Bladder contractions and micturition in fetal sheep: their relation to behavioral states

1989 ◽  
Vol 257 (6) ◽  
pp. R1526-R1532 ◽  
Author(s):  
M. E. Wlodek ◽  
G. D. Thorburn ◽  
R. Harding

Fetal bladder contractions, indicative of micturition (voiding), and behavioral states were monitored in unanesthetized fetal sheep in utero during the last third of gestation. Fetal voids began during low-voltage electrocortical activity (LV ECoG) at a greater frequency (91.4 +/- 1.0%) than expected (57.2%) and began during high-voltage electrocortical activity (HV ECoG) with a lower frequency (8.7 +/- 1.0%) than expected (42.8%). Fetal voids began significantly sooner after the onset of LV ECoG (5.84 +/- 0.13 min) than after the onset of HV ECoG (10.88 +/- 0.04 min). Electroocular and nuchal muscle activities were associated with 96.2 and 66.0% of the voids, respectively, but there was no significant association between fetal voiding and swallowing episodes. Abolition of spontaneous voiding, by urine drainage (24 h), caused no significant differences, relative to a 24-h control period, in the duration or number of episodes of LV or HV ECoG or percentage of time spent in these states. Also, induction of voiding by infusing saline into the bladder did not significantly alter the time to the next change of ECoG state. However, the mean time to the next void and the mean volume of saline infused into the bladder to induce voiding tended to be less during LV ECoG than HV ECoG, although not significantly less. Our data show that most spontaneous voids in the fetus begin during LV ECoG, suggesting that voiding is regulated by descending information from the brain. Furthermore, these experiments demonstrate that fetal bladder contractions and voiding, either spontaneous or induced, do not influence the normal cycling of fetal ECoG states.

1996 ◽  
Vol 8 (3) ◽  
pp. 423 ◽  
Author(s):  
RE Alvaro ◽  
V Rehan ◽  
Almeida V de ◽  
Z Haider ◽  
M Robertson ◽  
...  

We have found previously that the infusion of a placental extract inhibits breathing induced by 100% O2 plus umbilical cord occlusion in the fetal sheep, suggesting that a placental factor is responsible for the inhibition of fetal breathing. To test whether this factor is specific to the placenta and whether it also inhibits spontaneous fetal breathing (occurring in the absence of cord occlusion), we administered extracts from the placenta, muscle and liver of the pregnant ewe, extracts of fetal liver, and Krebs solution to 16 chronically instrumented fetal sheep at 135 +/- 5 days of gestation. Infusions were made during low-voltage electrocortical activity, 5 to 15 min after a switch from high voltage, when breathing was well established. Within 90 s of the infusion of the placental extract in the carotid artery of the fetus, breathing decreased in 79% (33/42) of the experiments and was completely abolished in 71% (30/42) of them (P < 0.0001 compared with the other infusates). No apnoeas were observed with the Krebs solution (0/19) and the maternal muscle (0/20). Extracts of maternal and fetal liver abolished breathing in only 17% (4/23) and 21% (6/29) of the experiments respectively (NS compared with Krebs solution). There were no significant changes in blood gas tensions, pH, blood pressure and heart rate associated with the infusion of the extracts. The electrocortical activity (ECoG) switched from low to high voltage in 50% of the experiments using placental extract compared with 0% with Krebs solution and maternal muscle, and with 9% and 17% with maternal and fetal liver respectively (P < 0.005). Breathing output (integral of EMGdi x f) during and after the infusions significantly decreased only with the placental extract. These findings indicate the presence of a factor produced by the placenta which inhibits fetal breathing and may be responsible for the normal inhibition of breathing observed in fetal life.


2008 ◽  
Vol 294 (3) ◽  
pp. G694-G698 ◽  
Author(s):  
Hariprasad Korsapati ◽  
Arash Babaei ◽  
Valmik Bhargava ◽  
Ravinder K. Mittal

In healthy subjects, a close temporal correlation exists between contractions of the circular muscle (CM) and longitudinal muscle (LM) layers of the esophagus. Patients with nutcracker esophagus show disassociation between the peak of contractions of the CM and LM layers and the peak of contraction 1–3 s apart (Jung HY, Puckett JL, Bhalla V, Rojas-Feria M, Bhargava V, Liu J, Mittal RK. Gastroenterology 128: 1179–1186, 2005). The purpose of the present study was to evaluate the effect of acetylcholinesterase inhibitor (edrophonium) and acetylcholine receptor antagonist (atropine) on human esophageal peristalsis in normal subjects. High-frequency intraluminal ultrasound imaging and manometry were performed simultaneously during swallow-induced peristalsis in ten normal subjects. Standardized 5-ml water swallows were recorded 2 cm above the lower esophageal sphincter under three study conditions: control, edrophonium (80 μg/kg iv), and atropine (10 μg/kg iv). A close temporal correlation exists between the peak pressure and peak wall thickness during the control period. The mean time lag between the peak LM and peak CM contraction was 0.03 s. After edrophonium administration, the mean contraction amplitude increased from 101 ± 9 mmHg to 150 ± 20 mmHg ( P < 0.05) and mean peak muscle thickness increased from 3.0 ± 0.2 mm to 3.6 ± 0.3 mm ( P < 0.01), and duration of both CM and LM contractions were also increased. Furthermore, the mean time difference between the peak LM and CM was increased to 1.1 s, (ranging 0.2 to 3.4 s) ( P < 0.0001). We conclude that cholinomimetic agent induces discoordination between the two muscle layers of the esophagus.


1995 ◽  
Vol 21 (4) ◽  
pp. 553-560 ◽  
Author(s):  
P.M. Duggan ◽  
G.C. Liggins ◽  
S.B. Barnett
Keyword(s):  
In Utero ◽  

1987 ◽  
Vol 62 (3) ◽  
pp. 1033-1039 ◽  
Author(s):  
B. J. Koos ◽  
H. Sameshima ◽  
G. G. Power

Graded isocapnic hypoxemia was produced in unanesthetized fetal sheep by varying the inspired O2 concentration (21, 12, 10.5, and 9%) of the ewe. This produced corresponding mean preductal arterial O2 tension (PaO2) values of 25.2 +/- 1.1 (control), 20.1 +/- 1.0 (mild hypoxia), 17.8 +/- 0.9 (moderate hypoxia), and 16.8 +/- 1.4 Torr (severe hypoxia). These were associated with mean arterial O2 contents (CaO2) of 7.18 +/- 0.44, 5.19 +/- 0.34, 4.24 +/- 0.33, and 3.27 +/- 0.20 ml/dl, respectively. The most severe hypoxia was associated with metabolic acidosis and fetal bradycardia. Hypoxia did not reduce significantly the incidence of low-voltage electrocortical activity. The incidence of breathing and rapid eye movements was not affected by mild hypoxia; however, the incidence of both was significantly reduced during moderate and severe hypoxia. It is concluded that 1) acute reductions in the mean PaO2 of 5.9 +/- 0.6 Torr and CaO2 of 2.00 +/- 0.23 ml/dl are critical in that greater reductions inhibit fetal eye and breathing activity and 2) hypoxia probably inhibits eye and breathing movements by altering sleep state.


1993 ◽  
Vol 264 (6) ◽  
pp. R1139-R1149
Author(s):  
S. A. Joseph ◽  
D. W. Walker

The effects of intracisternal administration of tyramine on fetal breathing movements (FBM), electrocortical (ECoG) and nuchal muscle activities, and cerebrospinal fluid (CSF) monoamine concentrations have been studied in unanesthetized fetal sheep (124-140 days gestation) in utero. In 18 trials (8 fetuses) infusion of 50 or 100 micrograms/kg tyramine increased the incidence of FBM from 32.2 +/- 2.0 to 79.4 +/- 4.7%/h (P < 0.05) and increased mean breath amplitude from 6.4 +/- 0.4 to 11.8 +/- 1.6 mmHg (P < 0.05). FBM incidence during high-voltage ECoG activity increased from 3.3 +/- 0.6 to 22.5 +/- 3.6%/h (P < 0.05). Tyramine infusion (100 micrograms/kg) significantly increased (P < 0.05) the CSF concentrations of dopamine from 129.5 +/- 26.2 to 10,222.4 +/- 1,103.6 pg/ml, of norepinephrine from 74.7 +/- 11.0 to 2,238.6 +/- 143.5 pg/ml, and of serotonin from 1,824.5 +/- 340.7 to 3,888.7 +/- 1,335.2 pg/ml. Intracisternal injection of dopamine or norepinephrine (10-20 micrograms) caused the rapid onset of large-amplitude FBM, which often continued throughout high-voltage ECoG activity. In contrast, serotonin (20-40 micrograms) caused cessation of FBM and change of the ECoG from low- to high-voltage activity. These results indicate that neuronal release of catecholamines in the CNS has excitatory effects on FBM.


1994 ◽  
Vol 76 (4) ◽  
pp. 1476-1480 ◽  
Author(s):  
I. M. Kuipers ◽  
W. J. Maertzdorf ◽  
D. S. De Jong ◽  
M. A. Hanson ◽  
C. E. Blanco

We hypothesized that the level of arterial PCO2 (PaCO2) affects the incidence of fetal breathing movements and electrocorticographic (ECoG) states in chronically instrumented fetal sheep. Six fetuses of 128–132 days gestational age were instrumented for recording fetal behavior and for later connection to an extracorporeal membrane oxygenation (ECMO) system to change fetal blood gases. Before ECMO fetal arterial pH and blood gases were pH 7.40 +/- 0.01, PaCO2 42.9 +/- 1.5 Torr, and arterial PO2 (PaCO2) 19.2 +/- 1.7 Torr; during ECMO in normocapnia they were pH 7.37 +/- 0.01, PaCO2 46.1 +/- 0.7 Torr, and PaCO2 27.6 +/- 3.0 Torr; and during ECMO in mild hypocapnia they were pH 7.47 +/- 0.01, PaCO2 35.3 +/- 1.7 Torr, and PaCO2 26.6 +/- 1.7 Torr. The overall incidence of breathing movements, the incidence of breathing movements during low-voltage (LV) ECoG activity, and the mean duration of periods of breathing decreased significantly during hypocapnia. Fetal ECoG activity showed normal cycling during the periods of mild hypocapnia, and the mean duration of LV ECoG periods did not change. During mild hypocapnia, eye movements remained associated with LV ECoG activity and nuchal electromyographic activity remained associated with high-voltage ECoG activity. These results suggest that the presence of breathing movements in fetal life is not only dependent on the behavioral state but also on the level of fetal PaCO2.


1989 ◽  
Vol 257 (5) ◽  
pp. R1251-R1257 ◽  
Author(s):  
B. S. Richardson ◽  
L. Carmichael ◽  
J. Homan ◽  
R. Gagnon

Cerebral oxidative metabolism and regional blood flow were studied, with changes in behavioral state over the immediate perinatal period, to determine the change in cerebral metabolism at birth and the relationship to behavioral activity. Nine unanesthetized fetal sheep (139-142 days gestation) were each studied during a period of high-voltage and low-voltage electrocorticogram (ECOG) activity and then again after cesarean delivery at 2 h of age while awake and at 24 h of age while awake and during a period of high-voltage ECOG sleep. Preductal arterial and sagittal vein blood samples were analyzed for O2 content, blood gases, and pH. Blood flow was measured with a radioactive microsphere technique. Cerebral oxidative metabolism showed no significant perinatal change, although a coupling to behavioral state was evident with significant increases during both the perinatal low-voltage ECOG state and the awake state at 24 h. Blood flow to the brain showed a significant perinatal decrease after birth and state-related increases during both the prenatal low-voltage ECOG state and the awake state at 24 h consistent with the tight coupling of flow and/or O2 delivery to metabolic needs reported for normal brain tissue. The cerebral metabolic rate of the prenatal low-voltage ECOG state suggested a level of functional excitation comparable with that of the awake state after birth, supporting the importance of the rapid-eye-movement (REM) state mechanism as a source of endogenous stimulation during the perinatal period of brain growth and development.


1986 ◽  
Vol 60 (2) ◽  
pp. 526-531 ◽  
Author(s):  
L. D. Wallen ◽  
D. T. Murai ◽  
R. I. Clyman ◽  
C. H. Lee ◽  
F. E. Mauray ◽  
...  

In fetal sheep, plasma prostaglandin (PG) E2 concentrations are high, and fetal breathing movements (FBM) occur intermittently, primarily during low-voltage fast electrocortical activity (LVFA). There is evidence suggesting that prostaglandins, specifically PGE2, may regulate FBM. To define the physiological role of PGE2 in regulation of FBM, we infused meclofenamate (0.9 mg X kg-1 X h-1), a prostaglandin synthetase inhibitor, into six fetal sheep to suppress endogenous prostaglandin production. Afterward, PGE2 was added in mean doses of 9, 18, 36, and 90 ng X kg-1 X min-1. Meclofenamate decreased PGE2 concentrations and increased FBM, especially during high-voltage slow electrocortical activity (HVSA). Addition of PGE2 reversed the effects of meclofenamate, increasing PGE2 concentrations and decreasing FBM, especially during HVSA. The response to PGE2 was dose dependent; the overall incidence of FBM and incidences of FBM during HVSA and LVFA were inversely correlated with both the infused PGE2 dose and the mean PGE2 concentration. At higher doses of PGE2, FBM occurred intermittently and only during LVFA; thus PGE2 infusion restored the physiological pattern of FBM. These results indicate that PGE2 regulates FBM by inhibiting FBM during HVSA.


1995 ◽  
Vol 78 (2) ◽  
pp. 531-538 ◽  
Author(s):  
R. D. Savich ◽  
F. A. Guerra ◽  
C. C. Lee ◽  
J. A. Kitterman

During transition from fetal to extrauterine life, respiration increases in incidence and magnitude as pulmonary blood flow dramatically increases. To determine whether alterations in pulmonary blood flow in utero are directly related to alterations in fetal breathing movements (FBM), we studied six chronically instrumented fetal sheep late in gestation to assess the effects of continuous FBM caused by a 4-h infusion of meclofenamate, a prostaglandin synthase inhibitor, on mean pulmonary blood flow to the fetus. We found a striking increase in FBM from 46 +/- 15% (SD) of the time during control to > 85% of the time by 1 h (P < 0.001), with the fetuses exhibiting continuous FBM by the last 1 h of infusion. The mean pulmonary blood flow also increased significantly during the first 90 min of the infusion as the incidences of FBM were increasing (26 +/- 14 and 56 +/- 23 ml.min-1.kg-1 for control and infusion, respectively; P < 0.01). Despite the simultaneous initial increase in FBM and mean pulmonary blood flow, the increase in left pulmonary artery blood flow was not sustained and decreased back to baseline by 2 h, even though the incidence of FBM continued to increase at this time. During the infusion, the mean pulmonary blood flow was not different between the presence or absence of FBM. There were no changes in fetal heart rate or pulmonary or systemic blood pressures during the infusion nor in arterial pH or blood gas tensions. We conclude that this increase in mean pulmonary blood flow in utero was not solely related to the increase in breathing movements.


1990 ◽  
Vol 68 (4) ◽  
pp. 1597-1604 ◽  
Author(s):  
R. J. Baier ◽  
S. U. Hasan ◽  
D. B. Cates ◽  
D. Hooper ◽  
B. Nowaczyk ◽  
...  

To test the hypothesis that continuous fetal breathing could be induced by hyperoxemia alone or by hyperoxemia and umbilical cord occlusion, even in the absence of a rise in arterial PCO2 (PaCO2), we studied 18 chronically instrumented fetal sheep on 34 occasions using our window model (18). After a resting cycle (1 low-voltage followed by 1 high-voltage electrocortical activity epoch), the fetal lung was distended via an endotracheal tube using mean airway pressure of approximately cmH2O. Inspired N2, 17% O2, and 100% O2 were given to the fetus during one cycle each. While 100% O2 was given, the umbilical cord was occluded (balloon cuff).(ABSTRACT TRUNCATED AT 250 WORDS)


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