Coronary vasoconstrictor pathway from anterior hypothalamus includes neurons in RVLM

1993 ◽  
Vol 265 (6) ◽  
pp. R1311-R1317 ◽  
Author(s):  
A. R. Goodson ◽  
T. S. LaMaster ◽  
D. D. Gutterman
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Chemical Activation ◽  
Ventrolateral Medulla ◽  
Coronary Vascular Resistance ◽  
Gamma Aminobutyric Acid ◽  
Coronary Vasoconstriction ◽  
Coronary Vasoconstrictor

We have previously identified discrete brain sites [anterior (AHA) and lateral hypothalamus, periaqueductal gray, pontine parabrachial nucleus, lateral reticular formation, and rostral ventrolateral medulla (RVLM)] in the cat, in which electrical or chemical activation produces coronary vasoconstriction. This study examines whether the most rostral (AHA) and caudal (RVLM) of these sites are connected as part of a common pathway mediating coronary vasoconstriction. In chloralose-anesthetized cats, electrical stimulation in the AHA produced maximum increases in arterial pressure (41 +/- 10%) and coronary vascular resistance (28 +/- 9%). Microinjection of lidocaine into the RVLM attenuated the increases in arterial pressure (10 +/- 3%) and coronary vascular resistance (5 +/- 1%) in response to electrical stimulation in the AHA (P < 0.05 vs. before lidocaine). Lidocaine nonspecifically inhibits neural elements in the region. gamma-Aminobutyric acid in the RVLM, which selectively inhibits cell bodies and not fibers passing through the RVLM, attenuated the increase in coronary vascular resistance (38 +/- 8 to 14 +/- 3%; P < 0.05) but not the increase in arterial pressure (87 +/- 12 to 92 +/- 16%) in response to electrical stimulation in the AHA. These data indicate that coronary vasoconstriction in response to electrical stimulation in the AHA requires cell bodies in the RVLM; however, the associated pressor response is mediated by fibers passing through the RVLM. We conclude that a polysynaptic descending pathway that mediates sympathetic coronary vasoconstriction descends from the AHA through a synaptic connection in the RVLM.

Patterns of hemodynamic responses associated with central activation of coronary vasoconstriction

1992 ◽  
Vol 262 (2) ◽  
pp. R276-R283
Author(s):  
L. F. Jones ◽  
D. D. Gutterman ◽  
M. J. Brody
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Ventral Surface ◽  
Ventrolateral Medulla ◽  
Defense Reaction ◽  
Hemodynamic Responses ◽  
Coronary Vasoconstriction ◽  
Integrated Response ◽  
Coronary Vasoconstrictor

Previous studies in our laboratory have identified several central sites from which coronary vasoconstriction can be elicited by electrical stimulation. The present study was conducted to determine if specific patterns of hemodynamic responses are associated with activation of the coronary vasoconstrictor pathway in the hypothalamus, pons, and medulla. Cats anesthetized with chloralose were instrumented for recording arterial pressure, heart rate, and coronary, femoral, renal, and mesenteric blood flow velocities. After vagotomy and atenolol (1 mg/kg iv), anterior hypothalamus (AHA), parabrachial nucleus (PBN), a site very close to the ventral surface of the pons lateral to the pyramidal tract, and rostral ventrolateral medulla (RVLM) were stimulated electrically. Stimulation produced a decrease in coronary blood flow that was associated with all of the cardiovascular components of the defense reaction, an integrated response that included a decrease in hindquarter vascular resistance (blocked by methyl atropine), increases in renal and mesenteric vascular resistances, and a pressor response, except no change in renal vascular resistance from RVLM. Different patterns of hemodynamic responses were obtained from sites outside the coronary vasoconstrictor areas. From these results we conclude that coronary vasoconstriction is a frequent component of the defense reaction.

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.

Activation in the region of parabrachial nucleus elicits neurogenically mediated coronary vasoconstriction

1991 ◽  
Vol 261 (5) ◽  
pp. H1585-H1596 ◽  
Author(s):  
F. J. Miller ◽  
M. L. Marcus ◽  
M. J. Brody ◽  
D. D. Gutterman
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Chemical Activation ◽  
Parabrachial Nucleus ◽  
Coronary Vasoconstriction ◽  
Coronary Blood Flow Velocity

A role for parabrachial nucleus in cardiovascular regulation is suggested by evidence that electrical stimulation in this region elicits increase in heart rate and arterial pressure. We hypothesized that parabrachial nucleus may also be involved in control of coronary vasomotor tone. After beta-adrenergic receptor blockade in anesthetized cats, electrical stimulation in the region of parabrachial nucleus produced no change in heart rate, an increase in arterial pressure (34 +/- 6 mmHg), and a transient reduction in coronary blood flow velocity (-21 +/- 2%). Coronary resistance (72 +/- 9%) and femoral resistance (189 +/- 31%) increased markedly. The decrease in coronary blood flow velocity was abolished by stellate ganglionectomy or alpha 1-adrenergic blockade without altering pressor or femoral responses. Injection of the neurotransmitter L-glutamate or kainic acid into parabrachial nucleus also elicited coronary vasoconstriction. We conclude that electrical or chemical activation in the region of parabrachial nucleus elicits coronary vasoconstriction as part of a generalized sympathetic activation. The fact that the coronary response is elicited by chemical activation suggests that cell bodies in the region of medial parabrachial nucleus and subceruleus, as opposed to fibers of passage, are involved in this central neural coronary vasoconstriction.

Neurons of C1 area mediate cardiovascular responses initiated from ventral medullary surface

1986 ◽  
Vol 250 (5) ◽  
pp. R932-R945 ◽  
Author(s):  
E. E. Benarroch ◽  
A. R. Granata ◽  
D. A. Ruggiero ◽  
D. H. Park ◽  
D. J. Reis
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Ventral Surface ◽  
Aminobutyric Acid ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Pressor Responses ◽  
Ventral Medullary Surface

We sought to establish whether neurons of the C1 area of the rostral ventrolateral medulla (RVL) mediate changes in arterial pressure and heart rate evoked by topical application of drugs to the ventral medullary surface of the rat. Animals were anesthetized, paralyzed, and ventilated. The ventral surface was mapped with L-glutamate, and a restricted zone was identified from which L-glutamate, as well as kainic acid, bicuculline, strychnine, carbachol, or physostigmine, increased arterial pressure and heart rate. The hypertensive effects of carbachol and physostigmine were blocked by previous local application of atropine but not hexamethonium. Application of gamma-aminobutyric acid (GABA) or glycine to this area produced hypotension and bradycardia. Located caudal to the trapezoid bodies and lateral to the pyramids, this area corresponded to points with lowest threshold for pressor responses evoked by electrical stimulation and overlapped the distribution of epinephrine-synthesizing cells of the RVL. Processes arising from these neurons were identified reaching and contacting the ventral surface. Unilateral lesions involving the C1 area or phenylethanolamine-N-methyltransferase-labeled descending axons derived from this area imparied by greater than 70% the response to ipsilateral application of L-glutamate, GABA, or glycine to the ventral surface. We suggest that neurons within the C1 area of RVL adjacent to or including epinephrine cells may mediate cardiovascular changes elicited from a restricted chemosensitive zone of the ventral medullary surface of the rat.

Vasoconstrictor and vasodilator sites within anteroventral third ventricle region

1987 ◽  
Vol 253 (6) ◽  
pp. R827-R831 ◽  
Author(s):  
M. L. Mangiapane ◽  
M. J. Brody
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Third Ventricle ◽  
Renal Vascular Resistance ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Tungsten Microelectrode ◽  
Renal Vascular ◽  
Stimulation Of

Previous studies have shown that electrical stimulation of the rat anteroventral third ventricle (AV3V) region produces a characteristic pattern of hemodynamic effects, i.e., renal and mesenteric vasoconstriction, and hindquarters vasodilation. In the present study, we localized the vasoconstrictor and vasodilator effects to specific subregions of the AV3V. In urethan-anesthetized rats prepared with arterial catheters and pulsed Doppler flow probes, we assessed the effects of electrical stimulation of four nuclei within AV3V on mean arterial pressure and renal, mesenteric, and hindquarters resistance. These nuclei were the organum vasculosum lamina terminalis (OVLT), ventral nucleus medianus (median preoptic nucleus), anterior (precommissural) nucleus medianus (median preoptic nucleus), and periventricular preoptic nuclei. Stimulation was carried out by use of a tungsten microelectrode. Stimulation of the OVLT consistently provoked stimulus-locked increases in arterial pressure coupled with increases in mesenteric and renal vascular resistance. Ganglionic blockade with chlorisondamine prevented these responses, demonstrating that they were mediated neurogenically. Stimulation of the three remaining nuclei produced decreases in arterial pressure, hindquarters vasodilation, and little change in mesenteric and renal vascular resistance. No changes in heart rate were observed with stimulation of any of the four nuclei. These results suggest that the vasoconstrictor and pressor functions of the AV3V region are localized in or near the OVLT region, whereas the remaining nuclei of the AV3V region mediate vasodilator and depressor responses.

Subregions of rostral ventral medulla control arterial pressure and regional hemodynamics

1989 ◽  
Vol 257 (3) ◽  
pp. R635-R640 ◽  
Author(s):  
B. F. Cox ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Tidal Volume ◽  
Vascular Resistance ◽  
Neural Control ◽  
Cardiovascular Response ◽  
Cardiovascular Effects ◽  
Ventrolateral Medulla ◽  
Ventral Medulla ◽  
Ventromedial Medulla ◽  
Regional Hemodynamics

The cardiovascular effects of inactivating rostral ventromedial medulla (RVMM) under conditions of normal (2.5 ml) and reduced (1.5 ml) tidal volume were studied in urethan-anesthetized rats. Bilateral microinjection of lidocaine (200 nl, 4%) reduced mean arterial pressure (MAP), renal, mesenteric, and particularly hindquarter vascular resistance. These effects were not significantly altered by reducing tidal volume. Electrical stimulation of RVMM increased MAP and regional vascular resistances, again with the hindquarter change most prominent. The integrated cardiovascular response to stimulating rostral ventrolateral medulla (RVLM) appears to require integrity of RVMM; however, the converse is not true. Overall, these studies indicate that 1) the potential for RVMM to maintain neurogenic control of arterial pressure is as great as RVLM; 2) RVMM is capable of playing a proportionally greater role in the controlling hindquarter vascular resistance; 3) the integrity of RVMM appears to be important for responses elicited from RVLM; and 4) unlike RVLM, neural control of arterial pressure is sustained by RVMM under conditions of reduced tidal volume. We conclude that RVLM and RVMM are functionally and anatomically distinct subregions of rostral ventral medulla with equivalent capacity to maintain vasomotor tone.

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.

Powerful depressor and sympathoinhibitory effects evoked from neurons in the caudal raphe pallidus and obscurus

1995 ◽  
Vol 268 (5) ◽  
pp. R1295-R1302 ◽  
Author(s):  
M. J. Coleman ◽  
R. A. Dampney
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Raphe Nuclei ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Medullary Raphe ◽  
Dose Dependent Decrease ◽  
Raphé Nuclei ◽  
Raphe Pallidus ◽  
Dose Dependent

Microinjection of glutamate into sites within the medullary raphe nuclei (pallidus and obscurus) at levels caudal to the obex resulted in a dose-dependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate in anesthetized rabbits. The depressor and sympathoinhibitory responses were similar in magnitude to those elicited from the previously described depressor region in the caudal ventrolateral medulla (CVLM) but had a shorter duration, in both intact and barodenervated animals. The bradycardia was not altered by barodenervation but was reduced after administration of propranolol or atropine and abolished after administration of both drugs. The neuroinhibitory compounds gamma-aminobutyric acid or muscimol had no effect on MAP or RSNA when injected into the caudal medullary raphe nuclei but evoked a pressor and sympathoexcitatory response when injected into the CVLM. The results indicate that neurons within the caudal raphe pallidus and obscurus can powerfully inhibit sympathetic activity, but unlike sympathoinhibitory neurons in the CVLM, they are not tonically active and are not capable of producing sustained changes in arterial pressure and sympathetic activity.

Effect of Large Doses of Head Irradiation in Dogs

1958 ◽  
Vol 194 (2) ◽  
pp. 344-350 ◽  
Author(s):  
Ming-Tsung Peng ◽  
Shu Chien ◽  
Magnus I. Gregersen
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Respiratory Rate ◽  
Cause Of Death ◽  
Carotid Sinus ◽  
Pressor Response ◽  
Respiratory Response ◽  
Neurological Signs ◽  
X Irradiation

Dogs in which the head was x-irradiated with 23,500 r survived from 14 to 28 hours. The chief neurological signs were disturbance of equilibrium and extensor rigidity. Throughout the whole postirradiation course, the blood volume showed very little change. Arterial pressure, heart rate and respiratory rate remained essentially unchanged until about 1 hour before death. The carotid sinus reflex did not change until 30–60 minutes before death, but then deteriorated rapidly. Generally, the respiratory response to cyanide injection was still present after the disappearance of the carotid sinus reflex. At the terminal stage, the pressor response of the medullary vasomotor center to electrical stimulation decreased in parallel to that of the carotid sinus reflex. The vital centers in the medulla oblongata are directly damaged by large doses of x-irradiation. The failure of respiration is the cause of death.

Increased myocardial perfusion and sympathoadrenal activation during mild core hypothermia in awake humans

2003 ◽  
Vol 104 (5) ◽  
pp. 503-508 ◽  
Author(s):  
Steven M. FRANK ◽  
Patricia SATITPUNWAYCHA ◽  
Simon R. BRUCE ◽  
Peter HERSCOVITCH ◽  
David S. GOLDSTEIN
Keyword(s):  
Myocardial Perfusion ◽  
Vascular Resistance ◽  
Plasma Catecholamines ◽  
Saline Control ◽  
Coronary Vascular Resistance ◽  
Cardiac Work ◽  
Plasma Adrenaline ◽  
Coronary Vasoconstriction ◽  
Cold Saline ◽  
Sympathoadrenal Activation

Potential mechanisms of cold-induced myocardial ischaemia are sympathetically mediated coronary vasoconstriction and/or catecholamine-induced increases in cardiac work. To examine these parameters, 11 human volunteers were each studied on one day with, and on another day without, β-adrenoceptor blockade. On each day, warm (37 °C) saline (control) and cold (4 °C) saline (hypothermia) were given intravenously. Myocardial perfusion was assessed by positron emission tomography using H215O, and coronary vascular resistance was calculated. Plasma catecholamines were measured to assess sympathoadrenal activation. The core temperature decreased by 1.0 ± 0.2 °C with the cold saline, and was unchanged with warm saline. Myocardial perfusion increased by 20% (P = 0.01) and the rate–pressure product by 33% (P = 0.0004) with cold saline compared with warm saline. β-Blockade eliminated these increases. Coronary vascular resistance was similar with warm and cold saline, and was unaffected by β-blockade. Plasma adrenaline increased by 120% and noradrenaline by 251% during cold saline, but were unchanged during warm saline. In conclusion, core hypothermia triggers β-adrenoceptor-mediated increased cardiac work, sympathoadrenal activation and increased myocardial perfusion. There is no evidence for hypothermia-induced coronary vasoconstriction.

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