Role of ventrolateral medulla in vasomotor response to cerebral ischemia

1980 ◽  
Vol 239 (3) ◽  
pp. H349-H358 ◽  
Author(s):  
R. A. Dampney ◽  
E. A. Moon
Keyword(s):  
Cerebral Ischemia ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Medullary Reticular Formation ◽  
Norepinephrine Infusion ◽  
Pressor Responses ◽  
Highly Sensitive ◽  
Dorsal Medulla ◽  
Stimulation Of

The ventrolateral medulla has been postulated to contain chemosensitive neurons. This study investigated the role of this region in the generation of the pressor response to cerebral ischemia (CIR) in anesthetized paralyzed artificially ventilated rabbits. A circumscribed and highly sensitive pressor area in the ventrolateral medullary reticular formation 2-4 mm rostral to the obex, separate from the well-known dorsal pressor area, was mapped by use of a stimulating electrode. Electrolytic destruction of this area resulted in a profound reduction in resting mean arterial pressure (MAP). After restoration of baseline MAP with norepinephrine infusion, the CIR was greatly reduced (by mean 70.2% of control), but pressor responses from the dorsal medulla were unaffected. In contrast, lesions of greater size placed in the ventrolateral medulla more caudally did not significantly alter resting MAP and only slightly reduced the CIR (by mean 17.0% of control). Vasomotor responses to stimulation of the ventrolateral pressor area were unaffected by caudal ventrolateral lesions, but greatly reduced by dorsomedial lesions in the same plane. It is concluded that the ventrolateral area is either the site of origin or an essential part of the central vasomotor pathway mediating the CIR and that this pathway projects dorsomedially before descending to the spinal cord.

Mechanisms of pressor response produced by stimulation of nucleus ambiguus

1990 ◽  
Vol 259 (5) ◽  
pp. R955-R962
Author(s):  
B. H. Machado ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Pressor Responses ◽  
Regional Vascular Resistance ◽  
Parasympathetic Control ◽  
Renal Vascular ◽  
Stimulation Of

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

Pressor response from rostral dorsomedial medulla is mediated by excitatory amino acid receptors in rostral VLM

1994 ◽  
Vol 267 (1) ◽  
pp. R309-R315 ◽  
Author(s):  
Y. Hirooka ◽  
J. W. Polson ◽  
R. A. Dampney
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Amino Acid Receptors ◽  
Control Value ◽  
Afferent Fibers ◽  
Pressor Responses ◽  
Before And After ◽  
Stimulation Of

Excitatory amino acid (EAA) receptors in the rostral part of the ventrolateral medulla (VLM) have been shown to mediate pressor responses elicited by stimulation of various peripheral afferent fibers as well as other central nuclei. This study tested the hypothesis that these receptors are a critical component in the central pathway mediating the powerful pressor response that is produced by stimulation of a group of neurons within a circumscribed region in the rostral dorsomedial medulla (RDM). In anesthetized rabbits, the pressor response elicited by unilateral microinjection of glutamate into this RDM region was measured before and after injection of kynurenic acid (Kyn), a broad-spectrum EAA receptor antagonist, into the physiologically identified pressor region of either the ipsilateral or contralateral rostral VLM. The pressor response to RDM stimulation was greatly reduced (to 24 +/- 4% of control) 5-10 min after injection of Kyn (but not the vehicle solution) into the ipsilateral rostral VLM; this response returned completely to its control value within 30-60 min after Kyn injection. By contrast, after Kyn injection into the contralateral rostral VLM, the pressor response to RDM stimulation was not affected (106 +/- 15% of control). The results indicate that the descending pressor pathway from the RDM to the spinal cord is mediated by EAA receptors in the rostral VLM pressor region. Furthermore, the pathway from the RDM to the rostral VLM is predominantly, if not exclusively, ipsilateral.

Glutamatergic and GABAergic inputs to the RVL mediate cardiovascular adjustments to noxious stimulation

2001 ◽  
Vol 280 (2) ◽  
pp. R434-R440 ◽  
Author(s):  
Olga S. Possas ◽  
Oswaldo U. Lopes ◽  
Sérgio L. Cravo
Keyword(s):  
Blood Flow ◽  
Pressor Response ◽  
Muscle Afferents ◽  
Ventrolateral Medulla ◽  
Noxious Stimulation ◽  
Glutamatergic Synapses ◽  
Pressor Responses ◽  
Gabaergic Synapses ◽  
Sciatic Nerve Stimulation

Stimulation of cutaneous and muscle afferents induces several cardiovascular adjustments such as hypertension, tachycardia, and muscle vasodilation. Although previous studies have demonstrated that the rostral ventrolateral medulla (RVL) mediates sympathoexcitation and pressor responses to sciatic nerve stimulation (SNS), whether it also mediates blood flow adjustments remains unclear. Therefore, in the present study, we examined the role of the RVL in the vasodilation induced by SNS and the possible neurotransmitters involved. In Urethane-anesthetized, paralyzed, and artificially ventilated rats, SNS (square pulses, 1 ms, 20 Hz, 800–1200 μA, 10 s) produced increases in blood pressure, heart rate, blood flow, and vascular conductance of the stimulated limb. Unilateral microinjection of kainic acid (2 nmol/100 nl) into the RVL contralateral to the stimulated limb abolished cardiovascular adjustments to SNS. Unilateral microinjections of kynurenic acid (2 nmol/100 nl) selectively abolished the pressor response to SNS, whereas bicuculline (400 pmol/100 nl) abolished the increases in blood flow without changing the pressor response. These results suggest that glutamatergic synapses within the RVL mediate pressor responses, whereas GABAergic synapses may mediate the vasodilation to SNS.

Role of rostral ventrolateral medulla in centrally mediated pressor responses

1994 ◽  
Vol 267 (4) ◽  
pp. H1549-H1556 ◽  
Author(s):  
J. M. Kiely ◽  
F. J. Gordon
Keyword(s):  
Synaptic Transmission ◽  
Excitatory Amino Acid ◽  
Receptor Activation ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Synaptic Activation ◽  
Axonal Conduction ◽  
Pressor Responses ◽  
Stimulation Of

The region of the rostral ventrolateral medulla (RVLM) plays an important role in central nervous system regulation of cardiovascular function. The initial purpose of these studies was to determine whether synaptic activation of excitatory amino acid (EAA) receptors in the RVLM might mediate central pressor responses. Blockade of EAA receptors in the RVLM with kynurenic acid abolished pressor responses evoked by stimulation of sciatic nerve afferents but had no effect on increases in arterial pressure produced by stimulation of hypothalamic sites. To determine whether synaptic transmission in the RVLM, independent of EAA receptor activation, was a prerequisite for the production of hypothalamic pressor responses, axonal conduction and/or synaptic transmission were pharmacologically interrupted in the RVLM. Blockade of synaptic transmission with muscimol or kainic acid attenuated, but did not eliminate, hypothalamic pressor responses. Concurrent blockade of synaptic and axonal transmission in the RVLM with lidocaine produced the greatest reduction of hypothalamic pressor responses. Collectively, these results suggest that central pressor responses are not uniformly mediated by synaptic activation of neurons within the RVLM. Instead, a combination of synaptic transmission and axonal conduction within and possibly outside the region of the RVLM may be required for the production of many centrally mediated pressor responses.

Involvement of the ventrolateral medulla in the mediation of pressor responses of the rat to afferent vagal stimulation

1985 ◽  
Vol 63 (12) ◽  
pp. 1612-1614 ◽  
Author(s):  
T. Kubo
Keyword(s):  
Spinal Cord ◽  
Vagal Stimulation ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Vasopressin Antagonist ◽  
Caudal Ventrolateral Medulla ◽  
Pressor Responses ◽  
Electrolytic Lesions ◽  
Afferent Vagal ◽  
Stimulation Of

Electrical stimulation of afferent vagal fibres evoked a pressor response in rats after transection of the spinal cord. The pressor response was accounted for by an increased release of vasopressin because it was abolished by the intravenous injection of a vasopressin antagonist. Bilateral electrolytic lesions at the sites of the caudal ventrolateral medulla markedly reduced the pressor response to afferent vagal stimulation but not that to carotid occlusion. It is concluded that the area of the caudal ventrolateral medulla is involved in mediation of the vasopressin-induced pressor response to afferent vagal stimulation.

Ventrolateral medullary neurons modulate pressor reflex to muscular contraction

1989 ◽  
Vol 257 (5) ◽  
pp. R1154-R1161 ◽  
Author(s):  
R. M. Bauer ◽  
G. A. Iwamoto ◽  
T. G. Waldrop
Keyword(s):  
Arterial Pressure ◽  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Minute Ventilation ◽  
Muscular Contraction ◽  
Posterior Hypothalamus ◽  
Ventrolateral Medulla ◽  
Pressor Reflex ◽  
Stimulation Of

Cardiorespiratory alterations during exercise are mediated through feedback from contracting muscles and descending drive from rostral brain sites such as the posterior hypothalamus. The role of medullary sites, which process this information, was examined in this study. In anesthetized cats, muscular contraction elicited by stimulation of L7 and S1 ventral roots and electrical stimulation of sites in the posterior hypothalamus both evoked increases in arterial pressure, heart rate, and minute ventilation. The reflex increase in arterial pressure produced by muscular contraction was attenuated significantly 15-20 min after bilateral microinjections of an excitatory amino acid (EAA) receptor antagonist, kynurenic acid (KYN), into the ventrolateral medulla (VLM). The reflex increase in arterial pressure evoked by muscular contraction returned to control levels 90 min after VLM microinjections of KYN. Microinjection of KYN into the VLM had no effect on the cardiorespiratory responses to posterior hypothalamic stimulation. These findings suggest that neurons in the VLM modulate the reflex pressor response evoked by muscular contraction. This reflex may be mediated through an interaction with EAA receptors on neurons in the VLM.

Methylene blue potentiates vascular reactivity in isolated rat lungs

1989 ◽  
Vol 66 (3) ◽  
pp. 1040-1045 ◽  
Author(s):  
G. M. Mazmanian ◽  
B. Baudet ◽  
C. Brink ◽  
J. Cerrina ◽  
S. Kirkiacharian ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Vascular Reactivity ◽  
Bolus Injection ◽  
Pressor Response ◽  
Hypoxic Response ◽  
Pressor Responses ◽  
Isolated Rat Lung ◽  
Lung Preparation ◽  
Isolated Rat

A bolus injection of methylene blue (1 mg), a guanylate cyclase inhibitor, or aspirin (3 mg) in the isolated rat lung preparation had little or no effect on resting perfusion pressure under normoxic condition. In contrast, methylene blue markedly potentiated hypoxic vasopressor response (4-fold) when injected before or during the alveolar hypoxic stimulation. Hemoglobin also potentiated the hypoxic pressor response. Similarly, methylene blue or aspirin augmented the pressor responses to angiotensin II (0.1–1 microgram). The increased hypoxic response induced by methylene blue was immediate and sustained. Methylene blue, when added during hypoxia in the presence of aspirin, further augmented the response to hypoxia compared with the enhanced hypoxic response observed with aspirin alone. Our results suggest that, in addition to the role of cyclooxygenase products, the pulmonary vascular bed may be regulated by endothelium-dependent factors that can be antagonized directly or indirectly by methylene blue.

Role of adrenal catecholamines in cerebrovasodilation evoked from brain stem

1987 ◽  
Vol 252 (6) ◽  
pp. H1183-H1191
Author(s):  
C. Iadecola ◽  
P. M. Lacombe ◽  
M. D. Underwood ◽  
T. Ishitsuka ◽  
D. J. Reis
Keyword(s):  
Brain Function ◽  
Blood Gases ◽  
Brain Regions ◽  
Elevated Plasma ◽  
Regional Cerebral Blood ◽  
Medullary Reticular Formation ◽  
Alpha Chloralose ◽  
The Brain ◽  
Stimulation Of

We studied whether adrenal medullary catecholamines (CAs) contribute to the metabolically linked increase in regional cerebral blood flow (rCBF) elicited by electrical stimulation of the dorsal medullary reticular formation (DMRF). Rats were anesthetized (alpha-chloralose, 30 mg/kg), paralyzed, and artificially ventilated. The DMRF was electrically stimulated with intermittent trains of pulses through microelectrodes stereotaxically implanted. Blood gases were controlled and, during stimulation, arterial pressure was maintained within the autoregulated range for rCBF. rCBF and blood-brain barrier (BBB) permeability were determined in homogenates of brain regions by using [14C]iodoantipyrine and alpha-aminoisobutyric acid (AIB), respectively, as tracers. Plasma CAs (epinephrine and norepinephrine) were measured radioenzymatically. DMRF stimulation increased rCBF throughout the brain (n = 5; P less than 0.01, analysis of variance) and elevated plasma CAs substantially (n = 4). Acute bilateral adrenalectomy abolished the increase in plasma epinephrine (n = 4), reduced the increases in flow (n = 6) in cerebral cortex (P less than 0.05), and abolished them elsewhere in brain (P greater than 0.05). Comparable effects on rCBF were obtained by selective adrenal demedullation (n = 7) or pretreatment with propranolol (1.5 mg/kg iv) (n = 5). DMRF stimulation did not increase the permeability of the BBB to AIB (n = 5). We conclude that the increases in rCBF elicited from the DMRF has two components, one dependent on, and the other independent of CAs. Since the BBB is impermeable to CAs and DMRF stimulation fails to open the BBB, the results suggest that DMRF stimulation allows, through a mechanism not yet determined, circulating CAs to act on brain and affect brain function.

Effects on breathing of ventrolateral medullary cooling in awake goats

1995 ◽  
Vol 78 (1) ◽  
pp. 258-265 ◽  
Author(s):  
H. V. Forster ◽  
P. J. Ohtake ◽  
L. G. Pan ◽  
T. F. Lowry ◽  
M. J. Korducki ◽  
...  
Keyword(s):  
Pulmonary Ventilation ◽  
Control Level ◽  
Control Of Breathing ◽  
Ventrolateral Medulla ◽  
Neuronal Dysfunction ◽  
Subsequent Increase ◽  
Initial Decrease ◽  
Caudal Area ◽  
Stimulation Of

Our objective was to investigate the role of the ventrolateral medulla (VLM) in the control of breathing during the awake state. In 17 awake adult goats, chronically implanted thermodes were used to cool the VLM and thereby cause reversible neuronal dysfunction in all or portions of the area between the first hypoglossal rootlet and the ponto-medullary junction (so-called area M (rostral) and area S). Within 5 s after the initiation of cooling, 60–100% of areas M and S, pulmonary ventilation (VE) decreased uniformly over conditions of eucapnia, hypercapnia, hypoxia, and exercise (P < 0.05). Between 10 and 20 s of cooling, the reduction in VE was approximately 10% greater during eucapnia and hypercapnia than during hypoxia and exercise (P < 0.05). For the remaining 10 s of cooling and for about 1 min after cooling, VE increased to and above control level. Cooling only rostral area M or only caudal area M-rostral area S affected breathing qualitatively in the same manner as when 60–100% of areas M and S were cooled. However, cooling caudal area S had effects that differed significantly (P < 0.05) from more rostral cooling in that the initial decrease in VE was attenuated and the subsequent increase was accentuated. The initial uniform decreased VE during cooling suggests that superficial VLM nonchemoreceptor neurons facilitate breathing. The subsequent relatively greater effect of cooling during eucapnia and hypercapnia probably reflects dysfunction of chemoreceptor-related neurons that normally stimulate breathing. The stimulation of breathing during the later stages and after cooling may suggest that some VLM neurons inhibit breathing.

Effects of hypoxia, hyperoxia and hypercapnia on graded cerebral ischemic responses in rabbits

1992 ◽  
Vol 263 (6) ◽  
pp. H1839-H1846
Author(s):  
T. Takeuchi ◽  
J. Horiuchi ◽  
N. Terada ◽  
M. Nagao ◽  
H. Terajima
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Arterial Pressure ◽  
Internal Carotid ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Left Internal Carotid Artery ◽  
Renal Nerve ◽  
Tissue Po2 ◽  
Cerebral Ischemic

This study was designed to determine how several factors interact to modify the cerebral ischemic pressor response (CIR) in anesthetized rabbits. After the carotid sinus and aortic nerves were bilaterally sectioned, blood flow through the left internal carotid artery (ICF), which was surgically restricted as the sole route of blood supply to the brain, was reduced by a servo-controller during ventilation with room air, and 8% and 90% O2 and 2 and 5% CO2 gas mixtures. Blood flow (MBF), tissue PO2, PCO2, and interstitial pH were measured in the rostral ventrolateral medulla. Internal carotid arterial pressure, tissue PO2, and MBF decreased proportionately as ICF decreased in the range from 4 to 0 ml/min. Hypoxia significantly increased the rise in renal nerve activity (RNA) and CIR caused by cerebral ischemia, while hyperoxia significantly decreased them. Hypercapnia had almost no influence on the increases in RNA and mean arterial pressure produced by cerebral ischemia. CIR showed a much higher correlation with changes in tissue PO2 than with the other factors. We examined how these factors interact to modify CIR and found that central hypoxia is the main factor in producing CIR.

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