Analysis of factors related to vagally mediated reflex bradycardia during gastrectomy

2015 ◽  
Vol 29 (6) ◽  
pp. 874-880 ◽  
Author(s):  
Duk-Kyung Kim ◽  
Hyun Joo Ahn ◽  
Seung Won Lee ◽  
Ji Won Choi
Keyword(s):  
Reflex Bradycardia

Reflex bradycardia in facial surgery

1990 ◽  
Vol 43 (1) ◽  
pp. 128 ◽  
Author(s):  
E.R. Emmanuel ◽  
W.E. Morcos
Keyword(s):  
Facial Surgery ◽  
Reflex Bradycardia

Effects of temperature and wind on facial temperature, heart rate, and sensation

1976 ◽  
Vol 40 (2) ◽  
pp. 127-131 ◽  
Author(s):  
J. LeBlanc ◽  
B. Blais ◽  
B. Barabe ◽  
J. Cote
Keyword(s):  
Heart Rate ◽  
Skin Temperature ◽  
Subjective Evaluation ◽  
Temperature Measurements ◽  
Wind Speeds ◽  
Reflex Bradycardia ◽  
The Face ◽  
Cooling Effects ◽  
Effects Of Temperature ◽  
Cold Wind

Skin temperature measurements of the face have shown that the cheek cools faster than the nose and the nose faster than the forehead. The cooling effect of wind is maximum at wind speeds between 4.5 and 6.7 m/s. Cold winds produce significant bradycardia, which is, however, much more pronounced during the expiratory phase of respiration. A significant correlation was noted between cooling of face and the reflex bradycardia observed. Similarly, a very significant correlation was noted between drop in skin temperature and subjective evaluation of cold discomfort. Consequently, the drop in skin temperature, reflex bradycardia, and subjective evaluation are parameters which are directly affected by cold wind and can be used as adequate indicators of the degree of discomfort. When comparing the present results with the windchill index, it was found that in the zone described as “dangerously cold” the index fits well with the physiological measurements. In the zone described as “bitterly cold,” the index by comparison with actual skin temperature measurements and subjective evaluation underestimates the cooling effects of combined temperature and wind by approximately 10 degrees C.

Isoflurane Depresses Baroreflex Control of Heart Rate in Decerebrate Rats

2002 ◽  
Vol 96 (5) ◽  
pp. 1214-1222 ◽  
Author(s):  
Jong S. Lee ◽  
Don Morrow ◽  
Michael C. Andresen ◽  
Kyoung S. K. Chang
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Baroreflex Sensitivity ◽  
Baroreflex Control ◽  
Beta Adrenoceptor ◽  
Reflex Bradycardia ◽  
Reflex Tachycardia ◽  
Map Data ◽  
Regulatory Sites

Background Isoflurane inhibits baroreflex control of heart rate (HR) by poorly understood mechanisms. The authors examined whether suprapontine central nervous system cardiovascular regulatory sites are required for anesthetic depression. Methods The effects of isoflurane (1 and 2 rat minimum alveolar concentration [MAC]) on the baroreflex control of HR were determined in sham intact and midcollicular-transected decerebrate rats. Intravenous phenylephrine (0.2-12 microg/kg) and nitroprusside (1-60 microg/kg) were used to measure HR responses to peak changes in mean arterial pressure (MAP). Sigmoidal logistic curve fits to HR-MAP data assessed baroreflex sensitivity (HR/MAP), HR range, lower and upper HR plateau, and MAP at half the HR range (BP50). Four groups (two brain intact and two decerebrate) were studied before, during, and after isoflurane. To assess sympathetic and vagal contributions to HR baroreflex, beta-adrenoceptor (1 mg/kg atenolol) or muscarinic (0.5 mg/kg methyl atropine) antagonists were administered systemically. Results Decerebration did not alter resting MAP and HR or baroreflex parameters. Isoflurane depressed baroreflex slope and HR range in brain-intact and decerebrate rats. In both groups, 1 MAC reduced HR range by depressing peak reflex tachycardia. Maximal reflex bradycardia during increases in blood pressure was relatively preserved. Atenolol during 1 MAC did not alter maximum reflex tachycardia. In contrast, atropine during 1 MAC fully blocked reflex bradycardia. Therefore, 1 MAC predominantly depresses sympathetic components of HR baroreflex. Isoflurane at 2 MAC depressed both HR plateaus and decreased BP50 in both groups. Conclusions Isoflurane depresses HR baroreflex control by actions that do not require suprapontine central nervous system sites. Isoflurane actions seem to inhibit HR baroreflex primarily by the sympathetic nervous system.

Baroreflex modulation by angiotensins at the rat rostral and caudal ventrolateral medulla

2006 ◽  
Vol 290 (4) ◽  
pp. R1027-R1034 ◽  
Author(s):  
Andréia C. Alzamora ◽  
Robson A. S. Santos ◽  
Maria J. Campagnole-Santos
Keyword(s):  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Opposite Effect ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Differential Modulation ◽  
Baroreflex Control ◽  
Caudal Ventrolateral Medulla ◽  
Angiotensin Peptides ◽  
Reflex Bradycardia

We determined the effect of microinjection of ANG-(1–7) and ANG II into two key regions of the medulla that control the circulation [rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively)] on baroreflex control of heart rate (HR) in anesthetized rats. Reflex bradycardia and tachycardia were induced by increases and decreases in mean arterial pressure produced by intravenous phenylephrine and sodium nitroprusside, respectively. The pressor effects of ANG-(1–7) and ANG II (25 pmol) after RVLM microinjection (11 ± 0.8 and 10 ± 2 mmHg, respectively) were not accompanied by consistent changes in HR. In addition, RVLM microinjection of these angiotensin peptides did not alter the bradycardic or tachycardic component of the baroreflex. CVLM microinjections of ANG-(1–7) and ANG II produced hypotension (−11 ± 1.5 and −11 ± 1.9 mmHg, respectively) that was similarly not accompanied by significant changes in HR. However, CVLM microinjections of angiotensins induced differential changes in the baroreflex control of HR. ANG-(1–7) attenuated the baroreflex bradycardia (0.26 ± 0.06 ms/mmHg vs. 0.42 ± 0.08 ms/mmHg before treatment) and facilitated the baroreflex tachycardia (0.86 ± 0.19 ms/mmHg vs. 0.42 ± 0.10 ms/mmHg before treatment); ANG II produced the opposite effect, attenuating baroreflex tachycardia (0.09 ± 0.06 ms/mmHg vs. 0.31 ± 0.07 ms/mmHg before treatment) and facilitating the baroreflex bradycardia (0.67 ± 0.16 ms/mmHg vs. 0.41 ± 0.05 ms/mmHg before treatment). The modulatory effect of ANG II and ANG-(1–7) on baroreflex sensitivity was completely abolished by peripheral administration of methylatropine. These results suggest that ANG II and ANG-(1–7) at the CVLM produce a differential modulation of the baroreflex control of HR, probably through distinct effects on the parasympathetic drive to the heart.

The Effects of Branchial Denervation and Pseudobranch Ablation on Cardioventilatory Control in an Air-Breathing Fish

1991 ◽  
Vol 161 (1) ◽  
pp. 347-365 ◽  
Author(s):  
DAVID J. McKENZIE ◽  
MARK L. BURLESON ◽  
DAVID J. RANDALL
Keyword(s):  
Cardiovascular Responses ◽  
Sodium Cyanide ◽  
Air Breathing ◽  
Ventilatory Responses ◽  
Reflex Bradycardia ◽  
Afferent Information ◽  
Gill Ventilation ◽  
Air Ventilation ◽  
Amia Calva

Present address and address for reprint requests: Istituto di Scienze Farmacologiche, via Balzaretti 9, Università di Milano, Milano 20133, Italy. The role of sensory afferent information from the gills of Amia calva in cardiovascular and ventilatory control was investigated by bilateral branchial denervation and pseudobranch ablation. Aquatic hypoxia or 1 mg of sodium cyanide (NaCN) in the water flowing over the gills stimulated bradycardia, and gill and air ventilation in sham-operated fish. Sodium cyanide, noradrenaline (NA) and adrenaline (A) infusion into the dorsal aorta increased gill ventilation, and NA and A infusion also stimulated tachycardia and an increase in blood pressure. Following denervation and pseudobranch ablation, O2 consumption (V·OO2), airbreathing frequency (fAB) and arterial O2 tension (PaOO2) declined, and circulating NA levels increased, as compared with sham-operated fish. Cardiovascular and air-breathing responses to hypoxia were abolished and gill ventilatory responses attenuated. All ventilatory and cardiovascular responses to NaCN were abolished and gill ventilatory responses to NA and A were attenuated in animals following denervation and pseudobranch ablation. These results demonstrate that O2-sensitive chemoreceptors in the gills and pseudobranch control reflex bradycardia and air-breathing responses in Amia, but that gill ventilatory responses to hypoxia, NA and A are partially mediated by extrabranchial mechanisms. Plasma NA levels increased during hypoxia in shamoperated and denervated animals, indicating that circulating NA may have mediated gill ventilatory responses in denervated animals.

scholarly journals K+ channel blockade in the NTS alters efficacy of two cardiorespiratory reflexes in vivo

1998 ◽  
Vol 274 (3) ◽  
pp. R677-R685 ◽  
Author(s):  
James W. Butcher ◽  
Julian F. R. Paton
Keyword(s):  
Potassium Channel ◽  
Neuronal Excitability ◽  
Baroreceptor Reflex ◽  
Right Atrial ◽  
K Channel ◽  
Reflex Bradycardia ◽  
Potassium Conductances ◽  
Voltage Dependent

We investigated the role of potassium conductances in the nucleus of the solitary tract (NTS) in determining the efficacy of the baroreceptor and cardiopulmonary reflexes in anesthetized rats. The baroreceptor reflex was elicited with an intravenous injection of phenylephrine to evoke a reflex bradycardia, and the cardiopulmonary reflex was evoked with a right atrial injection of phenylbiguanide. Microinjection of two Ca-dependent potassium channel antagonists (apamin and charybdotoxin) into the NTS potentiated the baroreceptor reflex bradycardia. This may reflect the increased neuronal excitability observed previously in vitro with these blockers. In contrast, the Ca-dependent potassium channel antagonists attenuated the cardiopulmonary reflex, whereas voltage-dependent potassium channel antagonists (4-aminopyridine and dendrotoxin) attenuated both the baro- and cardiopulmonary reflexes when microinjected into the NTS. The possibility that the reflex attenuation observed indicates a predominant distribution of certain potassium channels on γ-aminobutyric acid interneurons is discussed.

Mechanisms of pressor and bradycardic responses to L-glutamate microinjected into the NTS of conscious rats

1994 ◽  
Vol 266 (3) ◽  
pp. R730-R738 ◽  
Author(s):  
E. Colombari ◽  
L. G. Bonagamba ◽  
B. H. Machado
Keyword(s):  
Amino Acid ◽  
Kynurenic Acid ◽  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Excitatory Amino Acid Receptors ◽  
Amino Acid Receptors ◽  
Conscious Rats ◽  
Reflex Bradycardia ◽  
Autonomic Pathways ◽  
Related Pattern

Microinjection of increasing doses of L-glutamate (L-Glu, 0.03-5.0 nmol/100 nl) into the nucleus tractus solitarii (NTS) produced a dose-related pressor and bradycardic response. Prazosin virtually abolished the pressor response but produced no changes in the bradycardic response to L-Glu, indicating that bradycardia is not reflex in origin. The bradycardic response was blocked by atropine. In three different groups of rats, excitatory amino acid receptors in the NTS were blocked by increasing doses of kynurenic acid (0.5, 2.0, and 10.0 nmol/100 nl) and the pressor and bradycardic responses to L-Glu (1 nmol/100 nl) were reduced in a dose-related pattern. Reflex bradycardia induced by an increase in pressure caused by phenylephrine (iv) was also blocked by kynurenic acid. These data show that microinjection of L-Glu into the NTS of conscious rats produced pressor and bradycardic responses, which are due to the activation of two independent autonomic pathways. The data also indicate that the activation of both pathways is mediated by excitatory amino acid receptors. Considering that reflex bradycardia was also blocked by kynurenic acid, we suggest that L-Glu and excitatory amino acid receptors are part of the parasympathetic limb of the baroreceptor reflex. The pressor response to L-Glu is also mediated by excitatory amino acid receptors, but its physiological meaning is still unclear.

ANP, BNP, and CNP enhance bradycardic responses to cardiopulmonary chemoreceptor activation in conscious sheep

2001 ◽  
Vol 280 (1) ◽  
pp. R282-R288 ◽  
Author(s):  
Colleen J. Thomas ◽  
Clive N. May ◽  
Atul D. Sharma ◽  
Robyn L. Woods
Keyword(s):  
Heart Rate ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Normal Saline ◽  
Jugular Vein ◽  
Resting Heart Rate ◽  
Reflex Bradycardia ◽  
Cardiac Slowing ◽  
Vagal Reflex ◽  
Conscious Sheep

We demonstrated previously that atrial natriuretic peptide (ANP) enhances reflex bradycardia to intravenous serotonin [5-hydroxytryptamine (5-HT)] (von Bezold-Jarisch reflex) in rats. To determine whether 1) ANP affects this cardiopulmonary vagal reflex in another species and 2) B-type (BNP) and C-type (CNP) natriuretic peptides share with ANP the ability to modulate this reflex, we used intravenous phenylbiguanide (PBG), a 5-HT3agonist, as the stimulus to evoke a von Bezold-Jarisch reflex (dose-related, reproducible bradycardia) in conscious adult sheep ( n = 5). Three doses of PBG (13 ± 3, 20 ± 3, and 31 ± 4 μg/kg) injected into the jugular vein caused reflex cardiac slowing of −7 ± 1, −15 ± 2, and −36 ± 3 beats/min, respectively, under control conditions. These doses of PBG were repeated during infusions of ANP, BNP, or CNP (10 pmol · kg−1 · min−1 iv), or vehicle (normal saline). Each of the natriuretic peptides significantly ( P < 0.05) enhanced the sensitivity of bradycardic responses to PBG by 94 ± 8% (ANP), 142 ± 55% (BNP), and 61 ± 16% (CNP). Thus not only did ANP sensitize cardiopulmonary chemoreceptor activation in a species with resting heart rate close to that in humans, but BNP and CNP also enhanced von Bezold-Jarisch reflex activity in conscious sheep.

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