Apparatus for study of ventricular function and metabolism in the isolated perfused rat heart.

Fallen, Ernest L.; Elliott, William C.; Gorlin, Richard

doi:10.1152/jappl.1967.22.4.836

Cited by 90 publications

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“…Weight and tail cuff blood pressure were recorded weekly during the 7-week treatment period. Figure 1 illustrates the isolated isovolumic working rat heart preparation which has been previously described in detail (Fallen et al, 1967b;Apstein et al, 1977). Rats were injected intraperitoneally with 1-1.5 ml pentobarbital (15 mg/ml) and the thorax was rapidly opened.…”

Section: Methodsmentioning

confidence: 99%

The influence of pressure overload left ventricular hypertrophy on diastolic properties during hypoxia in isovolumically contracting rat hearts.

Lorell¹,

Wexler²,

Momomura³

et al. 1986

Circulation Research

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SUMMARY. We tested the hypothesis that there is an enhanced susceptibility in hypertrophied cardiac muscle to develop decreased diastolic distensibility of the left ventricle in response to hypoxia. The effects of brief hypoxia (3 minutes) were studied in rats with and without chronic left ventricular pressure overload hypertrophy using an isolated buffer-perfused and isovolumic (balloon-in-left ventricle) heart preparation with excised pericardium and vented right ventricle. We compared hypertrophied hearts from hearts from hypertensive uninephrectomized WistarKyoto rats (» = 12) with normotensive uninephrectomized age-matched controls (n = 13). Coronary flow was held constant and adjusted so that an identical flow per gram left ventricular weight was achieved in both groups. The left ventricular balloon volume was adjusted to produce an initial left ventricular end-diastolic pressure of 10 mm Hg in both groups and was held constant thereafter so that changes in left ventricular end-diastolic pressure during hypoxia represented changes in diastolic chamber distensibility. Under aerobic conditions, left ventricular systolic pressure was 66% higher in the hypertrophied hearts than in the controls, but there was no difference in the rate or extent of left ventricular relaxation as estimated by the exponential time constant of pressure decay and the asymptote to which pressure decayed. In response to hypoxia, left ventricular end-diastolic pressure was significantly higher in the hypertrophied hearts than in the controls (37 ± 5 vs. 22 ± 5 mm Hg, P < 0.001). In response to hypoxia, the rate of left ventricular relaxation was depressed to a comparable degree in both groups, but there was a greater upward shift in the asymptote to which pressure decayed in the hypertrophied hearts. Hypoxia-induced coronary vasodilation as assessed by the change in coronary vascular resistance was similar in the hypertrophied and control hearts (2.9 ± 0.5 vs. CARDIAC hypertrophy is a compensatory response to chronic pressure or volume overload of the heart. However, adaptive cardiac hypertrophy may result in an enhanced vulnerability to ischemia or hypoxia,* as manifested by a decrease in diastolic distensibility. Bache et al. (1984a) have shown that pacing tachycardia in dogs with chronic left ventricular (LV) hypertrophy without coronary stenoses produces myocardial ischemia associated with a substantial increase in left ventricular end-diastolic pressure. A similar dramatic and reversible decrease in left ventricular diastolic distensibility has been * In this paper, hypoxia will be used to indicate an abnormally low level of tissue oxygenation due to hypoxemia, an abnormally low arterial oxygen content. Ischemia will mean an abnormally low level of myocardial perfusion.

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Section: Methodsmentioning

confidence: 99%

The influence of pressure overload left ventricular hypertrophy on diastolic properties during hypoxia in isovolumically contracting rat hearts.

Lorell¹,

Wexler²,

Momomura³

et al. 1986

Circulation Research

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“…The signals from the force transducer were recorded on an oscillograph and the data expressed as 'force of contraction'. The force of contraction of the heart was also recorded in isovolumic conditions by implanting a water-filled vinyl balloon into the left ventricle according to the method described by Fallen, Elliott & Gorlin (1967); in this preparation the balloon was connected to a pressure transducer (Statham P23 Db).…”

Section: Methodsmentioning

confidence: 99%

Coronary Reactions to Cardiac Hyperactivity and to Hypoxia in Isolated Perfused Heart of Rat

Sen

Sunahara

Talesnik

et al. 1977

British J Pharmacology

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I Continuous recording of cardiac force of contraction, heart rate and coronary flow from isolated perfused hearts of rats was used to study coronary reactions: (a) to cardiostimulation with noradrenaline, CaCl2, or electrically induced tachycardia; (b) to short duration stoppage of coronary inflow (hypoxia). 2 The heart rate was controlled by electrical pacing. Coronary vasodilatation resulted from cardiostimulation or hypoxia. This coronary response was greater at higher heart rates. 3 In parallel experiments administration of noradrenaline to hearts paced at different frequencies resulted in a rate-dependent elevation of adenosine-3',5'-cyclic monophosphate (cyclic AMP). 4 Duration of hypoxia leading to different degrees of reactive hyperaemia did not change the cardiac cyclic AMP levels. SCoronary vasodilatation due to increased cardiac metabolism produced by noradrenaline, Ca2+ or tachycardia was enhanced by the phosphodiesterase inhibitors diazoxide and papaverine while it was inhibited during the administration of prostaglandin E2. 6 Reactive hyperaemia was unaffected by diazoxide, papaverine or prostaglandin E2. 7 Catecholamine depletion by reserpine did not influence metabolic coronary dilatation nor the reactive hyperaemic responses. 8 We postulate that there are at least two types of coronary reactions: one in response to hypoxia, 'reactive hyperaemia', and another resulting from cardiac hyperactivity, 'metabolic coronary dilatation'. The latter, blocked by prostaglandin E2 and enhanced by diazoxide or papaverine, would be triggered by cyclic AMP while reactive hyperaemia would result from other mechanisms.

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“…Исследования проведены на модели изолированного изово люмически сокращающегося сердца белых беспородных крыс по методу E. L. Fallen et al (1967) [3]. Было проведено две серии экс периментов.…”

Section: материал и методыunclassified

“…Ла тексный баллончик соединяли с датчиком монитора Mindray MEC 1200 для регистрации давления в левом желудочке. На осно вании графического материала рассчитывали комплекс силовых (систолическое, диастолическое и развиваемое давление) и скоро стных (+ dp/dt max -максимальная скорость увеличения и -dp/dt max -максимальная скорость снижения внутрижелудочко вого давления), а также дефект диастолы, позволявшие оценивать сократительную функцию сердца [3].…”

Section: материал и методыunclassified

Mechanisms of the Cardiotoxic Action of Amitriptyline

Чекмарев¹,

Долгих²

2011

rmt

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Первые случаи острого отравления психотропны ми препаратами отмечены в 50 х годах прошлого столе тия [1]. В последние годы увеличивается число отравле ний новыми препаратами с психотропным эффектом: амитриптилином, азалептином, финлепсином. В насто ящее время такие нозологические формы занимают од но из ведущих мест в общей структуре отравлений «ле карственной этиологии», составляя, по данным Всемирной организации здравоохранения, от 10 до 15% [2]. Токсичность амитриптилина, как и всех трицикли ческих антидепрессантов, обусловлена, в первую оче редь, их высокой способностью связываться с белками крови (до 96%), а также длительным периодом полувы ведения из организма, который для амитриптилина со ставляет, по данным литературы, от 31 до 46 часов [2].Цель настоящего исследования -изучить механизмы токсического действия амитриптилина на миокард. Материал и методыИсследования проведены на модели изолированного изово люмически сокращающегося сердца белых беспородных крыс по методу E. L. Fallen et al. (1967) [3]. Было проведено две серии экс периментов. В одной серии (I группа) в раствор Кребса Хензе лайта был добавлен амитриптилин в дозе 250 нг/мл, исходя из то го, что средняя терапевтическая концентрация амитриптилина в крови при назначении терапевтических доз составляет 250 нг/мл [5]. В другой -концентрация амитриптилина в растворе, прохо дившем через коронарное русло, составила 1250 нг/мл (II груп па). Таким образом, проведение подобных экспериментов позво лило оценить непосредственное влияние амитриптилина на сократимость и метаболизм изолированного сердца.Эксперименты выполнены на 30 белых беспородных крысах самцах массой 210-250 г, наркотизированных тиопенталом натрия (25 мг/кг внутрибрюшинно). Через 15 минут после наркотизации животного выполняли срединную торакотомию, сердце быстро из влекали и погружали с целью кардиоплегии в охлажденный до 2-4°С раствор Кребса Хензелайта. Предсердия частично удаляли, а сердце фиксировали, надев аорту на канюлю перфузионной уста Objective: to study the mechanisms of toxic action of amitriptyline on the myocardium. Material and methods. Investigations were conducted using the hearts from 30 outbred albino rats, which had been isolated and perfused according to the proce dure described by Fallen et al. There were two series of experiments: 1) amitriptyline was added in a dose of 250 ng/ml to Krebs Henseleit solution (Group 1); 2) the agent was added at another concentration (1250 ng/ml) to the solution passing through the coronary bed (Group 2). The animals were anesthetized with thiopental sodium (25 mg/kg) peritoneally. Results. Amitriptyline depresses myocardial contractility, which is particularly obvious with high rate pacing. This manifests itself as reduced contractile velocity and force power parameters and elevated left ventricular diastolic pressure. Amitriptyline lowers the efficacy of glucose and increases the release of enzymes into the coronary duct. Conclusion. Hypoergosis, membrane destruction, and cardiomyocyte ion pump failure have been shown to underlie nega...

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Apparatus for study of ventricular function and metabolism in the isolated perfused rat heart.

Cited by 90 publications

References 0 publications

The influence of pressure overload left ventricular hypertrophy on diastolic properties during hypoxia in isovolumically contracting rat hearts.

The influence of pressure overload left ventricular hypertrophy on diastolic properties during hypoxia in isovolumically contracting rat hearts.

Coronary Reactions to Cardiac Hyperactivity and to Hypoxia in Isolated Perfused Heart of Rat

Mechanisms of the Cardiotoxic Action of Amitriptyline

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