Peripheral chemoreceptors respond to hypoxia in pontine-lesioned fetal lambs in utero

1993 ◽  
Vol 75 (3) ◽  
pp. 1027-1034 ◽  
Author(s):  
B. M. Johnston ◽  
P. D. Gluckman
Keyword(s):  
Acute Hypoxia ◽  
In Utero ◽  
Fetal Life ◽  
Peripheral Chemoreceptors ◽  
Fetal Breathing Movements ◽  
Pontine Lesion ◽  
Regulation Of Breathing ◽  
Peripheral Arterial ◽  
Stimulation Of

Acute hypoxia inhibits, rather than stimulates, fetal breathing movements (FBM), but there has been controversy as to the activity and role of the peripheral arterial chemoreceptors in the regulation of breathing movements in the unanesthetized fetus in utero. However, after midcollicular brain stem transection or lateral pontine lesion, hypoxia causes FBM to become continuous and stimulated in rate and depth. To determine whether this stimulatory response involves peripheral chemoreceptors, we used a two-stage approach to examine the response to hypoxia after peripheral chemodenervation in lateral pontine-lesioned fetal lambs. The lateral pons was lesioned at 119–121 days, and the response to hypoxia was tested in the unanesthetized fetus 4 days afterward. Fourteen fetuses in which hypoxia stimulated FBM underwent either peripheral chemodenervation or sham denervation in a second operation. Hypoxia had no effect when the fetus was tested 4–5 days after peripheral chemodenervation, and the basal incidence of FBM was significantly lower. The stimulatory response was unchanged by sham denervation. We conclude that the peripheral chemoreceptors are active in fetal life and that they mediate the stimulation of FBM seen in response to hypoxia after removal of the lateral pontine inhibition. In addition, after pontine lesion there is evidence of tonic chemoreceptor-mediated influences on FBM, which are normally overriden in the intact fetus.

Denervation of peripheral chemoreceptors decreases breathing movements in fetal sheep

1985 ◽  
Vol 59 (2) ◽  
pp. 575-579 ◽  
Author(s):  
D. T. Murai ◽  
C. C. Lee ◽  
L. D. Wallen ◽  
J. A. Kitterman
Keyword(s):  
Low Voltage ◽  
Fetal Life ◽  
Fetal Sheep ◽  
Peripheral Chemoreceptors ◽  
Arterial Blood ◽  
Several Variables ◽  
Arterial Ph ◽  
Fetal Breathing ◽  
Fetal Breathing Movements

The role of the peripheral chemoreceptors in the control of fetal breathing movements has not been fully defined. To determine whether denervation of the peripheral chemoreceptors affects fetal breathing movements, we studied 14 chronically catheterized fetal sheep from 120 to 138 days of gestation. In seven fetuses the chemoreceptors were denervated by bilateral section of the vagus and carotid sinus nerves; in seven others, sham operations were performed. We compared several variables during two study periods: 0–5 and 6–13 days after operation. In the denervated fetuses there were significant decreases in the incidence and amplitude of fetal breathing movements during both study periods. There were no differences between the two groups in incidence of low-voltage electrocortical activity, arterial pH and blood gas tensions, fetal heart rate, mean arterial blood pressure, or duration of survival after operation or birth weight. We conclude that denervation of the peripheral chemoreceptors decreases fetal breathing movements. These results indicate that the peripheral chemoreceptors are active during fetal life and participate in the control of fetal breathing movements.

Role of central and peripheral chemoreceptors in diving responses of ducks

1982 ◽  
Vol 243 (5) ◽  
pp. R537-R545 ◽  
Author(s):  
D. R. Jones ◽  
W. K. Milsom ◽  
G. R. Gabbott
Keyword(s):  
Carotid Body ◽  
Significant Contribution ◽  
Cardiovascular Responses ◽  
Peripheral Circulation ◽  
Blood Gas ◽  
Peripheral Chemoreceptors ◽  
Central Chemoreceptors ◽  
The Right ◽  
Stimulation Of

Using techniques of vascular isolation and subsequent perfusion we have investigated the effects of altering blood gas tensions, in the cerebral and carotid body circulations, on some cardiovascular responses to diving in unanesthetized ducks. After denervating the right carotid body, perfusion of the innervated left carotid body with hyperoxic blood significantly reduced diving bradycardia and reduced the increase in hindlimb vascular resistance (HLVR) in 1-min dives compared with dives in which the innervated carotid body was autoperfused. Denervation of systemic arterial baroreceptors reduced the fall in heart rate (HR) and increased the rise in HLVR in all dives. Cross-perfusion of the head, from a donor with blood of normal blood gas tensions, did not significantly affect HR or HLVR in 2-min dives compared with dives in which the head was autoperfused. however, cross-perfusing the cerebral circulation with blood of elevated PaCO2 caused significantly greater increases in HLVR than when high PaCO2 only affected the peripheral circulation. We conclude that peripheral chemoreceptors cause virtually all the bradycardia in the later stages of a dive but only about one-half the increase in HLVR, a significant contribution comes from the stimulation of central chemoreceptors with blood of high PaCO2.

Effects of prostaglandins on fetal breathing do not involve peripheral chemoreceptors

1987 ◽  
Vol 62 (1) ◽  
pp. 271-277 ◽  
Author(s):  
D. T. Murai ◽  
L. D. Wallen ◽  
C. C. Lee ◽  
R. I. Clyman ◽  
F. Mauray ◽  
...  
Keyword(s):  
Carotid Sinus ◽  
Vagus Nerves ◽  
Fetal Sheep ◽  
Peripheral Chemoreceptors ◽  
Respective Control ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Site Of Action ◽  
Pg E2 ◽  
Stimulation Of

In sheep, prostaglandin (PG) E2 inhibits fetal breathing movements and meclofenamate, a PG synthetase inhibitor, causes a marked stimulation of fetal breathing movements; the site of action of these agents is not known. To determine whether these effects are mediated through the peripheral chemoreceptors, we studied 13 fetal sheep at gestational ages of 127 to 138 days. Seven fetuses had bilateral section of the carotid sinus and vagus nerves (denervated); six had sham operations. Beginning at least 6 days after the operation, we infused PGE2 (0.6 microgram X kg-1 X min-1) into five denervated and five sham-operated fetuses and meclofenamate (0.4 mg X kg-1 X h-1) into six denervated and four sham-operated fetuses. Infusions averaged 20 h in duration. During preinfusion control periods, the incidence of fetal breathing movements (% of time) was lower in denervated than in sham-operated fetuses (18.9% vs. 31.5%; P less than 0.005). In both groups, the incidence of fetal breathing movements was decreased by PGE2 and was increased by meclofenamate; when expressed as absolute values, the magnitude of the changes with both agents was greater in sham-operated fetuses than denervated fetuses. However, the effects were similar in both groups when the changes were expressed as a percent of the respective control values. The incidence of fetal breathing movements (% of control) was decreased by PGE2 to 25.4% in denervated and to 28.2% in sham-operated fetuses and was increased by meclofenamate to 297.3% in denervated and to 304.0% in sham-operated fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)

Generation and regulation of breathing in utero: fetal CO2 response test

1979 ◽  
Vol 47 (3) ◽  
pp. 527-531 ◽  
Author(s):  
I. R. Moss ◽  
E. M. Scarpelli
Keyword(s):  
In Utero ◽  
Fetal Life ◽  
Respiratory Drive ◽  
Endogenous Opioid ◽  
Co2 Response ◽  
Fetal Breathing ◽  
Regulation Of Breathing ◽  
Increased Sensitivity ◽  
Sciatic Nerve Stimulation ◽  
Spontaneously Breathing

Breathing responses to increasing fetal arterial CO2 pressure (PaCO2) were measured in 15 mature fetal lambs in utero during hyperoxic CO2 rebreathing in the ewe. Fetal breathing was expressed as 1) respiratory drive (RD), i.e., the early slope of intratracheal pressure during inspiration, and 2) ventilation equivalent (VEq), i.e., the product of intratracheal pressure and frequency of breathing. RD and VEq increased linearly with increasing PaCO2. CO2 threshold beyond which apneic fetuses started breathing was higher than the extrapolated CO2 threshold in spontaneously breathing fetuses. Afferent sciatic nerve stimulation, which induced regular breathing in apneic fetuses, lowered their CO2 threshold but did not alter their sensitivity to CO2. Naloxone resulted in initiation of fetal breathing, decreased CO2 threshold, and increased sensitivity to CO2. These studies demonstrate that respiratory center responsivity can be quantified in the lamb fetus in utero, that nonspecific somatic stimulation lowers fetal breathing threshold to CO2, and that endogenous opioid peptides could participate in the physiological suppression of breathing in fetal life.

Ventilatory control in peripheral chemoreceptor-denervated ponies during chronic hypoxemia

1976 ◽  
Vol 41 (6) ◽  
pp. 878-885 ◽  
Author(s):  
H. V. Forster ◽  
G. E. Bisgard ◽  
B. Rasmussen ◽  
J. A. Orr ◽  
D. D. Buss ◽  
...  
Keyword(s):  
Sea Level ◽  
Hypobaric Hypoxia ◽  
Acute Hypoxia ◽  
Inhibitory Influence ◽  
Ventilatory Control ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Chronic Hypoxemia ◽  
Insight Into

The present study was designed to provide further insight into the role of the carotid and aortic chemoreceptors in ventilatory (VE) acclimatization during sojourn at altitude. Measurements were made: 1) on 10 ponies near sea level(SL, 740 Torr) under normal conditions, 2) on 6 of these at SL following chemoreceptor denervation (CD), and 3) subsequently on all 10 during 4 days of hypobaric hypoxia (PaO2 = 40–47 Torr). CD resulteo in hypoventilation at SL (deltaPaCO2 = d8 Torr, P less than 0.05), and it prevented hyperventilation normally observed with injection of NaCN and acute exposure to hypoxia (less than 1 h). In contrast, hyperventilation was evidentin normal ponies during acute hypoxia (deltaPaCO2 = -6.7 Torr). Ventilationincreased in both groups between the 2nd and 8th h of hypoxia (deltaPaCO2 from 1 h = -4 Torr, P less than 0.05). This change, a common characteristic of acclimatization, persisted throughout 4 days of hypoxia in the normal ponies. However, in the CD ponies this change was evident consistently only through the 12th h and after the 44 h hyperventilation was no longer evident.We conclude that the peripheral chemoreceptors are essential in ponies for normal VE acclimatization to this degree of hypoxemia. Two additional findingsin CD ponies suggest the presence of a CNS inhibitory influence on theVEcontrol center during chronic hypoxemia. First, acute hyperoxygenation on the 4th day of hypoxemia induced hyperventilation (deltaPaCO2 = -5 Torr, P less than 0.05). Second, again on the 4th day and during hyperoxygenation, VE responsiveness to CO2 and doxapram HCl was greater than at sea level.

Role of chemical afferents in the maintenance of rhythmic respiratory movements

1983 ◽  
Vol 54 (2) ◽  
pp. 453-459 ◽  
Author(s):  
W. R. See ◽  
M. E. Schlaefke ◽  
H. H. Loeschcke
Keyword(s):  
Respiratory Rhythm ◽  
Afferent Input ◽  
Vagal Afferents ◽  
Peripheral Chemoreceptors ◽  
Central Chemosensitivity ◽  
Relative Contribution ◽  
Ventilatory Drive ◽  
Respiratory Movements ◽  
Stimulation Of

In seven anesthetized cats central chemosensitivity was eliminated (cold block) and peripheral chemoreceptors were either stimulated or eliminated (sectioned) to test whether nonchemical vagal afferents can maintain rhythmic ventilation and to determine the relative contribution of the carotid and aortic chemoreceptors to ventilatory drive without central chemosensitivity. Elimination of all chemical afferents invariably induced apnea, whereas ventilation was reduced from 533 to 159 ml X min-1 during cold block of central chemosensitivity and to 478 ml X min-1 after sectioning both sinus nerves. Cold block with only the aortic chemoreceptors and vagal afferents intact produced apnea in four of six cases tested. Stimulation of peripheral chemoreceptors during cold block remained effective and interrupted apnea in three of the four cats with only aortic chemoreceptors intact. We conclude that the nonchemical vagal respiratory afferents alone are unable to maintain rhythmic ventilation. Respiratory rhythm generation is, under the conditions of our experiments, critically dependent on sufficient afferent input from chemical afferents. Of these, central chemosensitivity plays the major role, followed by carotid body and, least importantly, by aortic afferents.

Differential role of the paraventricular nucleus of the hypothalamus in modulating the sympathoexcitatory component of peripheral and central chemoreflexes

2005 ◽  
Vol 289 (3) ◽  
pp. R789-R797 ◽  
Author(s):  
Maram K. Reddy ◽  
Kaushik P. Patel ◽  
Harold D. Schultz
Keyword(s):  
Paraventricular Nucleus ◽  
Potassium Cyanide ◽  
Reflex Response ◽  
Nerve Activity ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Arterial Blood ◽  
Central Chemoreceptors ◽  
Stimulation Of

In the present study we investigated the involvement of the hypothalamic paraventricular nucleus (PVN) in the modulation of sympathoexcitatory reflex activated by peripheral and central chemoreceptors. We measured mean arterial blood pressure (MAP), heart rate (HR), renal sympathetic nerve activity (RSNA), and phrenic nerve activity (PNA) before and after blocking neurotransmission within the PVN by bilateral microinjection of 2% lidocaine (100 nl) during specific stimulation of peripheral chemoreceptors by potassium cyanide (KCN, 75 μg/kg iv, bolus dose) or stimulation of central chemoreceptors with hypercapnia (10% CO2). Typically stimulation of peripheral chemoreceptors evoked a reflex response characterized by an increase in MAP, RSNA, and PNA and a decrease in HR. Bilateral microinjection of 2% lidocaine into the PVN had no effect on basal sympathetic and cardiorespiratory variables; however, the RSNA and PNA responses evoked by peripheral chemoreceptor stimulation were attenuated ( P < 0.05). Bilateral microinjection of bicuculline (50 pmol/50 nl, n = 5) into the PVN augmented the RSNA and PNA response to peripheral chemoreceptor stimulation ( P < 0.05). Conversely, the GABA agonist muscimol (0.2 nmol/50 nl, n = 5) injected into the PVN attenuated these reflex responses ( P < 0.05). Blocking neurotransmission within the PVN had no effect on the hypercapnia-induced central chemoreflex responses in carotid body denervated animals. These results suggest a selective role of the PVN in processing the sympathoexcitatory and ventilatory component of the peripheral, but not central, chemoreflex.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

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