scholarly journals Carotid sinus nerve section and the increase in plasma cortisol during acute hypoxia in fetal sheep.

1994 ◽  
Vol 477 (1) ◽  
pp. 75-80 ◽  
Author(s):  
D A Giussani ◽  
H H McGarrigle ◽  
P J Moore ◽  
L Bennet ◽  
J A Spencer ◽  
...  
Keyword(s):  
Plasma Cortisol ◽  
Carotid Sinus ◽  
Acute Hypoxia ◽  
Carotid Sinus Nerve ◽  
Nerve Section ◽  
Fetal Sheep

Endogenous prostanoids modulate the ACTH and AVP responses to hypotension in late-gestation fetal sheep

1998 ◽  
Vol 275 (3) ◽  
pp. R735-R741 ◽  
Author(s):  
Haiyan Tong ◽  
Farahaba Lakhdir ◽  
Charles E. Wood
Keyword(s):  
Carotid Sinus ◽  
Vena Cava ◽  
Cardiovascular Responses ◽  
Late Gestation ◽  
Arterial Hypotension ◽  
Prostaglandin E ◽  
Nerve Section ◽  
Fetal Sheep ◽  
Hormonal Responses ◽  
Indomethacin Treatment

We have previously reported that prostaglandin E2 and thromboxane A2 stimulate endocrine and cardiovascular responses similar to the responses to arterial hypotension. The present experiments were designed to test the hypothesis that prostanoids are involved in the generation of responses to hypotension induced by vena cava occlusion. Fetal sheep were either intact or subjected to a prior carotid sinus denervation and bilateral vagosympathetic nerve section. Indomethacin or vehicle was injected intravenously 90 min before the start of arterial hypotension. In intact fetuses treated with phosphate buffer, ACTH increased significantly from 83 ± 39 to 3,611 ± 774 pg/ml, arginine vasopressin (AVP) increased from 3.9 ± 0.5 to 1,079 ± 549 pg/ml, and cortisol increased from 4.7 ± 0.8 to 9.5 ± 1.7 ng/ml. Indomethacin treatment significantly reduced the magnitudes of the hormonal responses. Baroreceptor and chemoreceptor denervation attenuated the ACTH and AVP responses, but these responses were not further inhibited by indomethacin. We conclude that endogenous prostanoids partially mediate the reflex hormonal and hemodynamic responses to arterial hypotension in late-gestation fetal sheep.

Effects of decortication and carotid sinus nerve section on ventilation of the rat

1981 ◽  
Vol 43 (3) ◽  
pp. 263-273 ◽  
Author(s):  
M. Maskrey ◽  
D. Megirian ◽  
S.C. Nicol
Keyword(s):  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Nerve Section

scholarly journals Essential role of hemoglobin beta-93-cysteine in posthypoxia facilitation of breathing in conscious mice

2014 ◽  
Vol 116 (10) ◽  
pp. 1290-1299 ◽  
Author(s):  
Benjamin Gaston ◽  
Walter J. May ◽  
Spencer Sullivan ◽  
Sean Yemen ◽  
Nadzeya V. Marozkina ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Essential Role ◽  
Carotid Sinus ◽  
Acute Hypoxia ◽  
Carotid Sinus Nerve ◽  
Short Term ◽  
Ventilatory Responses ◽  
Term Potentiation ◽  
Β Chain

When erythrocyte hemoglobin (Hb) is fully saturated with O2, nitric oxide (NO) covalently binds to the cysteine 93 residue of the Hb β-chain (B93-CYS), forming S-nitrosohemoglobin. Binding of NO is allosterically coupled to the O2 saturation of Hb. As saturation falls, the NO group on B93-CYS is transferred to thiols in the erythrocyte, and in the plasma, forming circulating S-nitrosothiols. Here, we studied whether the changes in ventilation during and following exposure to a hypoxic challenge were dependent on erythrocytic B93-CYS. Studies were performed in conscious mice in which native murine Hb was replaced with human Hb (hB93-CYS mice) and in mice in which murine Hb was replaced with human Hb containing an alanine rather than cysteine at position 93 on the Bchain (hB93-ALA). Both strains expressed human γ-chain Hb, likely allowing a residual element of S-nitrosothiol-dependent signaling. While resting parameters and initial hypoxic (10% O2, 90% N2) ventilatory responses were similar in hB93-CYS mice and hB93-ALA mice, the excitatory ventilatory responses (short-term potentiation) that occurred once the mice were returned to room air were markedly diminished in hB93-ALA mice. Further, short-term potentiation responses were virtually absent in mice with bilateral transection of the carotid sinus nerves. These data demonstrate that hB93-CYS plays an essential role in mediating carotid sinus nerve-dependent short-term potentiation, an important mechanism for recovery from acute hypoxia.

The Effect of Acute Hyhoxia and Carotid Sinus Nerve Section on Hypothalamic Blood Flow in the Rabbit

1975 ◽  
Vol 49 (3) ◽  
pp. 11P-12P ◽  
Author(s):  
R. A. F. Linton ◽  
Roxana Miller ◽  
I. R. Cameron
Keyword(s):  
Blood Flow ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Nerve Section

Integration of chemoreceptor stimuli by rostral brainstem respiratory areas

1975 ◽  
Vol 39 (2) ◽  
pp. 209-214 ◽  
Author(s):  
W. M. Saint John ◽  
G. C. Bond ◽  
J. N. Pasley
Keyword(s):  
Tidal Volume ◽  
Respiratory Activity ◽  
Carotid Sinus ◽  
Minute Volume ◽  
Carotid Sinus Nerve ◽  
Nerve Section ◽  
Bilateral Vagotomy ◽  
Pneumotaxic Center ◽  
Decerebrate Cats ◽  
Paco2 Level

Ventilatory regulation by brainstem sites rostral to the midpontile level was assessed in decerebrate cats by comparing the effects of punctate pneumotaxic center lesions with those of midpontile transection. After either procedure, PACO2 was significantly elevated. Moreover an equal suppression of hypercapnia-induced minute volumes and maintenance, at some PACO2 levels, of minute volume responses to hypoxia was observed. Tidal volume elevations accounted for the maintenance of hypoxia-induced minute volumes. Following pneumotaxic center lesions, hypercapnia-induced tidal volumes were higher than those exhibited subsequent to midpontile transection. After carotid sinus nerve section, PACO2 was elevated and hypoxia-induced alterations were abolished. Bilateral vagotomy resulted in apneusis. These data demonstrate that, in the brainstem area examined, only the pneumotaxic center influences the PACO2 level or set point for respiratory activity. A locus of tidal volume generation is ascribed to rostral brainstem sites outside this pneumotaxic center. Data obtained support the hypothesis of a differential brainstem integration of peripheral and central chemoreceptor afferent stimuli.

Adult carotid chemoafferent responses to hypoxia after 1, 2, and 4 wk of postnatal hyperoxia

2003 ◽  
Vol 95 (3) ◽  
pp. 946-952 ◽  
Author(s):  
G. E. Bisgard ◽  
E. B. Olson ◽  
Z.-Y. Wang ◽  
R. W. Bavis ◽  
D. D. Fuller ◽  
...  
Keyword(s):  
Phrenic Nerve ◽  
Carotid Sinus ◽  
Acute Hypoxia ◽  
Carotid Sinus Nerve ◽  
Newborn Rats ◽  
Adult Rats ◽  
Neural Input ◽  
Hyperoxic Exposure ◽  
Depressed Response

Exposing newborn rats to postnatal hyperoxia (60% O2) for 1-4 wk attenuates the ventilatory and phrenic nerve responses to acute hypoxia in adult rats. The goal of this research was to increase our understanding of the carotid chemoreceptor afferent neural input in this depressed response with different durations of postnatal hyperoxic exposure. Rats were exposed from a few days before birth to 1, 2, or 4 wk of 60% O2 and studied after 3-5 mo in normoxia. The rats were anesthetized with urethane. Whole carotid sinus nerve (CSN) responses to NaCN (40 μg/kg iv), 10 s of asphyxia and acute isocapnic hypoxia (arterial Po2 45 Torr) were determined. Mean CSN responses to stimuli after postnatal hyperoxia were reduced compared with controls. Responses in rats exposed to 1 wk of postnatal hyperoxia were less affected than those exposed to 2 and 4 wk of hyperoxia, which were equivalent to each other. These studies illustrate the importance of normoxia during the first 2 wk of life in development of carotid chemoreceptor afferent function.

Respiration in awake cats: sympathectomy and deafferentation of carotid bifurcations

1987 ◽  
Vol 62 (3) ◽  
pp. 932-940 ◽  
Author(s):  
P. C. Szlyk ◽  
D. B. Jennings
Keyword(s):  
Carotid Sinus ◽  
Minute Ventilation ◽  
Reflex Modulation ◽  
Carotid Sinus Nerve ◽  
Inspiratory Time ◽  
Nerve Section ◽  
Arterial Pco2 ◽  
Bilateral Carotid ◽  
Arterial Po2 ◽  
Awake Cats

Respiratory effects of sympathectomy of the carotid bifurcations and, in a subsequent experiment, bilateral carotid sinus nerve section were examined in six awake resting cats. In each intact and denervated state, sequential breaths were analyzed at 10-min intervals up to 80 min. Individual breath frequency (f), tidal volume (VT), and ventilation (V = f X VT) were determined. In individual cats, sympathectomy or deafferentation could cause significant increases or decreases in ventilation or no change. Thus the range of spontaneous variability in breath V as well as minute ventilation (VE), averaged for the group, were not consistently altered in the same direction by either sympathectomy or deafferentation of the carotid bifurcations. Interestingly, in most cats after both sympathectomy (5 of 6) and deafferentation (4 of 6), VT increased and f decreased relative to V. Despite this, after sinus nerve section in two cats arterial PO2 decreased and arterial PCO2 tended to increase relative to VE, suggesting possible effects of deafferentation on ventilation-perfusion balance. Sympathectomy also affected timing such that inspiratory time began to exceed 0.5 of the breath duration at a lower breath f; this effect of sympathectomy was reversed to intact values by subsequent sinus deafferentation. Thus, in eupneic awake cats, sympathetics normally suppress reflex modulation of central timing from carotid chemoreceptors and/or baroreceptors.

Cerebrovascular response to hypoxia in baroreceptor- and chemoreceptor-denervated dogs

1981 ◽  
Vol 241 (5) ◽  
pp. H724-H731 ◽  
Author(s):  
R. J. Traystman ◽  
R. S. Fitzgerald
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Nerve Section ◽  
Carotid Baroreceptor ◽  
Aortic Baroreceptors ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

Cerebral hemodynamic responses to arterial hypoxemia were studied in anesthetized paralyzed dogs that were or that had undergone carotid baroreceptor denervation, carotid chemoreceptor denervation, vagotomy, or both vagotomy and carotid sinus nerve section. Arterial O2 content was lowered from control (19.0 vol%) to 9.6 vol% by either decreasing arterial O2 tension [hypoxic hypoxemia (HH)] or increasing carboxyhemoglobin saturation[carbon-monoxide hypoxemia (COH)] at normal O2 tension. In intact animals (composite control values from all groups) HH and COH resulted in similar increases in cerebral blood flow (to 205 and 197% of control, respectively). Cerebral vascular resistance decreased more with COH than with HH (to 42 vs. 60% of control). The response from carotid baroreceptor-denervated animals and from vagotomized animals did not differ from that of the intact animals. After carotid chemoreceptor denervation and combined carotid sinus nerve section and vagotomy, both HH and COH increased cerebral blood flow to 194% of control (same increase as in intact animals, carotid baroreceptor-denervated animals, and vagotomized animals) and produced equal reductions in cerebral vascular resistance (to 34% of control). These data show that the carotid and aortic chemoreceptors are not necessary for the increase in cerebral blood flow provoked by hypoxemia and that this response is not modified by the carotid and aortic baroreceptors.

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