Chronotropic, inotropic, and coronary artery blood flow responses to stimulation of specific canine sympathetic nerves and ganglia

1984 ◽  
Vol 62 (11) ◽  
pp. 1374-1381 ◽  
Author(s):  
R. D. Janes ◽  
D. E. Johnstone ◽  
J. A. Armour
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Coronary Blood Flow ◽  
Stellate Ganglion ◽  
Sympathetic Nerves ◽  
Neural Stimulation ◽  
Intramyocardial Pressure ◽  
Intact Heart ◽  
Cardiac Nerves ◽  
Stimulation Of

Electrical stimulation of the major sympathetic cardiac nerves and ganglia in chloralose-anesthetized, open-chest dogs elicited specific changes in heart rate, coronary blood flow, regional intramyocardial pressure, or intraventricular pressure. The effects produced by stimulation of a cardiac nerve were similar to, but never greater than those produced by stimulation of the ipsilateral stellate ganglion. Coronary blood flow was increased when neural stimulation increased intramyocardial pressure. In contrast, coronary blood flow was not altered significantly when neural stimulation induced tachycardia without increasing intramyocardial pressure. It is concluded that in the intact heart, electrical stimulation of the sympathetic cardiac nerves or ganglia increases coronary blood flow by augmenting intramyocardial pressure, not chronotropism.

Uterine arterial vasoconstrictions mediated by ovarian nerves in virgin and postpartum rats

1997 ◽  
Vol 272 (1) ◽  
pp. R318-R325 ◽  
Author(s):  
S. M. Hutchison ◽  
A. E. Tietz ◽  
K. A. Trostel ◽  
L. P. Schramm
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Uterine Artery ◽  
Sympathetic Nerves ◽  
Adrenergic Blockade ◽  
Sympathetic Vasoconstriction ◽  
Femoral Vessels ◽  
Ovarian Nerves ◽  
Stimulation Of

In most mammals, including humans, pregnancy results in the loss of most uterine vasomotor fibers. These experiments determined whether, despite this denervation, sympathetic nerves mediated uterine vasoconstrictions in the rat 24 h after delivery. Both virgin and uniparous postpartum rats were anesthetized with urethan. Femoral vessels were cannulated for measurement of arterial pressure and intravenous administration of fluids and drugs. Blood flow was measured in a uterine artery after ligation of all anastomotic ovarian vessels. Electrical stimulation of ovarian nerve efferents elicited frequency-dependent uterine vasoconstrictions in both virgin and postpartum rats. Vasoconstrictions in postpartum rats were not significantly different from those observed in virgins. In both virgin and postpartum rats, neurogenic vasoconstrictions were reduced by combined alpha 1- and alpha 2-adrenergic blockade. We conclude that the uterine branches of the ovarian nerve mediate adrenergic uterine vasoconstrictions. In the largely denervated uterus of the postpartum rat, these vasoconstrictions may be mediated by surviving innervation of the uterine artery and its major branches. Sympathetic vasoconstriction acting at these sites would constitute an effective defense against postpartum hemorrhage.

Effect of changes in myocardial epinephrine stores on plasma norepinephrine gradient across the dog heart

1994 ◽  
Vol 266 (6) ◽  
pp. H2404-H2409 ◽  
Author(s):  
F. Peronnet ◽  
G. Boudreau ◽  
J. de Champlain ◽  
R. Nadeau
Keyword(s):  
Electrical Stimulation ◽  
Adrenal Medulla ◽  
Pulse Width ◽  
Stellate Ganglion ◽  
Plasma Norepinephrine ◽  
Direct Support ◽  
Left Stellate Ganglion ◽  
Ici 118,551 ◽  
Beta 2 ◽  
Stimulation Of

Plasma norepinephrine (NE) concentration ([NE]) gradient across the heart was measured under electrical stimulation of the left stellate ganglion (LSG; 4 Hz, 4 V, 2 ms pulse width, 1 min) in control (Ctrl) and in adrenalectomized (Adrx) dogs, without and with a 10-min epinephrine (Epi) infusion (92 ng.kg-1.min-1), which partly restored myocardial Epi stores in Adrx dogs (2.9 +/- 0.7 ng/g vs. 6.4 +/- 0.7 ng/g in Ctrl dogs) and slightly increased tissue Epi stores in Ctrl dogs (10.5 +/- 1.3 pg/g). Compared with Ctrl dogs (1,069 +/- 172 pg/ml), the [NE] gradient across the heart under stimulation of the LSG was not modified 1 wk after bilateral adrenalectomy (1,190 +/- 122 pg/ml) or after Epi infusion in Ctrl (1,134 +/- 276 pg/ml) and Adrx (1,259 +/- 279 pg/ml) dogs. The beta 2-antagonist ICI-118,551 significantly reduced the stimulation-induced [NE] gradient across the heart in Ctrl dogs (621 +/- 190 and 603 +/- 86 pg/ml without and with a 10-min Epi infusion, respectively) but not in Adrx dogs deprived of tissue Epi (1,345 +/- 345 pg/ml). Partial repletion of myocardial Epi stores in Adrx dogs restored the effect of ICI-118,551 on the stimulation-induced [NE] gradient (776 +/- 121 pg/ml). These results provide direct support of the hypothesis that tissue Epi, which originates from the adrenal medulla and which is released locally along with NE, is the endogenous agonist for presynaptic beta 2-receptors and potentiates NE release.

Effects of Electrical Stimulation of the Superior Cervical Ganglion on Cochlear Blood Flow in Guinea Pig

1993 ◽  
Vol 113 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Tian-Ying Ren ◽  
E. Laurikainen ◽  
W. S. Quirk ◽  
J. M. Miller ◽  
A. L. Nuttall
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Guinea Pig ◽  
Superior Cervical Ganglion ◽  
Cochlear Blood Flow ◽  
Cervical Ganglion ◽  
Stimulation Of

Autoradiographic Evidence for Flow-Metabolism Uncoupling During Stimulation of the Nucleus Basalis of Meynert in the Conscious Rat

1997 ◽  
Vol 17 (6) ◽  
pp. 686-694 ◽  
Author(s):  
Elvire Vaucher ◽  
Josiane Borredon ◽  
Gilles Bonvento ◽  
Jacques Seylaz ◽  
Pierre Lacombe
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Metabolic Activity ◽  
Nucleus Basalis ◽  
Nucleus Basalis Of Meynert ◽  
Conscious Rat ◽  
Local Flow ◽  
Cortical Blood Flow ◽  
Subcortical Regions ◽  
Stimulation Of

We earlier reported that electrical stimulation of the rat nucleus basalis of Meynert (NBM) induces large cerebral blood flow increases, particularly in frontal cortical areas but also in some subcortical regions. The present study was designed to address the issue of blood flow control exerted by NBM projections. To this aim, we have determined whether these flow increases were associated with proportionate changes in metabolic activity as evaluated by cerebral glucose utilization (CGU) strictly under the same experimental conditions in the conscious rat. An electrode was chronically implanted in a reactive site of the NBM as determined by laser-Doppler flowmetry (LDF) of the cortical circulation. One to two weeks later, while the cortical blood flow was monitored by LDF, we measured CGU using the [14C]2-deoxyglucose autoradiographic technique during unilateral electrical stimulation of the NBM, and analyzed the local flow-metabolism relationship. The large increases in cortical blood flow induced by NBM stimulation, exceeding 300% in various frontal areas, were associated with at most 24% increases in CGU (as compared with the control group) in one frontal area. By contrast, strong increases in CGU exceeding 150% were observed in subcortical regions ipsilateral to the stimulation, especially in extrapyramidal structures, associated with proportionate CBF changes. Thus, none of the blood flow changes observed in the cortex can be ascribed to an increased metabolic activity, whereas CBF and CGU were coupled in many subcortical areas. This result indicates that different mechanisms, which do not necessarily involve any metabolic factor, contribute to the regulation of the cerebral circulation at the cortical and subcortical level. Because the distribution of the uncoupling is coincident with that of cholinergic NBM projections directly reaching cortical microvessels, these data strongly support the hypothesis that NBM neurons are capable of exerting a neurogenic control of the cortical microcirculation.

THROMBOLYSIS BY TISSUE-PLASMNOCEN ACTIVATOR AND A FIBRIN (OCEN) -DEGRADATION PRODUCT, PEPTIDE 6A, IN A CANINE MDDEL OF ELECTRICALLY-INDUCED CORONARY THROMBOSIS

1987 ◽  
Author(s):  
T Saldeen ◽  
J Mehta ◽  
W Nichols ◽  
D Lew
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Thrombosis ◽  
Canine Model ◽  
Peak Effect ◽  
Endothelial Surface ◽  
Tissue Plasminogen ◽  
Flow Restoration ◽  
Mean Time ◽  
Stimulation Of

Intracoronary thrombus resulting in acute myocardial ischemia can be lysed by thrombolytic agents, such as, streptokinase or t-PA. We examined the potential of a recombitant tissue-plasminogen activator (rt-PA)and a fibrin (ogen)-degradation productpentapeptide 6A, Ala-Arg-Pro-Ala-Lys, corresponding to aminoacids 43-47 in the BB-chain of fibrinogen, which causes marked increase in coronary blood flow and stimulates prostacyclin release, in restoring coronary blood flow in dqgs with experimentally-induced thrombus. An occlusive thrombus was created in the circumflex (Cx) coronary artery in 8 dcgs by electricalstimulation of the endothelial surface. The electrically-induced Cx thrombus consisted primarily of platelets and fibrin. After the occlusive thrcmbus was stable without electrical currant, rt-PA (10ug/kg/minute for 30 minutes intravenously)or peptide 6A (5 unoles/minute for 20 minutes intracorcnary) were randomly administered. Infusion of t-PA restored coronar blood flow (peak 22 ±12 ml/minute, mean ±SD) in five of seven animlas. The time to flow restoration was 12.3 ± 9.1 minutes and the reflow persistedfor20.0 ± 10.9 minutes. Peptide 6A administration also restored coronary blood flow (peak 20 ± 4 ml/ minute) in seven of eight animals with occlusive coronary thrombus. Mean time to blood flow restoration (4.3 ±2.9 minutes) wasshorter(P>0.05) than with rt-PA, but thereflow persisted only for the duration of tine infusion (16.3 ± 10.2 minutes).Peptide 6A adninistration was associatedwith a significant (P±0.05) increase in plasma 6-keto-PGF1α indicating stimulation of prostacyclin release. In addition, plasma t-PA concentrations also increased (F>0.01) at the peak effect of peptide 6A indicating releaseof endogenous t-PA as another potentialmechanism of the thrombolytic effects of peptide 6A. This study demonstrates that peptide 6A exerts coronary thrombolytic effectsccmpa rable to those of t-PA in a canine model of coronary thrombosis.

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