia (MH) after cardiac arrest attenuates hypoxic brain injury and improves survival. As MH increases contractility in normal hearts, we hypothesized that MH improves cardiovascular function after cardiac arrest. Methods: In 16 anaesthetized pigs (64 ± 2 kg), ventricular fibrillation was induced electrically for 5 min. At 10 min after resuscitation and return of spontaneous circulation (ROSC), pigs were assigned to normothermia (NT, 38 °C, n = 8) or MH (33 °C, n = 8, intravascular cooling). Results: At ROSC 6 h vs. baseline, heart rate (HR) was unchanged in NT, but decreased in MH. Cardiac output (CO, l min−1) decreased in MH (3.5 ± 0.2 vs. 5.5 ± 0.4, P < 0.05) more than in NT (4.8 ± 0.4 vs. 5.7 ± 0.4, P = ns). Mixed venous oxygen saturation decreased in NT (56 ± 2 vs. 66 ± 3%, P < 0.05), but remained constant in MH (64 ± 2 vs. 65 ± 2%) due to a 35% decrease of whole body oxygen consumption. Left ventricular (LV) dP/dtmax (mmHg s−1) decreased in NT (1163 ± 97 vs. 1665 ± 134, P < 0.05), but was preserved in MH (1602 ± 102 vs. 1603 ± 96), whereas LV relaxation was profoundly slowed during MH. Pressure-volume analysis confirmed improved LV systolic function during MH, but also demonstrated decreased LV end-diastolic distensibility, which was further potentiated by right atrial pacing at baseline HR. MH did not increase plasma catecholamine levels. Spectral analysis of heart rate variability revealed reduced sympathetic activation during MH. Conclusion: The induction of MH after cardiac resuscitation improves systolic myocardial function without further sympathetic activation. A reduced metabolism during MH outweighs a decreased CO and thereby acts favourably on systemic oxygen supply/demand balance. [ABSTRACT FROM AUTHOR]

Published
2011
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3. Arterial hypertension promotes atrial remodelling and fibrillation in pigs.

Author

Antoons, G., Schwarzl, M., Jin, G., Zweiker, D., Huber, S., Verderber, J., Alogna, A., Schoenleitner, P., Wakula, P., Lueger, A., Heinzel, F. R., Pieske, B., and Post, H.

Subjects
*HYPERTENSION, *ATRIAL fibrillation, *EXTRACELLULAR matrix
Abstract

Arterial hypertension is an independent risk factor for atrial fibrillation (AF). The occurrence of AF is related to atrial dilation and extracellular matrix remodelling, shortening of atrial refractory period (AERP), and disturbed Ca2+ handling. In this study, we investigate if chronic hypertension in a porcine model induces structural and electrical changes in the atria, including Ca2+ homeostasis, and whether these changes enhance susceptibility to AF. To induce hypertension, 8 landrace pigs received subcutaneous DOCA-pellets (aldosterone analogon, 90-day release) and high-lipid/salt diet for 12 weeks. Eight weight-matched pigs served as controls. AERP was determined at different cycle lengths, S0, followed by a premature extrastimulus with 5 ms decrements. To test for AF susceptibility, a separate group of pigs (N=16) was instrumented with a telemetry-controlled pacemaker. Surgical procedures and in vivo interventions were performed under anesthesia (1.0 % isoflurane, 35 μg/kg/h fen-tanyl, 1 mg/kg/h midazolam, and 0.2 mg/kg/h pancouronium). A number of 5/16 pigs received DOCA/salt starting 2 weeks before the onset of rapid atrial pacing (600 bpm). After 2 weeks pacing, spontaneous atrial rhythm was monitored in unsedated pigs. AF susceptibility was defined as no detectable sinus rhythm for > 1h. Atrial myocytes were isolated from 12 w-treated DOCA (N=3) and control pigs (N=4), from left (LA) or right atrium (RA). Calcium transients (CaT) and cell shortening were measured during field stimulation using Fura-2 AM (0.5 - 2 Hz, 37°C). Data are expressed as mean± s.e.m. After 12 w DOCA, systolic blood pressure was 139±1, vs 95±6 mmHg in control pigs (P<0.05, tail-cuff-method). LA area was enlarged (12.4±0.3 vs 9.7±0.6 cm² in control, p<0.05, echocardiography). Interstitial fibrosis was reduced (14.8±1.8 vs 20.5±1.7% in control, p<0.05, expressed as % stained area by Sirius Red). AERP was significantly shortened in DOCA (fig 1). In single atrial myocytes, CaT amplitude was comparable in DOCA and control, in LA and RA. In LA, but not in RA, diastolic Ca2+ levels were lower (0.54±0.02 F340/380, n=5, N=, vs 0.81±0.01 in control, n=7, N=,0.5 Hz), and Ca2+ decline was faster (RT50 81±24 ms, vs 197±21 ms in control, 0.5 Hz). While unchanged in RA, in LA cells, cell shortening was increased from 2.3±0.8% in control (n=, N=2) to 5.4±0.5% in DOCA (n=8, N=,0.5 Hz). DOCA pigs were more susceptible to AF. After 2 w of rapid pacing, sustained AF (>1h) occurred in 4/5 DOCA pigs, vs 2/11 control pigs (p<0.05). In conclusion, although sinus rhythm is maintained, hypertensive pigs develop left atrial dilation and reduced electrical refractoriness, which was related to enhanced AF susceptibility. At the myocyte level, faster Ca2+ kinetics and increased contractility may reflect compensatory mechanisms that primarily occur in the left atria during chronic hypertension. [ABSTRACT FROM AUTHOR]

Published
2013

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