Lesions Of Rostral Ventrolateral Medulla Research Articles

A brainstem area mediating cerebrovascular and EEG responses to hypoxic excitation of rostral ventrolateral medulla in rat.

We sought to identify the medullary relay area mediating the elevations of regional cerebral blood flow (rCBF) and synchronization of the electroencephalogram (EEG) in the rat cerebral cortex elicited by hypoxic excitation of reticulospinal sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM ). In anaesthetized spinalized rats electrical stimulation of RVLM elevated rCBF (laser-Doppler flowmetry) by 31 +/- 6 %, reduced cerebrovascular resistance (CVR) by 26 +/- 8 %, and synchronized the EEG, increasing the power of the 5-6 Hz band by 98 +/- 25 %. Stimulation of a contiguous caudal region, the medullary cerebral vasodilator area (MCVA), had comparable effects which, like responses of RVLM, were replicated by microinjection of L-glutamate (5 nmol, 20 nl). Microinjection of NaCN (300 pmol in 20 nl) elevated rCBF (17 +/- 5 %) and synchronized the EEG from RVLM, but not MCVA, while nicotine (1.2 nmol in 40 nl) increased rCBF by 13 +/- 5 % and synchronized the EEG from MCVA. In intact rats nicotine lowered arterial pressure only from MCVA (101 +/- 3 to 52 +/- 9 mmHg). Bilateral electrolytic lesions of MCVA significantly reduced, by over 59 %, elevations in rCBF and, by 78 %, changes in EEG evoked from RVLM. Bilateral electrolytic lesions of RVLM did not affect responses from MCVA. Anterograde tracing with BDA demonstrated that RVLM and MCVA are interconnected. The MCVA is a nicotine-sensitive region of the medulla that relays signals elicited by excitation of oxygen-sensitive reticulospinal neurons in RVLM to reflexively elevate rCBF and slow the EEG as part of the oxygen-conserving (diving) reflex initiated in these neurons by hypoxia or ischaemia.

P-346 - Splanchnic sympathetic nerve discharge and mean arterial pressure after heat lesion of rostral ventrolateral medulla in rats anesthetized with halothane or pentobarbital sodium.

P-346 - Splanchnic sympathetic nerve discharge and mean arterial pressure after heat lesion of rostral ventrolateral medulla in rats anesthetized with halothane or pentobarbital sodium.

Chronic lesion of rostral ventrolateral medulla in spontaneously hypertensive rats.

We studied the effects of chronic selective neuronal lesion of rostral ventrolateral medulla on mean arterial pressure, heart rate, and neurogenic tone in conscious, unrestrained spontaneously hypertensive rats. The lesions were placed via bilateral microinjections of 30 nmol/200 nl N-methyl-D-aspartic acid. The restimulation of this area with N-methyl-D-aspartic acid 15 days postlesion failed to produce a pressor response. One day postlesion, the resting mean arterial pressure was significantly decreased in lesioned rats when compared with sham rats (100 +/- 7 versus 173 +/- 4 mm Hg, p less than 0.05). Fifteen days later, the lesioned group still showed values significantly lower than the sham group (150 +/- 6 versus 167 +/- 5 mm Hg, p less than 0.05). No significant heart rate differences were observed between the sham and lesioned groups. The ganglionic blocker trimethaphan (5 mg/kg i.v.) caused similar reductions in mean arterial pressure in both lesioned and sham groups. The trimethaphan-induced hypotension was accompanied by a significant bradycardia in lesioned rats (-32 +/- 13 beats per minute) but a tachycardia in sham rats (+33 +/- 12 beats per minute) 1 day postlesion. Therefore, rostral ventrolateral medulla neurons appear to play a significant role in maintaining hypertension in conscious spontaneously hypertensive rats. Spinal or suprabulbar structures could be responsible for the gradual recovery of the hypertension in the lesioned rats.

Lesions of rostral ventrolateral medulla abolish some cardio- and cerebrovascular components of the cerebellar fastigial pressor and depressor responses

We sought to establish whether the C1 area of the rostral ventrolateral reticular nucleus (RVL) of the medulla oblongata mediates: (1) the elevations in arterial pressure (AP), heart rate (HR) and regional cerebral blood flow (rCBF) elicited by electrical stimulation of the rostral cerebellar fastigial nucleus (FN), the fastigial pressor response (FPR); (2) the reductions in AP and HR elicited by chemical stimulation of intrinsic neurons of FN with excitatory amino acids, the fastigial depressor response (FDR) 13. Studies were conducted on rats anesthetized (chloralose), paralyzed and artificially ventilated. The FN was stimulated electrically through microelectrodes and chemically by microinjection of d,l-homocysteic acid (100 nmol in 100 nl). rCBF was measured in homogenates of 11 brain regions by the 14C-iodoantipyrine technique. Bilateral electrolytic lesions restricted to the RVL abolished the elevations in AP, HR and rCBF elicited by electrical stimulation as well as the fall of AP and HR elicited by chemical stimulation of the FN. The disappearance of the responses was anatomically selective and could not be attributed to changes in resting AP, HR or rCBF, loss of reactivity of preganglionic sympathetic neurons, or variations in blood gases. Since the FN neither projects to nor receives afferents from the RVL the pathway to RVL is indirect. We conclude that: (1) the FPR results from excitation and the FDR inhibition of reticulospinal sympathoexcitatory axons of RVL; (2) the FPR is a consequence of excitation of axons arising from neurons in an as yet unidentified area of lower brainstem projecting to or through the FN and with collateral branches innervating RVL mono- or polysynaptically; (3) the FDR, in contrast, represents excitation of intrinsic FN neurons with a polysynaptic projection to RVL through unidentified regions of lower brainstem; (4) the RVL is a relay mediating the increase in rCBF associated with the FPR; and (5) the RVL plays a critical role in integrating actions on the systemic and cerebral circulation represented in cerebellum.

Brain stem area with C1 epinephrine neurons mediates baroreflex vasodepressor responses.

In anesthetized, paralyzed rats, bilateral electrolytic lesions of rostral ventrolateral medulla (RVL) containing epinephrine neurons of the C1 group 1) abolished the reflex hypotension and bradycardia elicited by electrical stimulation of the left vagus nerve or stretch of the left carotid sinus and 2) reduced arterial pressure (AP) and heart rate (HR) to values comparable to spinal cord transection. Combined lesions of the right nucleus tractus solitarii (NTS) and left or right C1 area did not alter AP. However, lesions of right NTS combined with lesions or microinjection of kainic acid into the left, but not right, C1 area abolished vasodepressor reflexes. Vasodepressor reflexes were unchanged by midcollicular decerebration, bilateral lesions of the parabrachial complex of the pons, or (after right NTS lesions) by lesions of the raphe or other reticular areas of the left half of the medulla. We conclude that neurons of the RVL, possibly belonging to the C1 epinephrine group, mediate vasodepressor responses from arterial baro- and other cardiopulmonary receptors, the pathway may be via a direct NTS-RVL projection, neurons in the C1 area of RVL are necessary for maintaining resting levels of arterial pressure.

TONIC AND REFLEX FUNCTIONS OF MEDULLARY SYMPATHETIC CARDIOVASCULAR CENTERS

TONIC AND REFLEX FUNCTIONS OF MEDULLARY SYMPATHETIC CARDIOVASCULAR CENTERS