The role of liver glucosensors in the integrated sympathetic response induced by deep hypoglycemia in dogs

Diabetes ◽  
1994 ◽  
Vol 43 (8) ◽  
pp. 1052-1060 ◽  
Author(s):  
M. Hamilton-Wessler ◽  
R. N. Bergman ◽  
J. B. Halter ◽  
R. M. Watanabe ◽  
C. M. Donovan
Keyword(s):  
2007 ◽  
Vol 184 (1) ◽  
pp. 135-140 ◽  
Author(s):  
Håkan Olausson ◽  
Jonathan Cole ◽  
Karin Rylander ◽  
Francis McGlone ◽  
Yves Lamarre ◽  
...  

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Jianhua Li ◽  
Jihong Xing ◽  
Lawrence Sinoway

2001 ◽  
Vol 280 (5) ◽  
pp. H1996-H2005 ◽  
Author(s):  
Kathleen P. O'Hagan ◽  
Kara A. Skogg ◽  
Jennifer B. Stevenson

The role of ANG II in the arterial baroreflex control of renal sympathetic nerve activity (RSNA) in eight term-pregnant (P) and eight nonpregnant (NP) conscious rabbits was assessed using sequential intracerebroventricular and intravenous infusions of losartan, an AT1 receptor antagonist. The blood pressure (BP)-RSNA relationship was generated by sequential inflations of aortic and vena caval perivascular occluders. Pregnant rabbits exhibited a lower maximal RSNA reflex gain (−44%) that was primarily due to a reduction in the maximal sympathetic response to hypotension (P, 248 ± 20% vs. NP, 357 ± 41% of rest RSNA, P < 0.05). Intracerebroventricular losartan decreased resting BP in P (by 9 ± 3 mmHg, P < 0.05) but not NP rabbits, and had no effect on the RSNA baroreflex in either group. Subsequent intravenous losartan decreased resting BP in NP and further decreased BP in P rabbits, but had no significant effect on the maximal RSNA reflex gain. ANG II may have an enhanced role in the tonic support of BP in pregnancy, but does not mediate the gestational depression in the arterial baroreflex control of RSNA in rabbits.


2010 ◽  
Vol 299 (5) ◽  
pp. R1407-R1414 ◽  
Author(s):  
Craig D. Steinback ◽  
Toni Breskovic ◽  
Maria Frances ◽  
Zeljko Dujic ◽  
J. Kevin Shoemaker

The within-breath modulation of muscle sympathetic nerve activity (MSNA) is well established, with greater activity occurring during expiration and less during inspiration. Whether ventilation per se affects the longer-term (i.e., minute-to-minute) regulation of MSNA has not been determined. We sought to define the specific role of ventilation in regulating sympathetic activation during chemoreflex activation, where both ventilation and MSNA are increased. Ten young healthy subjects performed both asphyxic rebreathing and repeated, rebreathing apneas to cause the same magnitude of chemoreflex stress in the presence or absence of ventilation. Both protocols caused increases in sympathetic burst frequency, burst amplitude, and burst incidence. However, burst frequency was increased more during repeated apneas (12 ± 6 to 25 ± 7 bursts/min) compared with rebreathing (12 ± 5 to 17 ± 7 bursts/min; P < 0.001) due to a greater burst incidence during apneas (36 ± 11 bursts/100 heart beats) vs. rebreathing (26 ± 8 bursts/100 heart beats, P < 0.001). The sympathetic gain to chemoreflex stress was also larger during repeated apneas (2.29 ± 1.29 au/% desaturation) compared with rebreathing (1.44 ± 0.53 au/% desaturation, P < 0.05). The augmented sympathetic response during apneas was associated with a larger pressor response and total peripheral resistance compared with rebreathing. These data demonstrate that ventilation per se restrains sympathetic activation during chemoreflex activation. Further, the augmented sympathetic response during apneas was associated with greater cardiovascular stress and may be relevant to the cardiovascular pathology associated with sleep-disordered breathing.


1962 ◽  
Vol 24 (1) ◽  
pp. 91-103 ◽  
Author(s):  
B. A. CROSS ◽  
I. A. SILVER

SUMMARY In rabbits under urethane anaesthesia sympathetico-adrenal vasoconstrictor activity was monitored by the reduction of oxygen tension (measured polarographically with needle electrodes) in the testis and lactating mammary gland, and by the inhibitory effect on milk ejection. Electrical stimulation of the dorsal, lateral and posterior hypothalamus evoked a sympathetic response in these organs, characterized by a rapid nervous effect and secondary humoral effect which outlasted the stimulus, resembled the response to intravenous adrenaline, and was abolished by removal of both adrenal glands. Hypoxia produced by making the animals inhale nitrous oxide or nitrogen for 15–30 sec. and hypercapnia induced by inhalation of a mixture of 80% CO2 and 20% O2 for 5–15 sec. both induced a sympathetic discharge similar to that resulting from hypothalamic stimulation. Hypercapnia was a notably more potent stimulus than hypoxia. The effects were reversibly blocked by thoraco-lumbar spinal anaesthesia. Placement of discrete bilateral lesions in the septum, hippocampus and medial thalamus did not impair the sympathetic activation elicited by hypercapnia. Hypothalamic lesions, on the other hand, often reduced and occasionally prevented the central sympathetic discharge. The possible role of the hypothalamus in cardiovascular regulation is discussed in the light of these findings.


Diabetes ◽  
1994 ◽  
Vol 43 (8) ◽  
pp. 1052-1060 ◽  
Author(s):  
Marianthe Hamilton-Wessler ◽  
Richard N Bergman ◽  
Jeffrey B Halter ◽  
Richard M Watanabe ◽  
Casey M Donovan
Keyword(s):  

Author(s):  
F. Derakhshan ◽  
E. Mosca ◽  
P. Ciechanski ◽  
A. Roy ◽  
R. Wilson
Keyword(s):  

2020 ◽  
pp. 150-165

In March, 2020, the world was confronted with the COVID-19 pandemic and worldwide governmental orders to “shelter in place.” Within days of this externally imposed hardship, threatening plans for gathering in every community, behavioral optometry organized a platform for virtual education which united the vision therapy community in mutual self-education, shared over 55 countries around the globe. The following article is distilled from a 4-part series of lectures presented by the author, Dr. Samantha Slotnick, on “Making Remote Vision Therapy Valuable.” These lectures constitute a guide for acting in a supportive capacity for our patients, with attention to the reciprocal roles of a balanced, open and available visual process, and a balanced autonomic nervous system. It addresses the impact of the sympathetic response on the visual system, and offers guidance to help patients selfmodulate the state of their nervous systems, with both bottom-up and top-down direction. In particular it elucidates the role of the peripheral visual field in both stress modulation and binocular visual skill development. It offers recommendations on conducting optometric assessments through the telehealth interface, as well as providing vision therapy through a video-based portal. Through the hardship the pandemic has created, and the wonder of technology, this isolating experience may in fact serve as an opportunity to hone our single most valuable tool in our practice: Ourselves, and our ability to facilitate change for others.


2001 ◽  
Vol 281 (4) ◽  
pp. E742-E748 ◽  
Author(s):  
Yoshiharu Koyama ◽  
Robert H. Coker ◽  
Joshua C. Denny ◽  
D. Brooks Lacy ◽  
Kareem Jabbour ◽  
...  

This study was aimed at assessing the role of carotid body function in neuroendocrine and glucoregulatory responses to exercise. The carotid bodies and associated nerves were removed (CBR, n = 6) or left intact (Sham, n = 6) in anesthetized dogs >16 days before experiments, and infusion and sampling catheters were implanted. Conscious dogs were studied at rest and during 150 min of exercise. Isotopic dilution was used to assess glucose production (Ra) and disappearance (Rd). Arterial glucagon was reduced in CBR compared with Sham at rest (29 ± 3 vs. 47 ± 3 pg/ml). During exercise, glucagon increased more in Sham than in CBR (47 ± 9 vs. 15 ± 2 pg/ml). Cortisol and epinephrine levels were similar in the two groups at rest and during exercise. Basal norepinephrine was similar in CBR and Sham. During exercise, norepinephrine increased by 432 ± 124 pg/ml in Sham, but by only 201 ± 28 pg/ml in CBR. Basal arterial plasma glucose was 108 ± 2 and 105 ± 2 mg/dl in CBR and Sham, respectively. Arterial glucose dropped by 10 ± 3 mg/dl at onset of exercise in CBR ( P < 0.01) but was unchanged in Sham (decrease of 3 ± 2 mg/dl, not significant). Basal glucose kinetics were equal in Sham and CBR. At onset of exercise, Raand Rdwere transiently uncoupled in CBR (i.e., Rd> Ra) but were closely matched in Sham. In steady-state exercise, Raand Rdwere closely matched in both groups. Insulin was equal in the basal period and decreased similarly during exercise. These studies suggest that input from the carotid bodies, or receptors anatomically close to them, 1) is important in control of basal glucagon and the exercise-induced increment in glucagon, 2) is involved in the sympathetic response to exercise, and 3) participates in the non-steady-state coupling of Rato Rd, but 4) is not essential to glucoregulation during sustained exercise.


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