Lateral reticular nucleus: a site of somatic and cardiovascular integration in the cat.
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Animals↗
Biomedical subjects
J Ciriello
Publications and source records attributed to J Ciriello.
Identification of pathways mediating cardiovascular responses elicited by stimulation of the septum in the rat.
1. Experiments were done in rats anaesthetized with sodium pentobarbitone to localize pathways mediating the cardiovascular responses elicited by electrical stimulation of the septum. The major efferent projections from the septum were first identified anatomically by the Fink-Heimer II technique and these pathways were subsequently lesioned in acute experiments to establish their role in the mediation of the cardiovascular responses elicited by septal stimulation. 2. Electrical stimulation of histologically localized sites in the lateral septum elicited hypotension and bradycardia whereas stimulation of sites in the medial septum elicited hypertension and bradycardia. 3. Selective lesions of cardiovascular responsive sites in either the lateral or medial septum produced a pattern of degeneration essentially similar to that of previous anatomical studies, i.e. the main efferent projections were localized to the fornix, stria medullaris and the medial forebrain bundle. 4. Stimulation of the fornix did not elicit cardiovascular changes and lesions of this pathway did not alter cardiovascular responses to septal stimulation. 5. Stimulation of the stria medullaris elicited hypotension and bradycardia whereas stimulation of the medial forebrain bundle elicited hypertension and bradycardia. Ipsilateral lesions of the stria medullaris, signicicantly attenuated the hypotension and bradycardia elicited by stimulation of the lateral septum but did not affect the responses to stimulation of the medial septum. Bilateral lesions of the medial forebrain bundle in the region of the lateral hypothalamus abolished the hypertension but did not affect the bradycardia elicited by medial septum stimulation. Cardiovascular, reponses elicited by stimulation of the lateral septum were not affected by medial forebrain bundle lesions. 6. It is suggested that the cardiovascular responses elicited by stimulation of the lateral septum are mediated via the stria medullaris and that the hypertension elicited by stimulation of the medial septum is mediated via the medial forebrain bundle. On the other hand, the bradycardia elicited by stimulation of the medial septum is probably mediated by a pathway presently unknown.
Animals↗
Convergence of ventrolateral medullary and aortic baroreceptor inputs in nucleus of the solitary tract.
Experiments were done in alpha-chloralose anesthetized rats to investigate the effect of stimulating the intermediate region of the ventrolateral medulla (VLM) on the response of single units in nucleus of the solitary tract (NTS) that altered their rate of discharge during aortic baroreceptor stimulation. Of 178 units recorded within NTS, 65 responded orthodromically to VLM stimulation. An additional 16 units were activated antidromically by VLM stimulation. The interaction between the aortic depressor nerve and VLM orthodromic inputs was investigated in 38 units that received converging inputs from VLM and the aortic depressor nerve. A conditioning stimulus applied to VLM, regardless of whether the NTS unit was excited by (n = 13) or did not respond to (n = 9) VLM stimulation, decreased the excitatory response of the unit to aortic depressor nerve stimulation. These data suggest that VLM neurons are involved in the modulation of aortic baroreceptor afferent information at the level of the NTS and that this interaction of inputs in NTS may involve both postsynaptic and presynaptic mechanisms.
Animals↗
Effect of renal denervation on arterial pressure in rats with aortic nerve transection.
The role of renal nerves in influencing the control of arterial pressure was studied in Wistar rats with aortic depressor nerve (ADN) transection. Renal denervation prevented or reversed the normal increase in arterial pressure seen after ADN transection. This effect was not due to an effect on the renin-angiotensin system, as the elevated arterial pressure after ADN section in rats with renal nerves intact was shown to be due to increased alpha-adrenergic activity. Food and water intake and urine output decreased significantly in both renal-denervated and sham-denervated rats after ADN section, suggesting that a pressure diuresis mechanism was not responsible for preventing the rise in pressure in renal-denervated rats. In another study, the concentration of norepinephrine in skeletal muscle and hypothalamus at 0 and 8 hours after inhibition of tyrosine hydroxylase with alpha-methyltyrosine was used as an index of norepinephrine turnover. Norepinephrine turnover in skeletal muscle was increased significantly over control values by ADN transection in sham renal-denervated rats, but was not significantly different from controls in renal-denervated rats with ADN section. In the hypothalamus, there was a significant difference between the turnover of norepinephrine in the two groups of ADN-sectioned rats. The results taken together suggest that renal denervation prevents the arterial pressure response to ADN transection by altering the central mechanisms governing sympathetic outflow. It is suggested that this effect may be due to elimination of information carried by afferent renal fibers.
Animals↗
Acute myocardial and plasma catecholamine changes in experimental stroke.
Focal cerebral ischemia in humans increases the incidence of cardiac arrhythmias, and serum cardiac enzyme and plasma norepinephrine levels. In addition, systemic administration of catecholamines causes myocardial damage. This suggests that cerebral ischemia may cause myocardial damage as a consequence of elevated plasma norepinephrine levels. Therefore, experiments were done in 23 chloralosed, paralyzed and artificially ventilated cats to investigate the effects of occluding (n = 17) or sham-occluding (n = 6) the left middle cerebral artery on the myocardium and on circulating levels of plasma catecholamines. After occlusion of the middle cerebral artery for 12-22 hr, 41% (7/17) of the hearts had either acute myocardial necrosis (3/7), focal hemorrhage (3/7), or both (1/7). In animals with acute myocardial damage the levels of plasma norepinephrine and epinephrine were significantly increased compared to pre- middle cerebral artery occlusion values (+46 +/- 18% and +142 +/- 45%, respectively). As well, in cats with acute myocardial damage, changes from initial levels of plasma norepinephrine and epinephrine were significantly increased over those of experimental cats without acute myocardial damage. In animals which did not have acute myocardial damage (10/17) the circulating plasma levels of catecholamines were not significantly different from pre-occlusion values. Similarly, sham occlusion did not alter plasma catecholamine levels. These data demonstrate that a percentage of animals subjected to middle cerebral artery occlusion have myocardial damage and an increase in plasma concentration of norepinephrine and epinephrine. This suggests that a rise in plasma catecholamine levels, due to increased sympathetic activity after middle cerebral artery occlusion, may cause myocardial damage.
Acute Disease↗