The role of sympathetic efferent activity in the regulation of brain temperature

1983 ◽  
Vol 396 (2) ◽  
pp. 138-143 ◽  
Author(s):  
O. S. Bamford ◽  
R. Eccles
Keyword(s):  
Brain Temperature ◽  
Efferent Activity ◽  
Sympathetic Efferent Activity

Role of afferent activity from the bladder in regulating its activity

1959 ◽  
Vol 196 (2) ◽  
pp. 351-353 ◽  
Author(s):  
Donald J. Marsh ◽  
George Suzuki ◽  
Frederick H. Meyers
Keyword(s):  
Local Anesthetic ◽  
Sympathetic Activity ◽  
Normal Function ◽  
Afferent Activity ◽  
Nerve Section ◽  
Efferent Activity ◽  
Afferent Nerves ◽  
Inhibitory Tone ◽  
Sympathetic Efferent Activity

Sympathetic efferent activity to the bladder was recorded from the hypogastric nerves of cats. When the pelvic (afferent) nerves were sectioned or a local anesthetic applied, sympathetic activity decreased. It is concluded from these data and from previous work that sympathetic inhibitory tone necessary for normal function is maintained by afferent activity from the bladder. Nerve section experiments are reinterpreted in the light of these data.

scholarly journals Dual role of cerebral blood flow in regional brain temperature control in the healthy newborn infant

2014 ◽  
Vol 37 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Sachiko Iwata ◽  
Ilias Tachtsidis ◽  
Sachio Takashima ◽  
Toyojiro Matsuishi ◽  
Nicola J. Robertson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Newborn Infant ◽  
Temperature Control ◽  
Brain Temperature ◽  
Dual Role ◽  
Healthy Newborn ◽  
Regional Brain

Attenuation of the cardiac effects of cocaine by dizocilpine

1993 ◽  
Vol 264 (6) ◽  
pp. H1890-H1895
Author(s):  
G. R. Hageman ◽  
T. Simor
Keyword(s):  
Ventricular Arrhythmias ◽  
Cardiovascular Effects ◽  
Sympathetic Stimulation ◽  
Efferent Nerve ◽  
Efferent Activity ◽  
Life Threatening ◽  
Innervation Patterns ◽  
The Right ◽  
Sympathetic Efferent Activity ◽  
Cardiac Nerves

Cocaine abuse causes autonomic and cardiovascular effects that may be life threatening. Attenuation of cocaine-induced seizures has been produced by the noncompetitive antagonist of the N-methyl-D-aspartate receptor channel complex, dizocilpine. The purpose of the present study was, first, to determine effects of dizocilpine on the incidence of pacing-induced ventricular arrhythmias and, second, to evaluate the effects of dizocilpine on cocaine-induced depression of sympathetic efferent activity to the heart. Adult dogs were anesthetized and instrumented for blood pressure and an electrocardiogram. After vagotomy and thoracotomy, electrodes and strain gauges were sutured onto the right atrium and ventricle. A left thoracic sympathetic efferent nerve was isolated and stimulated for analysis of the innervation pattern. Arrhythmias were induced with programmed electrical stimulation of the heart before and during left cardiac sympathetic efferent nerve stimulation. The control incidence of induced arrhythmias was only 2%, which increased to 21% during left sympathetic stimulation. Cocaine (2 mg/kg iv) significantly increased these to 11 and 42%, respectively. Dizocilpine (0.5 mg/kg iv) reduced the incidence of induced ventricular arrhythmias to 2% with cocaine (P < 0.05) and to 19% with cocaine and left sympathetic stimulation (P < 0.01). One or two sympathetic efferent cardiac nerves were stimulated to evaluate innervation patterns. These nerves were severed and prepared for recording multifiber efferent neurograms. Nerve traffic was analyzed by counting positive spikes for 15 s. Control activities were normalized at 100%. Within 6 min, cocaine (2 mg/kg iv) reduced the sympathetic efferent activity to 83 +/- 4% of control (n = 14 nerves).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of adenosine in regulation of brain temperature in fetal sheep

1999 ◽  
Vol 181 (3) ◽  
pp. 681-687 ◽  
Author(s):  
Shunji Suzuki ◽  
Gordon G. Power
Keyword(s):  
Brain Temperature ◽  
Fetal Sheep

Differential responses of regional sympathetic activity and blood flow to visceral afferent stimulation

2001 ◽  
Vol 280 (6) ◽  
pp. R1781-R1789 ◽  
Author(s):  
Hui-Lin Pan ◽  
Dwight D. Deal ◽  
Zemin Xu ◽  
Shao-Rui Chen
Keyword(s):  
Vascular Resistance ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Visceral Afferents ◽  
Cardiovascular Reflexes ◽  
Efferent Activity ◽  
Blood Flows ◽  
The Right ◽  
Sympathetic Efferent Activity ◽  
Stimulation Of

The sympathetic nervous system is essential for the cardiovascular responses to stimulation of visceral afferents. It remains unclear how the reflex-evoked sympathetic output is distributed to different vascular beds to initiate the hemodynamic changes. In the present study, we examined changes in regional sympathetic nerve activity and blood flows in anesthetized cats. Cardiovascular reflexes were induced by either electrical stimulation of the right splanchnic nerve or application of 10 μg/ml of bradykinin to the gallbladder. Blood flows were measured using colored microspheres or the Transonic flow meter system. Sympathetic efferent activity was recorded from the left splanchnic, inferior cardiac, and tibial nerves. Stimulation of visceral afferents decreased significantly blood flows in the celiac (from 49 ± 4 to 25 ± 3 ml/min) and superior mesenteric (from 35 ± 4 to 23 ± 2 ml/min) arteries, and the vascular resistance in the splanchnic bed was profoundly increased. Consistently, stimulation of visceral afferents decreased tissue blood flows in the splanchnic organs. By contrast, activation of visceral afferents increased significantly blood flows in the coronary artery and portal vein but did not alter the vascular resistance of the femoral artery. Furthermore, stimulation of visceral afferents increased significantly sympathetic efferent activity in the splanchnic (182 ± 44%) but not in the inferior cardiac and tibial nerves. Therefore, this study provides substantial new evidence that stimulation of abdominal visceral afferents differentially induces sympathetic outflow to the splanchnic vascular bed.

scholarly journals Body and brain temperature coupling: the critical role of cerebral blood flow

2009 ◽  
Vol 179 (6) ◽  
pp. 701-710 ◽  
Author(s):  
Mingming Zhu ◽  
Joseph J. H. Ackerman ◽  
Dmitriy A. Yablonskiy
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Temperature ◽  
Critical Role

EFFECT OF β-BLOCKING DRUGS ON SYMPATHETIC EFFERENT ACTIVITY AND SYMPATHETIC REFLEXES

Abstracts ◽  
1978 ◽  
pp. 875
Author(s):  
Katalin P. Gibiszer ◽  
J. Pórszász
Keyword(s):  
Efferent Activity ◽  
Sympathetic Reflexes ◽  
Sympathetic Efferent Activity

scholarly journals Vagotomy attenuates but does not prevent the somnogenic and febrile effects of lipopolysaccharide in rats

1998 ◽  
Vol 274 (2) ◽  
pp. R406-R411 ◽  
Author(s):  
Levente Kapás ◽  
Michael K. Hansen ◽  
Hee-Yoon Chang ◽  
James M. Krueger
Keyword(s):  
Vagus Nerve ◽  
Eye Movement ◽  
Slow Wave ◽  
Dark Period ◽  
Brain Temperature ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep

The role of the vagus nerve in the somnogenic and pyrogenic effects of lipopolysaccharide (LPS) was studied in rats. Control rats ( n= 8) and rats subjected to bilateral subdiaphragmal vagotomy (VX; n = 9) were injected with 100 μg/kg ip LPS at the beginning of the dark period. Sleep and brain temperature (Tbr) were recorded for 23 h after the injections. LPS caused increases in non-rapid eye movement sleep (NREMS) for 12 h after the injection in control rats. Sleep intensity, as indicated by the slow-wave activity (SWA) of the electroencephalogram during NREMS, was suppressed. LPS elicited biphasic Tbr responses: an initial hypothermia was followed by increases in Tbr that lasted for ∼20 h. In vagotomized rats, the NREMS responses to LPS were blunted. The magnitude of the LPS-induced NREMS increases was about one-half of that seen in control rats, and these sleep responses lasted only for 6 h. LPS did not affect SWA in VX animals. VX completely abolished the hypothermic responses to LPS and shortened the duration of the hyperthermia. The results suggest that the subdiaphragmal vagi play an important, but not exclusive, role in the somnogenic and pyrogenic actions of intraperitoneally injected LPS.

Brain O2 consumption and glutamate release during hypoglycemic coma in piglets are temperature sensitive

1999 ◽  
Vol 276 (6) ◽  
pp. H2053-H2062 ◽  
Author(s):  
R. N. Ichord ◽  
F. J. Northington ◽  
D. van Wylen ◽  
M. V. Johnston ◽  
C. Kwon ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Brain Temperature ◽  
Glutamate Release ◽  
Temperature Sensitive ◽  
Dependent Manner ◽  
Temperature Dependent ◽  
Immature Brain ◽  
Hypoglycemic Coma ◽  
Mature Brain

Hypoglycemic injury in the mature brain is mediated by excitotoxicity, which is worsened by disordered cellular energy metabolism. The role of excitotoxicity in relation to brain energy metabolism during hypoglycemia has not been studied in the immature brain. Brain oxygen consumption ([Formula: see text]) increases during hypoglycemia in piglets, whereas [Formula: see text] decreases in adult pig models. We tested the hypothesis that increased[Formula: see text] during hypoglycemic coma is temperature dependent and coincides with increased excitatory amino acids (EAA). We measured cerebral blood flow (CBF),[Formula: see text], and cortical microdiaysate EAA in pentobarbital-anesthetized piglets during hypoglycemic coma and during 2 h of recovery and in normoglycemic controls. In warmed animals brain temperature was kept normothermic (38.5°C). In unwarmed animals brain temperature was allowed to fall (37.6°C). During hypoglycemia CBF increased similarly in warmed animals and unwarmed animals;[Formula: see text] increased in warmed animals but not unwarmed animals. Glutamate increased during coma and increased more in warmed animals than unwarmed animals but normalized quickly during recovery. EEG recovered earlier in unwarmed animals. We conclude that during a hypoglycemic coma in the immature brain,[Formula: see text] and glutamate are increased in a temperature-dependent manner.

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