scholarly journals Trigeminocardiac reflex during surgery in the cerebellopontine angle

1998 ◽  
Vol 5 (3) ◽  
pp. E9 ◽  
Author(s):  
Bernhard Schall ◽  
Rudolf Probst ◽  
Stephan Strebel ◽  
Peter Fuhr ◽  
Otmar Gratzl
Keyword(s):  
Blood Pressure ◽  
Trigeminal Nerve ◽  
Cerebellopontine Angle ◽  
Experimental Studies ◽  
Ocular Surgery ◽  
Trigeminocardiac Reflex ◽  
Arterial Blood ◽  
Nerve System ◽  
Central Stimulation ◽  
Stimulation Of

In different experimental studies authors have analyzed the autonomic responses elicited by the electrical, mechanical, or chemical stimulation of the trigeminal nerve system. The trigeminocardiac reflex (TCR) is a well-recognized phenomenon that consists of bradycardia, arterial hypotension, apnea, and gastric hypermotility. It occurs during ocular surgery and during other manipulations in and around the orbit. Thus far, it has not been shown that central stimulation of the trigeminal nerve can also cause this reflex. The TCR was defined as clinical hypotension with a drop in mean arterial blood pressure (MABP) of more than 20% and bradycardia lower than 60 beats/minute. Pre-, intra-, and postoperative heart rate (HR) and blood pressure were reviewed retrospectively in 125 patients who underwent surgery for tumors of the cerebellopontine angle (CPA), and they were divided into a TCR group and a non-TCR group. Of the 125 patients, 14 (11%) showed evidence of TCR during dissection of the tumor near the trigeminal nerve at the brainstem. Their HR fell 38% and their MABP fell 48% during operative procedures as compared with preoperative levels. After cessation of manipulation, the HR and the MABP returned to preoperative levels. Risk factors for the occurrence of TCR were compared with results from the literature. The authors' results show the possibility of occurrence of a TCR during manipulation of the central part of the trigeminal nerve when performing surgery in the CPA.

Trigeminocardiac reflex during surgery in the cerebellopontine angle

1999 ◽  
Vol 90 (2) ◽  
pp. 215-220 ◽  
Author(s):  
Bernhard Schaller ◽  
Rudolf Probst ◽  
Stephan Strebel ◽  
Otmar Gratzl
Keyword(s):  
Trigeminal Nerve ◽  
Cerebellopontine Angle ◽  
Experimental Studies ◽  
Ocular Surgery ◽  
Content Type ◽  
Trigeminocardiac Reflex ◽  
Arterial Blood ◽  
Nerve System ◽  
Fine Print ◽  
Stimulation Of

Object. In different experimental studies authors have analyzed the autonomic responses elicited by the electrical, mechanical, or chemical stimulation of the trigeminal nerve system. The trigeminocardiac reflex (TCR) is a well-recognized phenomenon that consists of bradycardia, arterial hypotension, apnea, and gastric hypermotility. It occurs during ocular surgery and during other manipulations in and around the orbit. Thus far, it has not been shown that central stimulation of the trigeminal nerve can also cause this reflex.Methods. The TCR was defined as clinical hypotension with a drop in mean arterial blood pressure (MABP) of more than 20% and bradycardia lower than 60 beats/minute. Pre-, intra-, and postoperative heart rate (HR) and MABP were reviewed retrospectively in 125 patients who underwent surgery for tumors of the cerebellopontine angle (CPA), and they were divided into two groups on the basis of the occurrence of the TCR during surgery. Of the 125 patients, 14 (11%) showed evidence of the TCR during dissection of the tumor near the trigeminal nerve at the brainstem. Their HRs fell 38% and their MABPs fell 48% during operative procedures as compared with preoperative levels. After cessation of manipulation, the HRs and the MABPs returned to preoperative levels. Risk factors for the occurrence of the TCR were compared with results from the literature.Conclusions. The authors' results show the possibility of occurrence of a TCR during manipulation of the central part of the trigeminal nerve when performing surgery in the CPA.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

scholarly journals Blood pressure changes alter tracheobronchial cough: computational model of the respiratory-cough network and in vivo experiments in anesthetized cats

2011 ◽  
Vol 111 (3) ◽  
pp. 861-873 ◽  
Author(s):  
Ivan Poliacek ◽  
Kendall F. Morris ◽  
Bruce G. Lindsey ◽  
Lauren S. Segers ◽  
Melanie J. Rose ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Motor Pattern ◽  
Esophageal Pressure ◽  
Respiratory Neurons ◽  
Cycle Duration ◽  
In Vivo Experiments ◽  
Arterial Blood ◽  
Posterior Cricoarytenoid ◽  
Stimulation Of

We tested the hypothesis, motivated in part by a coordinated computational cough network model, that alterations of mean systemic arterial blood pressure (BP) influence the excitability and motor pattern of cough. Model simulations predicted suppression of coughing by stimulation of arterial baroreceptors. In vivo experiments were conducted on anesthetized spontaneously breathing cats. Cough was elicited by mechanical stimulation of the intrathoracic airways. Electromyograms (EMG) of inspiratory parasternal, expiratory abdominal, laryngeal posterior cricoarytenoid (PCA), and thyroarytenoid muscles along with esophageal pressure (EP) and BP were recorded. Transiently elevated BP significantly reduced cough number, cough-related inspiratory, and expiratory amplitudes of EP, peak parasternal and abdominal EMG, and maximum of PCA EMG during the expulsive phase of cough, and prolonged the cough inspiratory and expiratory phases as well as cough cycle duration compared with control coughs. Latencies from the beginning of stimulation to the onset of cough-related diaphragm and abdominal activities were increased. Increases in BP also elicited bradycardia and isocapnic bradypnea. Reductions in BP increased cough number; elevated inspiratory EP amplitude and parasternal, abdominal, and inspiratory PCA EMG amplitudes; decreased total cough cycle duration; shortened the durations of the cough expiratory phase and cough-related abdominal discharge; and shortened cough latency compared with control coughs. Reduced BP also produced tachycardia, tachypnea, and hypocapnic hyperventilation. These effects of BP on coughing likely originate from interactions between barosensitive and respiratory brainstem neuronal networks, particularly by modulation of respiratory neurons within multiple respiration/cough-related brainstem areas by baroreceptor input.

Mechanisms of action of sodium cromoglycate

1985 ◽  
Vol 63 (6) ◽  
pp. 760-765 ◽  
Author(s):  
D. F. Biggs ◽  
V. Goel
Keyword(s):  
Blood Pressure ◽  
Sodium Cromoglycate ◽  
Arterial Blood Pressure ◽  
Vagal Stimulation ◽  
Cardiovascular Responses ◽  
Bilateral Stimulation ◽  
Vagus Nerves ◽  
Arterial Blood ◽  
Efferent Pathways ◽  
Stimulation Of

The effects of sodium cromoglycate (SCG) on cardiovascular and pulmonary responses to phenylbiguanide, capsaicin, and vagal stimulation were studied in anesthetized guinea pigs. Phenylbiguanide had no bronchospastic activity but induced reflex changes in arterial blood pressure which were reduced or abolished by SCG. Capsaicin induced nonreflex bronchospasm, and decreases in arterial blood pressure that were unaffected by SCG. Sodium cromoglycate, given before or after atropine, had no effect on the bronchospasm and cardiovascular responses to unilateral or bilateral stimulation of the vagus nerves. We conclude that SCG may influence both the afferent and efferent pathways of responses to drugs.

Beta2-mediated hypotension and myocardial injury

1982 ◽  
Vol 60 (8) ◽  
pp. 1144-1148 ◽  
Author(s):  
Alison Brown-Lukacsko ◽  
Peter Lukacsko
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Myocardial Injury ◽  
Elevated Serum ◽  
Blocking Agent ◽  
Arterial Blood ◽  
Ganglionic Blocking ◽  
Elevated Heart Rate ◽  
Stimulation Of

This study was designed to investigate the importance of beta2 receptor mediated hypotension in the pathogenesis of myocardial injury. The effect of isoproterenol and the putative beta2 agonist albuterol on arterial blood pressure, heart rate, the myocardial content of ATP and cAMP, and the serum content of MB-CPK was examined in conscious rats. Isoproterenol (5.25 mg/kg, s.c.) and albuterol (45 mg/kg, s.c.) lowered blood pressure and elevated heart rate to the same extent. Also, both agonists increased the myocardial content of cAMP, decreased the myocardial content of ATP, and elevated serum MB-CPK. The beta1 antagonist practolol, but not the ganglionic blocking agent chlorisondamine, attenuated the elevation in heart rate to albuterol without reducing its effect on blood pressure. Practolol, but not chlorisondamine, abolished the effects of albuterol on cAMP, ATP, and MB-CPK. These data suggest that the myocardial injury which is associated with an increased heart rate and changes in cAMP, ATP, and MB-CPK following the administration of albuterol is not the result of beta2-mediated hypotension, but is due to stimulation of myocardial beta1 receptors.

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