Sinus node responses to perfusion pressure changes, ischaemia and hypothermia in the isolated blood-perfused dog atrium

Kobayashi, Miyoharu; Godin, D; Nadeau, Réginald

doi:10.1093/cvr/19.1.20

Cited by 16 publications

(12 citation statements)

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“…Shortening of the AP duration decreased refractoriness and facilitated the genesis of reentrant circuits in PVs. This study also demonstrated that a rise in temperature would increase the spontaneous activity of PV cardiomyocytes with pacemaker activity, which was similar to the results of previous studies on sinoatrial cells [2,16]. Moreover, this study demonstrated that rising temperatures induced the occurrence of oscillatory afterpotentials during spontaneous beating in PV cardiomyocytes.…”

Section: Effects Of Temperature On Ap Of Pv Cardiomyocytessupporting

confidence: 91%

“…Several researchers have evaluated the effects of temperature on cardiac arrhythmia, but their results remain controversial. Changes in temperature alter the spontaneous activity of sinoatrial cells [2,16]. Hypothermia has been shown to prevent the occurrence of ventricular arrhythmia [22], but it has also been shown to increase ventricular arrhythmia [25].…”

Section: Introductionmentioning

confidence: 99%

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Temperature Regulates the Arrhythmogenic Activity of Pulmonary Vein Cardiomyocytes

Chen¹,

Chen²,

Paul³

et al. 2003

J Biomed Sci

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Temperature plays an important role in the electrophysiology of cardiomyocytes. Pulmonary veins (PVs) are known to initiate paroxysmal atrial fibrillation. The effects of temperature on the arrhythmogenic activity of rabbit single PV and atrial cardiomyocytes were assessed using the whole-cell clamp technique. PV cardiomyocytes had different beating rates at low (22–25°C), normal (38–39°C) and high (40–41°C) temperatures (0.9 ± 0.1, 3.2 ± 0.4, 6.4 ± 0.6 Hz, respectively; p < 0.001). There were different action potential durations and incidences of delayed afterdepolarization in PV cardiomyocytes with pacemaker activity (31, 59, 63%; p < 0.05), PV cardiomyocytes without pacemaker activity (16, 47, 60%; p < 0.001), and atrial myocytes (0, 0, 21%; p < 0.05). However, oscillatory afterpotentials were only found in PV cardiomyocytes with pacemaker activity at normal (50%) or high (68%) temperatures, but not at low temperatures (p < 0.001). Both PV and atrial cardiomyocytes had larger transient inward currents and inward rectified currents at high temperatures. Additionally, PV cardiomyocytes with and without pacemaker activity had larger pacemaker currents at higher temperatures. This study demonstrated that PV cardiomyocytes have an increase in arrhythmogenic activity at high temperatures because of enhanced automaticity, induced triggered activity, or shortening of action potential duration.

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Section: Effects Of Temperature On Ap Of Pv Cardiomyocytessupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Temperature Regulates the Arrhythmogenic Activity of Pulmonary Vein Cardiomyocytes

Chen¹,

Chen²,

Paul³

et al. 2003

J Biomed Sci

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“…In vivo, lowering the temperature induces reduction of the SAN rhythm and conduction time (247,271). In the intact SAN, the effects of temperature on pacemaking can also be associated with pacemaker shift (271).…”

Section: E Electrolytes and Temperaturementioning

confidence: 99%

Genesis and Regulation of the Heart Automaticity

Mangoni

Nargeot²

2008

Physiological Reviews

507

565

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The heart automaticity is a fundamental physiological function in higher organisms. The spontaneous activity is initiated by specialized populations of cardiac cells generating periodical electrical oscillations. The exact cascade of steps initiating the pacemaker cycle in automatic cells has not yet been entirely elucidated. Nevertheless, ion channels and intracellular Ca(2+) signaling are necessary for the proper setting of the pacemaker mechanism. Here, we review the current knowledge on the cellular mechanisms underlying the generation and regulation of cardiac automaticity. We discuss evidence on the functional role of different families of ion channels in cardiac pacemaking and review recent results obtained on genetically engineered mouse strains displaying dysfunction in heart automaticity. Beside ion channels, intracellular Ca(2+) release has been indicated as an important mechanism for promoting automaticity at rest as well as for acceleration of the heart rate under sympathetic nerve input. The potential links between the activity of ion channels and Ca(2+) release will be discussed with the aim to propose an integrated framework of the mechanism of automaticity.

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“…The chronotropic effect of temperature has been widely documented in both hypothermic and hyperthermic conditions (3,10,28,73,100,119,121). Nakazawa and colleagues (168,169) observed consistent increases in heart rates when directly heating chick and rat embryos from 37 to either 40 or 42°C, followed by recovery of heart rate to basal levels when heating was discontinued.…”

Section: Heat Stress and Cardiac Responsesmentioning

confidence: 99%

Human Cardiovascular Responses to Passive Heat Stress

Crandall

Wilson

2014

Comprehensive Physiology

149

136

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Heat stress increases human morbidity and mortality compared to normothermic conditions. Many occupations, disease states, as well as stages of life are especially vulnerable to the stress imposed on the cardiovascular system during exposure to hot ambient conditions. This review focuses on the cardiovascular responses to heat stress that are necessary for heat dissipation. To accomplish this regulatory feat requires complex autonomic nervous system control of the heart and various vascular beds. For example, during heat stress cardiac output increases up to twofold, by increases in heart rate and an active maintenance of stroke volume via increases in inotropy in the presence of decreases in cardiac preload. Baroreflexes retain the ability to regulate blood pressure in many, but not all, heat stress conditions. Central hypovolemia is another cardiovascular challenge brought about by heat stress, which if added to a subsequent central volumetric stress, such as hemorrhage, can be problematic and potentially dangerous, as syncope and cardiovascular collapse may ensue. These combined stresses can compromise blood flow and oxygenation to important tissues such as the brain. It is notable that this compromised condition can occur at cardiac outputs that are adequate during normothermic conditions but are inadequate in heat because of the increased systemic vascular conductance associated with cutaneous vasodilation. Understanding the mechanisms within this complex regulatory system will allow for the development of treatment recommendations and countermeasures to reduce risks during the ever-increasing frequency of severe heat events that are predicted to occur.

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Sinus node responses to perfusion pressure changes, ischaemia and hypothermia in the isolated blood-perfused dog atrium

Cited by 16 publications

References 0 publications

Temperature Regulates the Arrhythmogenic Activity of Pulmonary Vein Cardiomyocytes

Temperature Regulates the Arrhythmogenic Activity of Pulmonary Vein Cardiomyocytes

Genesis and Regulation of the Heart Automaticity

Human Cardiovascular Responses to Passive Heat Stress

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