The effect of increased filling pressure on rhythmicity and atrioventricular conduction in isolated hearts

Keatinge, W. R.

doi:10.1113/jphysiol.1959.sp006334

Cited by 31 publications

(11 citation statements)

References 21 publications

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“…In the fetuses that had received hexamethonium, heart rate was significantly dependent on blood volume, probably due to an effect similar to that of filling pressure on heart rate in isolated hearts [Keatinge, 1959]. There is a suggestion in the data, which is not statistically reliable, that the direct relation between heart rate and blood volume is partially reversed when the fetal baroceptor mechanism is not deprived of its motor arms by ganglionic blockade.…”

Section: Discussioncontrasting

confidence: 40%

Arterial Blood Pressure in the Unanaesthetized Fetal Lamb After Changes in Fetal Blood Volume and Haematocrit

1974

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Fourteen sheep fetuses in the third trimester of gestation were surgically prepared with intravascular catheters and five were nephrectomized. All experiments were done on unanaesthetized fetuses in utero, 3 to 9 days after surgery. Mean arterial blood pressure was recorded while fetal blood volume was changed by injection or withdrawal of blood, or infusion of Ringer's or dextran solutions. Fetal arterial blood gases and pH changed little during the experiments and were shown not to have affected the results. Arterial blood pressure was strongly influenced by changes in fetal blood volume and was also found to depend on haematocrit. There were no detectable differences between the responses of normal and nephrectomized fetuses or between normal fetuses and fetuses treated with hexamethonium. In all preparations central venous pressure depended on blood volume. Heart rate did not depend on blood volume in normal fetuses, but an increase in heart rate with an increase in blood volume was seen after hexamethonium. The open loop gain of baroceptor control of arterial blood pressure could not be proved to differ significantly from zero. Venoconstrictor responses and heart rate responses of reflex origin did not occur when arterial blood pressure was changed. The absence of detectable baroceptor control appears to explain the great sensitivity of arterial blood pressure to blood volume in the unanaesthetized fetal lamb. Previously we found that fetal placental blood flow is almost proportional to fetal blood volume [Faber, Gault, Green and Thornburg, 1973]. Since placental resistance to flow is not known to be under fetal control, changes in placental blood flow were thought to be secondary to changes in arterial blood pressure, an explanation which would require that arterial blood pressure itself is also proportional to blood volume. Studies that demonstrate some control of arterial blood pressure by the baroceptors of the fetus [Brinkman, Ladner, Weston and Assali, 1969] and the neonate [Downing, 1960; Downing, Gardner and Rocamora, 1969] seem to argue against this supposition and we therefore investigated the relationship between arterial blood pressure and blood volume in unanaesthetized fetal lambs under near normal conditions. The contributions of the baroceptors, and of renal mechanisms, to the regulation of arterial blood pressure were assessed by experiments on fetuses with blocked ganglionic transmission or previous bilateral nephrectomy. Recordings of the pH, P02, and PCO2 of fetal arterial blood were made to monitor the condition of the preparations and to eliminate the possibility that the chemo-ceptors affected arterial blood pressure in these experiments. METHODS Animals Pregnant western mixed breed and Dorset ewes were starved for 24 hr prior to surgery and operated on under nitrous oxide-halothane anaesthesia, after induction 241

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Section: Discussioncontrasting

confidence: 40%

Arterial Blood Pressure in the Unanaesthetized Fetal Lamb After Changes in Fetal Blood Volume and Haematocrit

1974

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“…of cold immersion and this gives some support to the possibility that ventricular fibrillation is an occasional cause of sudden death in cold water. Several changes observed after cold immersion would tend to cause this; the venous pressure may rise briefly during sudden exposure to cold [Bondurant, Hickam and Isley, 1957;Keatinge and McCance, 1957] and an increase in filling pressure can precipitate ventricular fibrillation in isolated rabbit hearts [Keatinge, 1959], while it is well known that ventricular fibrillation can be precipitated by adrenaline [Levy, 1914;Goodford, 1958], which is probably released during cold immersion. The hyperventilation observed in these experiments is another possible factor, since a large fall in pCO2 can cause ventricular fibrillation in dogs [Brown and Miller, 1952].…”

Section: Discussionmentioning

confidence: 99%

“…The early increase in heart rate in the 15 and 50 C. immersions may be due to the intense sensation of cold causing reflex release of adrenaline and noradrenaline into the general circulation and into the vicinity of the pacemaker of the heart. The changes in heart rate may also have been due in part to a direct effect of increases in filling pressure on the pacemaker of the heart; moderate increases in filling pressure increase the rate of denervated or isolated mammalian hearts [Tiitso and Tootson, 1935;Blinks, 1956] while larger increases cause a fall [Pathak, 1958] whose size depends on duration of the high pressure [Keatinge, 1959].…”

Section: Discussionmentioning

confidence: 99%

“…However, it has seemed possible that ventricular fibrillation might be responsible for some of these cases; an increase in venous pressure may follow sudden exposure to cold [Bondurant, Hickam and Isley, 1957; Keatinge and McCance, 1957] and a rise in filling pressure may precipitate ventricular fibrillation in isolated hearts [Keatinge, 1959], while adrenaline is known sometimes to cause ventricular fibrillation after chloroform [Levy, 1914] and to facilitate it without chloroform in isolated hearts [Goodford, 1958].…”

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The Respiratory and Cardiovascular Response to Immersion in Cold and Warm Water

Keatinge

Evans

1961

Exp Physiol

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During their first few minutes of immersion in stirred water at 5 and 150 C. the pulmonary ventilation of twelve unclothed men was high, and their end-tidal PCO2 fell. The pCO2 then returned to or a little above its original level but did not greatly exceed it even in working experiments lasting 20 min. in water at 50 C. or 40 min. in water at 150 C. Although work reduced or reversed the initial fall in pCO2, these results therefore do not bear out predictions that the pCO2 would rise to dangerous levels during hard work in cold water, at least in immersions of moderate duration.In water at 37.80 C. the men's heart rates rose steadily, in water at 250 C. they fell and remained low, and in water at 5 and 150 C. they rose and then fell. Repeated immersion at 150 C. reduced or abolished the early respiratory and heart rate responses to immersion and the metabolic response, but did not significantly increase the falls in rectal temperature. Clothing also reduced the reflex responses to immersion. A number of ventricular extrasystoles were observed during the first 2 min. of immersion in water at 150 C., and it is suggested that ventricular fibrillation due to increased venous and arterial pressures, adrenaline, and hyperventilation, may be responsible for some cases of sudden death in cold water. THIS paper describes observations on the end-tidal pCO2, pulmonary ventilation, heart rate, and electrocardiographs of twelve men during immersion in water at temperatures between 5 and 37.80 C. Cotes [1954 and 1955] has reported that the pulmonary ventilation of a man could be predicted from his alveolar pCO2 and deep body temperature, and anticipated that CO2 would accumulate in the body to reach dangerous concentrations during hard work in cold water.Sudden death in cold water without drowning is generally [Simpson, 1958] attributed to vagal arrest of the heart following inhalation of cold water into the naso-pharynx and glottis. However, it has seemed possible that ventricular fibrillation might be responsible for some of these cases; an increase in venous pressure may follow sudden exposure to cold [Bondurant, Hickam and Isley, 1957; Keatinge and McCance, 1957] and a rise in filling pressure may precipitate ventricular fibrillation in isolated hearts [Keatinge, 1959], while adrenaline is known sometimes to cause ventricular fibrillation after chloroform [Levy, 1914] and to facilitate it without chloroform in isolated hearts [Goodford, 1958].The effect of adaptation by repeated immersion in cold water has also been assessed, since the heart rate and blood pressure responses to the immersion of a hand in ice water [Glaser and Whittow, 1957] are reduced by repetition. The design of the experiments and the subjects have been described in the preceding paper.*

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“…The maximum percentage increase in the frequency of the sinus venosus at this pressure was 1 2 6 % . Keatinge [1959a] observed only a 5 to 20 percent increase in the rate of frog hearts submitted to distension. On the basis of more recent observations using sensitive electronic recordings [Pathak, 1972a, b], the lower values observed by Keatinge [1959a] appear Autoregulation of Heart Rate 47 to be due to less effective distension and ectopic pacemaker foci.…”

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confidence: 94%

Autoregulation of Chronotropic Response of the Heart Through Pacemaker Stretch

Pathak¹

1973

Cardiology

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Mechanical stretch is a fundamental biological stimulus for pacemaker activity. Stretch-sensitiveness enables the heart to autoregulate its rate in relation to venous return. Phylogenetically the importance of this primitive mechanism has been diminished by the emergence of neurohumoral influences which permit a quicker and more effective adaptation of cardiac performance. Nevertheless, the intrinsic autoregulatory mechanism is capable of independent operation and may support extrinsic neurohumoral influences under various conditions.

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The effect of increased filling pressure on rhythmicity and atrioventricular conduction in isolated hearts

Cited by 31 publications

References 21 publications

Arterial Blood Pressure in the Unanaesthetized Fetal Lamb After Changes in Fetal Blood Volume and Haematocrit

Arterial Blood Pressure in the Unanaesthetized Fetal Lamb After Changes in Fetal Blood Volume and Haematocrit

The Respiratory and Cardiovascular Response to Immersion in Cold and Warm Water

Autoregulation of Chronotropic Response of the Heart Through Pacemaker Stretch

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