Analysis of the changes in tone of the vagal innervation center of the heart during hypoxic and anemic hypoxia in the adult dog

1965 ◽  
Vol 59 (4) ◽  
pp. 368-370
Author(s):  
R. G. Teregulov
Keyword(s):  
Vagal Innervation ◽  
Innervation Center

Asymmetric Dopaminergic Dysfunction in Brain-First versus Body-First Parkinson’s Disease Subtypes

2021 ◽  
pp. 1-11
Author(s):  
Karoline Knudsen ◽  
Tatyana D. Fedorova ◽  
Jacob Horsager ◽  
Katrine B. Andersen ◽  
Casper Skjærbæk ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
De Novo ◽  
Specific Binding ◽  
Asymmetry Index ◽  
The Body ◽  
Specific Binding Ratio ◽  
Dat Spect ◽  
Vagal Innervation ◽  
Nigrostriatal Degeneration

Background: We have hypothesized that Parkinson’s disease (PD) comprises two subtypes. Brain-first, where pathogenic α-synuclein initially forms unilaterally in one hemisphere leading to asymmetric nigrostriatal degeneration, and body-first with initial enteric pathology, which spreads through overlapping vagal innervation leading to more symmetric brainstem involvement and hence more symmetric nigrostriatal degeneration. Isolated REM sleep behaviour disorder has been identified as a strong marker of the body-first type. Objective: To analyse striatal asymmetry in [18F]FDOPA PET and [123I]FP-CIT DaT SPECT data from iRBD patients, de novo PD patients with RBD (PD +RBD) and de novo PD patients without RBD (PD - RBD). These groups were defined as prodromal body-first, de novo body-first, and de novo brain-first, respectively. Methods: We included [18F]FDOPA PET scans from 21 iRBD patients, 11 de novo PD +RBD, 22 de novo PD - RBD, and 18 controls subjects. Also, [123I]FP-CIT DaT SPECT data from iRBD and de novo PD patients with unknown RBD status from the PPPMI dataset was analysed. Lowest putamen specific binding ratio and putamen asymmetry index (AI) was defined. Results: Nigrostriatal degeneration was significantly more symmetric in patients with RBD versus patients without RBD or with unknown RBD status in both FDOPA (p = 0.001) and DaT SPECT (p = 0.001) datasets. Conclusion: iRBD subjects and de novo PD +RBD patients present with significantly more symmetric nigrostriatal dopaminergic degeneration compared to de novo PD - RBD patients. The results support the hypothesis that body-first PD is characterized by more symmetric distribution most likely due to more symmetric propagation of pathogenic α-synuclein compared to brain-first PD.

Efferent vagal innervation of canine ventricle

1985 ◽  
Vol 248 (1) ◽  
pp. H89-H97 ◽  
Author(s):  
N. Takahashi ◽  
M. J. Barber ◽  
D. P. Zipes
Keyword(s):  
Coronary Artery ◽  
Vagal Stimulation ◽  
Left Ventricular ◽  
Constant Infusion ◽  
Epicardial Surface ◽  
Before And After ◽  
Vagal Innervation ◽  
The Subject ◽  
Infusion Of Norepinephrine ◽  
The Right

The route efferent vagal fibers travel to reach the left ventricle is not clear and was the subject of this investigation. We measured left ventricular and septal effective refractory period (ERP) changes during vagal stimulation and a constant infusion of norepinephrine, before and after phenol was applied at selected sites of the heart to interrupt efferent vagal fibers that may be traveling in that area. Phenol applied to the atrioventricular (AV) groove between the origin of the right coronary artery anteriorly to the posterior descending branch of the circumflex coronary artery completely eliminated vagal-induced prolongation of ERP in the anterior and posterior left ventricular free wall and reduced, but did not eliminate, ERP prolongation in the septum. A large (3-cm radius) epicardial circle of phenol prevented vagal-induced ERP prolongation within the circle in all dogs, while a small (1-cm radius) epicardial circle of phenol failed to prevent vagal-induced ERP changes within the circle in any dog. An intermediate (2-cm radius) circle eliminated vagal effects on ERP in 13 of 18 dogs. Arcs of phenol, to duplicate the upper portion of the circle, applied sequentially from apex to base eliminated efferent vagal effects only when painted near or at the AV groove. We conclude that the majority of efferent vagal fibers enroute to innervate the anterior and posterior left ventricular epicardium cross the AV groove within 0.25-0.5 mm (depth of phenol destruction) of the epicardial surface.(ABSTRACT TRUNCATED AT 250 WORDS)

Pancreatic polypeptide responses to isoglycemic oral and intravenous glucose in humans with and without intact vagal innervation

Peptides ◽  
2015 ◽  
Vol 71 ◽  
pp. 229-231 ◽  
Author(s):  
Simon Veedfald ◽  
Astrid Plamboeck ◽  
Bolette Hartmann ◽  
Lars B. Svendsen ◽  
Tina Vilsbøll ◽  
...  
Keyword(s):  
Pancreatic Polypeptide ◽  
Intravenous Glucose ◽  
Vagal Innervation

Functional anatomy of the vagal innervation of the cervical trachea of the dog

2000 ◽  
Vol 89 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Robert L. Coon ◽  
Patrick J. Mueller ◽  
Philip S. Clifford
Keyword(s):  
Smooth Muscle ◽  
Vagus Nerve ◽  
Neural Control ◽  
Muscle Tone ◽  
Cuff Pressure ◽  
Vagal Innervation ◽  
Cervical Trachea ◽  
The Right ◽  
Left Vagus ◽  
Stimulation Of

The canine cervical trachea has been used for numerous studies regarding the neural control of tracheal smooth muscle. The purpose of the present study was to determine whether there is lateral dominance by either the left or right vagal innervation of the canine cervical trachea. In anesthetized dogs, pressure in the cuff of the endotracheal tube was used as an index of smooth muscle tone in the trachea. After establishment of tracheal tone, as indicated by increased cuff pressure, either the right or left vagus nerve was sectioned followed by section of the contralateral vagus. Sectioning the right vagus first resulted in total loss of tone in the cervical trachea, whereas sectioning the left vagus first produced either a partial or no decrease in tracheal tone. After bilateral section of the vagi, cuff pressure was recorded during electrical stimulation of the rostral end of the right or left vagus. At the maximum current strength used, stimulation of the left vagus produced tracheal constriction that averaged 28.5% of the response to stimulation of the right vagus (9.0 ± 1.8 and 31.6 ± 2.5 mmHg, respectively). In conclusion, the musculature of cervical trachea in the dog appears to be predominantly controlled by vagal efferents in the right vagus nerve.

Compensatory recovery of parasympathetic control of heart rate after unilateral vagotomy in rabbits

1992 ◽  
Vol 262 (4) ◽  
pp. H1122-H1127 ◽  
Author(s):  
D. D. Lund ◽  
G. A. Davey ◽  
A. R. Subieta ◽  
B. J. Pardini
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Vagal Stimulation ◽  
Acetylcholinesterase Inhibition ◽  
Baroreflex Control ◽  
Recovery Mechanism ◽  
Vagal Innervation ◽  
Increased Sensitivity ◽  
Parasympathetic Control

Compensatory recovery by the intact vagal innervation after unilateral vagotomy was investigated by measuring parasympathetic-mediated control of heart rate in beta-adrenergic-blocked rabbits. Direct contralateral vagal nerve stimulation produced greater bradycardia in anesthetized rabbits with chronic vagotomy compared with acutely vagotomized controls. Vagal stimulation during acetylcholinesterase inhibition by physostigmine and direct neuroeffector stimulation by methacholine indicated that a change in metabolism of the neurotransmitter or an increased sensitivity of the tissue to acetylcholine were not responsible for augmentation of vagal responses. Baroreflex control of heart rate in response to an increase in arterial pressure was also tested in urethan-anesthetized rabbits. There was a significant reduction in the prolongation of the R-R interval during baroreflex activation acutely after midcervical vagotomy. These values were subsequently above control levels in rabbits 28 days after vagotomy. In conscious rabbits, the decrease in baroreflex control of heart rate progressively recovered to control levels within 6 days. These results suggest that the recovery mechanism after unilateral vagotomy may be related to peripheral and central compensatory changes in the intact contralateral vagus nerve.

The Role of Vagal Innervation in Adaptive Cytoprotection

1995 ◽  
pp. 191-200
Author(s):  
Thomas A. Miller ◽  
Gregory S. Smith ◽  
Michael S. Tornwall ◽  
Rafael A. Lopez ◽  
Julia M. Henagan ◽  
...  
Keyword(s):  
Adaptive Cytoprotection ◽  
Vagal Innervation

Prospective comparison of Congo red and sham feeding testing to determine vagal innervation of the stomach

1992 ◽  
Vol 163 (5) ◽  
pp. 533-536 ◽  
Author(s):  
Richard C. Thirlby ◽  
David J. Patterson ◽  
Richard A. Kozarek
Keyword(s):  
Congo Red ◽  
Sham Feeding ◽  
Prospective Comparison ◽  
Vagal Innervation

Pancreatic polypeptide responses to isoglycemic oral and intravenous glucose in humans with and without intact vagal innervation

Neuropeptides ◽  
2016 ◽  
Vol 55 ◽  
pp. 25
Author(s):  
Simon Veedfald ◽  
Astrid Plamboeck ◽  
Bolette Hartmann ◽  
Lars Bo Svendsen ◽  
Tina Vilsbøll ◽  
...  
Keyword(s):  
Pancreatic Polypeptide ◽  
Intravenous Glucose ◽  
Vagal Innervation

The effect of ATP-sensitive potassium channel modulation on heart rate in isolated muskrat and guinea pig hearts.

1994 ◽  
Vol 197 (1) ◽  
pp. 101-118
Author(s):  
D R Streeby ◽  
T A McKean
Keyword(s):  
Heart Rate ◽  
Guinea Pig ◽  
Potassium Channel ◽  
Extracellular Potassium ◽  
Guinea Pig Heart ◽  
Channel Activation ◽  
Extracellular Potassium Concentration ◽  
Local Factors ◽  
Hypoxic Conditions ◽  
Vagal Innervation

Muskrats (Ondontra zibethicus) are common freshwater diving mammals exhibiting a bradycardia with both forced and voluntary diving. This bradycardia is mediated by vagal innervation; however, if hypoxia is present there may be local factors that also decrease heart rate. Some of these local factors may include ATP-sensitive potassium channel activation and extracellular accumulation of potassium ions, hydrogen ions and lactate. The purpose of this study was to investigate the role of these factors in the isolated perfused hearts of muskrats and of a non-diving mammal, the guinea pig. Although lactate and proton administration reduced heart rate in isolated muskrat and guinea pig hearts, there was no difference in the response to lactate and proton infusion between the two species. Muskrat hearts were more sensitive to the heart-rate-lowering effects of exogenously applied potassium than were guinea pig hearts. Early increases in extracellular potassium concentration during hypoxia are thought to be mediated by the ATP-sensitive potassium channel. Activation of these channels under normoxic conditions had a mildly negative chronotropic effect in both species; however, activation of these channels with Lemakalim under hypoxic conditions caused the guinea pig heart to respond with an augmented bradycardia similar to that seen in the hypoxic muskrat heart in the absence of drugs. Inhibition of these channels by glibenclamide during hypoxia was partially successful in blocking the bradycardia in guinea pig hearts, but inhibition of the same channels in hypoxic muskrat hearts had a damaging effect as two of five hearts went into contracture during the hypoxia. Thus, although ATP-sensitive potassium channels appear to have a major role in the bradycardia of hypoxia in guinea pigs, the failure to prevent the bradycardia by inhibition of these channels in muskrat hearts suggests that multiple factors are involved in the hypoxia-induced bradycardia in this species.

Effect of long-term parenteral feeding on gastric secretion in dogs.

1977 ◽  
Vol 232 (1) ◽  
pp. E39
Author(s):  
P J Thor ◽  
E M Copeland ◽  
S J Dudrick ◽  
L R Johnson
Keyword(s):  
Food Intake ◽  
Serum Gastrin ◽  
Oral Intake ◽  
Normal Diet ◽  
Parenteral Feeding ◽  
Gastric Fistula ◽  
Vagal Innervation ◽  
Intravenous Alimentation ◽  
Oral Diet

Three dogs were surgically prepared with gastric fistulas and Heidenhain (vagally denervated) pouches. Acid and pepsin responses to pentagastrin and food were determined before, at the end of a 1-mo period of total parenteral feeding, and 1 mo after the resumption of a normal oral diet. Acid and pepsin output from the denervated pouch in response to pentagastrin and food decreased significantly (P less than 0.001) after parenteral feeding and returned to control levels after the dogs resumed a normal diet. Secretory outputs from the gastric fistula in response to pentagastrin remained unchanged throughout the experiment. Basal serum gastrin levels decreased 50% during the period of intravenous feeding and returned to levels approximately twice the control levels following resumption of normal oral food intake. Serum gastrin responses to a meal also decreased during intravenous alimentation and returned to higher than normal levels following a 1-mo period of oral intake. These studies indicate that the absence of oral food intake in the dog does not result in decreased acid secretion from the innervated stomach. Vagal innervation in some way is responsible for the preservation of normal secretion during the absence of food from the gastrointestinal tract of the dog.

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