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F R Calaresu

Publications and source records attributed to F R Calaresu.

125 records · Page 7Linked to original sources

An experimental analysis of the tachycardia that follows vagal stimulation.

1. Postvagal tachycardia, the transient increase in heart rate that follows the sinus bradycardia elicited by vagal stimulation, was investigated in thirty chloralosed cats. Maximum postvagal tachycardia was elicited by stimulation at frequencies of 20-60 Hz with train durations of 30-90 sec. A positive correlation was demonstrated between the magnitudes of postvagal tachycardia and of the preceding sinus bradycardia.2. Postvagal tachycardia was not affected by either spinal transection at C7 or by administration of propranolol (1.5 mg/kg I.V.), but was abolished by the administration of atropine (2.0 mg/kg I.V.).3. Postvagal tachycardia was observed to follow the vagal bradycardia induced reflexly either by administration of phenyldiguanide (100-300 mug I.V.) or by stimulation of the aortic depressor nerve.4. In the isolated atria-vagus preparations from six rabbits a positive correlation was demonstrated between the magnitude of postvagal tachycardia and of the preceding bradycardia elicited by vagal stimulation.5. Continuous intracellular recordings were obtained from four sinuatrial node pace-maker cells in the isolated atria-vagus preparation of the rabbit before, during and after vagal stimulation. During postvagal tachycardia the slope of the diastolic prepotential, the maximum diastolic potential, threshold potential and the overshoot were found to be increased; these changes are different from those found in pace-maker cells during adrenergic activation.6. These findings demonstrate that postvagal tachycardia is not mediated by sympathetic adrenergic mechanisms, but suggest that it is dependent upon the preceding vagal bradycardia and may be related to an increase in net sodium influx into pace-maker cells initiated by the hyperpolarization of the pace-maker cell membrane during and immediately after vagal stimulation.

Animals↗

The function of the paramedian reticular nucleus in the control of heart rate in the cat.

1. Selective electrical stimulation of the paramedian reticular nucleus (PRN) in anaesthetized and decerebrate-anaesthetized cats elicited cardiac slowing which was shown to be due to inhibition of the sympathetic input to the heart.2. In decerebrate preparations stimulation of the PRN elicited cardioacceleration which was abolished by bilateral vagotomy.3. It is suggested that these changes in heart rate in opposite directions can be accounted for by an inhibitory influence of the PRN on both neural inputs to the heart. In the absence of vagal activity, demonstrated in anaesthetized and decerebrate-anaesthetized preparations, the response to stimulation of the PRN resulted in cardiac slowing. In contrast, when both sympathetic and parasympathetic pathways were active (decerebrate preparation) stimulation of the PRN resulted in cardio-acceleration, due to simultaneous inhibition of the two neural inputs to the heart.4. It is concluded that the two inhibitory functions of the PRN are probably mediated by two different populations of neurones and that the PRN plays an integrative role in the medullary control of heart rate.

Anesthesia, Intravenous↗

The mechanism of the cardio-acceleration elicited by electrical stimulation of the parahypoglossal area in the cat.

1. In chloralosed and in decerebrated cats localized electrical stimulation of a discrete parahypoglossal area (including the nucleus intercalatus and a discrete neighbouring region ventrolateral to the hypoglossal nucleus) elicited cardio-acceleration and arterial hypertension, either singly or together.2. The cardio-acceleratory response was decreased by intravenous administration of propranolol (2 mg/kg). In another group of experiments the response was abolished by acute bilateral cervical vagotomy but it was observed to return partially when stimulation was applied one or more hours after vagotomy. The hypertensive response was not affected by propranolol or by vagotomy.3. Evoked electrical activity with a latency of 3-10 msec was recorded from pre- and post-ganglionic sympathetic cardio-acceleratory nerves during stimulation of this region.4. These findings demonstrate the existence of a discrete medullary area which controls heart rate by activation of a sympathetic pathway and inhibition of a parasympathetic pathway.

Action Potentials↗

A group of neurons highly reactive for enkephalins in the rat hypothalamus.

Enkephalin-like immunoreactivity was demonstrated in a group of highly reactive neurons (HRN) of the rat hypothalamus by the biotin-avidin immunohistochemical technique. The location of the HRN spans several nuclei but the consistent immunoreactivity, the constant topography, and the uniform dimensions of the neurons suggest that they belong to one group. At its caudal end the group appears within the rostral dorso-medial nucleus. At the level of the caudal paraventricular nucleus (PVH) the HRN are assembled in a spherical pattern around a subgroup of neurons in the anterior hypothalamus (AH). The HRN then are found in a position directly between the PVH and the fornix. Before the HRN disappear at the level of the caudal preoptic area, many of the HRN become associated with the fornix. The close association of the HRN with the AH subgroup and the fornix suggests that the HRN may influence the activity of these structures. The HRN are small to medium in size and their short processes suggest that the HRN communicate with other neurons in their vicinity. The areas of the hypothalamus in which the HRN are found are involved in neuroendocrine and thermoregulatory functions suggesting that the HRN may play a role in modifying the activity of neurons and fibres involved in these functions.

Animals↗