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A H Jansen

Publications and source records attributed to A H Jansen.

At least 19 recordsLinked to original sources
PubMed2000

Effect of acute adrenalectomy on sympathetic responses to peripheral lipopolysaccharide or central PGE(2).

The impact of plasma corticosterone levels on the sympathetic nervous system (SNS) response to intravenous lipopolysaccharide (LPS) or intracerebroventricular injections of PG was studied in anesthetized (urethan-chloralose) male Sprague-Dawley rats. For this, electrophysiological recordings of splenic and renal nerves were completed in control or adrenalectomized (ADX) rats. LPS (10 microgram iv) similarly increased splenic and renal nerve activity in control rats with a shorter onset latency for the splenic nerve. Acute ADX enhanced the response of both nerves to LPS (P < 0.005) and reduced the onset latency of the renal nerve (P < 0.05). PGE(2) (2 microgram icv) rapidly increased the activity of both nerves but preferentially (magnitude and onset latency) stimulated the renal nerve (P < 0.05). The magnitude of the splenic nerve response to PGE(2) was unaffected by ADX. Unexpectedly, PGE(2) was less effective at stimulating renal nerve activity in ADX animals relative to intact controls (P < 0.05). Pretreatment of ADX rats with a CRF antagonist ([D-Phe(12), Nle(21,38), Calpha-MeLeu(37)]CRF-(12-41)) reversed this effect such that the renal nerve responded to central PGE(2) to a greater extent than the splenic nerve (P < 0.05), as was the case in non-ADX rats. These data indicate that enhanced sensitivity of central sympathetic pathways does not account for the enhanced SNS responses to LPS in ADX rats. Also, a CRF-related process appears to diminish renal sympathetic outflow in ADX rats.

Adrenalectomy↗
PubMed1997

Peripheral endotoxin increases splenic sympathetic nerve activity via central prostaglandin synthesis.

We tested whether prostaglandin synthesis mediates the lipopolysaccharide (LPS)-induced increase in splenic sympathetic nerve activity. Sprague-Dawley rats were pretreated with intravenous or intracerebroventricular injections of indomethacin, and splenic nerve activity was recorded after intravenous injections of LPS. In vehicle-pretreated rats, 100 micrograms LPS induced a 62.8 +/- 5.6% increase in splenic nerve activity beginning 22.7 +/- 2.7 min postinjection. All vehicle-pretreated animals responded to high (100 micrograms, 5 of 5 animals) and low (10 micrograms, 8 of 8 animals) doses of LPS. Both intravenous (15 mg/kg) and intracerebroventricular (50 micrograms) pretreatments with indomethacin delayed (F1.19 = 30.66, P < 0.001) the increase in nerve activity after 100 micrograms LPS. When given intravenously, 50 micrograms indomethacin (the intracerebroventricular dose) did not delay the response to intravenous LPS, indicating that the effects of intracerebroventricular indomethacin pretreatment were restricted to the central nervous system. Importantly, intracerebroventricular indomethacin reduced (2 of 7 animals) or completely blocked (5 of 7 animals) the splenic nerve response to the low dose of LPS (10 micrograms, iv). The indomethacin effects could not be accounted for by central release of vasopressin because intracerebroventricular injection of indomethacin did not alter baseline nerve activity or blood pressure, whereas intracerebroventricular injection of vasopressin rapidly increased both measures. Additionally, central injection of LPS did not elevate splenic nerve activity, whereas intracerebroventricular injection of prostaglandin E2 induced a rapid (2.2 +/- 2.7 min) increase in splenic nerve activity. These data indicate that central prostaglandin synthesis is an intermediate step whereby systemic LPS elicits an increase in sympathetic outflow to an immune organ.

Animals↗
PubMed1996

Effect of sinus denervation and vagotomy on c-fos expression in the nucleus tractus solitarius after exposure to CO2.

Exposure to hypercapnia and electrical stimulation of the carotid sinus nerve (CSN) has been shown to induce c-fos expression in several brain stem regions including the nucleus tractus solitarius (NTS). To test whether the labeled neurons were activated directly by hypercapnia or secondarily via the carotid bodies (sinus nerve), adult rats were exposed to either air or 14-16% CO2 for 1 h. Experiments were done on eight groups: (1) exposure to air, (2) exposure to CO2, (3) chronic CSN denervation/CO2, (4) chronic unilateral CSN denervation/CO2, (5) chronic sham CSN denervation/CO2, (6) anesthetized/CO2, (7) anesthetized and acute vagotomy/CO2, and (8) premedicated with morphine, 10 mg s.c., 20 min before exposure to CO2. After exposure to CO2 or air the rats were anesthetized, perfused with 4% paraformaldehyde and the brains processed for immunohistochemical staining for c-fos protein using the PAP (i.e. peroxidase anti-peroxidase) technique. Labeled neurons in the area of the NTS in every second 50- "mu"m section were counted and their position plotted using a microscope and camera lucida attachment. Rats exposed to CO2 had a significantly greater number of labeled neurons in the NTS than those exposed to air. Other interventions, such as CSN denervation, surgery, anesthesia, vagotomy or injection of morphine did not significantly affect the level of c-fos expression in rats exposed to hypercapnia, indicative of central stimulation rather than secondary peripheral input. These responsive neurons may be part of a widespread central chemoreceptive complex.

Animals↗
PubMed1996

Activation and selectivity of splenic sympathetic nerve electrical activity response to bacterial endotoxin.

Regulatory interactions and neuroanatomic pathways have been described between the sympathetic nervous system and the immune system. It is not clear whether these pathways are activated during immune responses and if target specificity provides selective regulation of immune organs. The present study examined whether systemic injection of endotoxin [lipopolysaccharide (LPS)] induces sympathetic outflow to an immune organ (spleen). Sympathetic nerve activity was recorded from either the splenic or renal nerve of adult male rats after intravenous injections of LPS. Splenic nerve activity increased in a dose-dependent manner up to 175% of control after injection of LPS, with an onset time of 17.1-23.5 min. In contrast, renal nerve recordings showed a significantly slower onset time of 37.1-52.6 min at similar doses. In addition, splenic nerve recordings of 8/8 rats responded to 10 micrograms of LPS, whereas only 4/11 positive renal nerve responses were observed at this dose. The magnitude of the responses of both splenic and renal nerves were comparable. These data suggest that the splenic nerve responds to and is more sensitive to LPS-stimulated sympathetic activation in terms of latency and frequency of responses. Thus sympathetic outflow can be directed to an immune organ in response to a stimulus known to activate the immune system.

Animals↗
PubMed1996

Technique for repetitive recording from fetal respiratory neurons.

We developed a new method for repetitive recording of medullary neurons in fetal sheep in situ. The technique involves chronically fixing the fetal head to the flank of the ewe by way of a Teflon plate that has a removable window. This window allows direct access of a recording electrode to the floor of the fourth ventricle of the fetus. In four of six fetuses, repetitive recordings lasting 3-4 h were possible for up to 6 days. By operating on younger fetuses and with care, this time span could be extended. This novel method should be useful in the future for extracellular and intracellular recordings of neurons in the developing fetus without disturbing the fetal state and for the study of putative neurotransmitters during development with iontophoretic techniques.

Animals↗
PubMed1993

Effect of medullary lesions, vagotomy and carotid sinus denervation on fetal breathing.

Chronically prepared fetal sheep were subjected to bilateral surface lesions of the Area "S" on the ventrolateral medulla and/or to peripheral chemoreceptor denervation by section of the vagus, sinus or both nerves. Sino-aortic denervation or Area "S" lesions reduced the incidence of fetal breathing (FB) for several days. Area "S" lesions also disrupted the pattern of FB; diaphragmatic EMG activity initially was mostly tonic and then of very high frequency, up to 7 Hz. Incidence and pattern of FB generally recovered by 7 days, but mean Ti was reduced in Area "S" lesioned fetuses (0.14 +/- 0.01 sec) compared to nonlesioned fetuses (0.19 +/- 0.01 sec) (P < 0.0001). Respiratory sensitivity to CO2 was variable but not different between control, denervated, and Area "S" lesioned groups. Eight of eight fetuses with Area "S" lesions were unable to initiate breathing at birth, but three sham operated fetuses were born normally. These data suggest that the classical peripheral and central chemoreceptors have a negligible influence on the control of FB, and that breathing activity in the fetus is mediated by a different mechanism than during postnatal life.

Animals↗
PubMed1993

Influence of prolonged adenosine receptor blockade on fetal sleep and breathing patterns.

Chronically prepared fetal sheep were subjected to 48 h infusions of theophylline, an adenosine antagonist, enprofylline, a xanthine without adenosine antagonism, or saline. Theophylline increased mean (+/- SD) incidence of REM sleep from 49.3 +/- 8.3% to 57.3 +/- 6.7% (p < 0.02) and wakefulness from 1.3 +/- 1.4% to 8.1 +/- 7.1% (p < 0.01). On the first day of theophylline infusion incidence of fetal breathing (FB) increased from 37.9 +/- 8.1% to 53.7 +/- 11.6% of total time (p < 0.002) and from 76.4 +/- 10.2% to 87.6 +/- 10.3% of REM sleep (p < 0.02). Diaphragmatic EMG/min increased from 6.9 +/- 4.0 to 17.3 +/- 13 arbitrary units (p < 0.02). By the second day of infusion, FB had returned to baseline value. Enprofylline and saline had no effect. 125 micrograms phenyl isopropyl adenosine (PIA) i.v. caused fetal apnea that was reduced from 143 +/- 45.5 min on the control day to 39.8 +/- 34.7 min (p < 0.001) during theophylline infusion. Enprofylline and saline had no effect, suggesting that the observed theophylline effect was due to its adenosine antagonism rather than to non-specific xanthine action. We conclude that endogenous adenosine suppresses FB, but since theophylline did not alter the basic relationship between FB and REM sleep it is not primarily responsible for apnea during NREM sleep.

Animals↗
PubMed1993

Anaerobic Nitrate Respiration by Erwinia carotovora subsp. atroseptica during Potato Tuber Invasion.

The in planta induction of anaerobic nitrate respiration by Erwinia carotovora subsp. atroseptica in relation to the in situ oxygen status in soft rotting potato tubers has been investigated. In vitro experiments have shown that nitrate was required for the induction of respiratory nitrate reductase activity in E. carotovora. In addition, oxygen was found to repress this activity. Expression of respiratory nitrate reductase was found in E. carotovora cells extracted from soft rotting potato tuber tissue. However, the rate of nitrite production in these cells was approximately 70-fold lower than the rate recorded in fully induced anaerobic cultures. Oxygen measurements in soft rotting potato tubers indicated that the invading bacteria encounter the lowest oxygen concentration at the interphase between healthy and macerated tissue. Consequently, growth of bacteria present in this specific zone will be stimulated by nitrate which is present in sufficient amounts in tuber tissue. A high nitrate content of the tuber will most likely facilitate the proliferation of E. carotovora in the tuber tissue.

Journal Article↗
PubMed1993

Fetal respiratory neuronal activity during REM and NREM sleep.

Chronically prepared near-term fetal lambs (129-133 days gestation) were exteriorized into a saline bath under maternal spinal anesthesia, and each head was rigidly connected to a stereotaxic frame. Multibarrel glass electrodes were inserted into the region of the nucleus tractus solitarius (NTS) during fetal breathing (FB) in rapid-eye-movement (REM) sleep. Of a total of 223 neurons, it was possible to record only 6 neurons for which firing amplitude did not change during the transition from REM to non-REM (NREM) sleep. The burst frequency, number of spikes per breath, and association with diaphragmatic activity were variable, with phasic activity preceding FB or disappearing and reappearing during FB. During the transition from REM to NREM sleep, phasic neuronal activity ceased, became tonic, and finally ceased altogether. L-Glutamate increased the number of spikes per breath and caused previous phasic activity to reappear but in NREM sleep produced only tonic activity. We conclude that during REM sleep the fetal respiratory neurons in the region of the NTS are to a large degree influenced by nonrespiratory REM sleep factors and that quiescence of respiratory neurons during NREM sleep is due to the lack of phasic input rather than to direct inhibition. Inhibition of FB during NREM sleep must occur upstream of the NTS neuron.

Animals↗
PubMed1992

Maturation of steady-state CO2 sensitivity in vagotomized anesthetized lambs.

The maturation of the respiratory sensitivity to CO2 was studied in three groups of anesthetized (ketamine, acepromazine) lambs 2-3, 14-16, and 21-22 days old. The lambs were tracheostomized, vagotomized, paralyzed, and ventilated with 100% O2. Phrenic nerve activity served as the measure of respiration. The lambs were hyperventilated to apneic threshold, and end-tidal PCO2 was raised in 0.5% steps for 5-7 min each to a maximum 7-8% and then decreased in similar steps to apneic threshold. The sinus nerves were cut, and the CO2 test procedure was repeated. Phrenic activity during the last 2 min of every step change was analyzed. The CO2 sensitivity before and after sinus nerve section was determined as change in percent minute phrenic output per Torr change in arterial PCO2 from apneic threshold. Mean apneic thresholds (arterial PCO2) were not significantly different among the groups: 34.8 +/- 2.08, 32.7 +/- 2.08, and 34.7 +/- 2.25 (SE) Torr for 2- to 3-, 14- to 16-, and 21- to 22-day-old lambs, respectively. After sinus denervation, apneic thresholds were raised in all groups [39.9 +/- 2.08, 40.9 +/- 2.08, and 45.3 +/- 2.25 (SE) Torr, respectively] but were not different from each other. CO2 response slopes did not change with age before or after sinus nerve section. We conclude that carotid bodies contribute to the CO2 response during hyperoxia by affecting the apneic threshold but do not affect the steady-state CO2 sensitivity and the central chemoreceptors are functionally mature shortly after birth.

Anesthesia↗
PubMed1992

Analysis of respiratory neuronal activity in fetal sheep.

We developed a new method to monitor fetal medullary respiratory neurons utilizing a two-stage approach. At 129-133 days of gestation, sheep were anesthetized, and a window was placed over the area of the fourth ventricle. After a recovery period of 3-5 days, the fetus was exteriorized into a saline bath under maternal spinal anesthesia, and the head was connected rigidly to a stereotaxic frame. Microelectrodes were inserted into the area of the nucleus tractus solitarius during rapid-eye-movement sleep, and extracellular recordings of 223 respiratory neurons were analyzed: 76% were inspiratory, 9% expiratory, and 15% phase spanning, as classified by visual and computer correlation to diaphragmatic activity. More detailed analysis of 100 neurons was done to assess the respiratory component (eta 2) by use of a modification of the method developed by Orem and Dick (J. Neurophysiol, 50: 1098-1107, 1983). With use of cohorts of 25 breaths, fetal respiratory neurons were found to frequently change their phase relationship to diaphragmatic activity. The eta 2 statistic of fetal respiratory neurons was not a stable characteristic but changed over time. This could be a reflection of an immature central respiratory system before birth or the lack of major sensory inputs.

Animals↗
PubMed1991

Fetal breathing and development of control of breathing.

Technical advances during the last several decades have greatly facilitated research into fetal physiology and behavior, specifically fetal breathing (FB). Breathing movements have been demonstrated in the fetuses of every mammalian species investigated and appear to be part of normal fetal development. In this review we focus on the methods of measuring FB and on some of the problems associated with these measurements and their interpretation. We also review fetal behavior, the role of the peripheral and central chemoreceptors in spontaneous FB, the fetal respiratory response to hypercapnia and hypoxia, and the transition to continuous breathing at birth. It is clear that in many ways the control of breathing movements in utero differs from that after birth. In particular, inhibitory influences are much more prominent before than after birth. Possibly this is due to the unique fetal situation, in which conservation of energy may be more important than any advantage breathing activity imparts to the fetus.

Animals↗
PubMed1989

Influence of naloxone on fetal breathing and the respiratory response to hypercapnia.

The effect of naloxone on fetal breathing and the respiratory sensitivity to CO2 was tested on chronically prepared fetal lambs on days one and four post-surgery. After a control period the fetus was challenged with hypercapnia for 10 min and after another control period 9 mg naloxone was administered to the fetus followed by another CO2 test 15 min later. An index of fetal breathing (Veq), tidal volume (VT) and frequency of breathing (f) was determined from tracheal pressure deflections and from the integrated diaphragmatic EMG, expressed as power of diaphragmatic activity per min. Naloxone consistently caused fetal arousal but the duration was variable. The respiratory response to naloxone was also variable and not statistically different from control. The respiratory sensitivity to CO2 (% delta Veq/Torr delta PaCO2 or % delta Diaph. Power/min/Torr delta PaCO2) was not changed by naloxone on either day. We conclude that endorphins do not have a significant direct role in the fetal respiratory response to CO2 but may be involved in the control of state.

Animals↗
PubMed1989

Control of organ blood flow in fetal sheep during normoxia and hypoxia.

The role of peripheral chemoreceptors in the circulatory adaptation to hypoxia and the effects of rapid-eye-movement (REM) and non-REM (NREM) sleep and breathing activity on organ blood flow were assessed in fetal sheep. Blood flow was measured with isotope-labeled microspheres on intact, vagotomized (VX), and sinoaortic-denervated (SAD) fetuses. Denervation did not change the biventricular cardiac output (Biv. CO) or organ blood flows during normoxia. In intact fetuses the blood flow was increased during hypoxemia in brain, adrenals, and heart but not in kidneys, skeletal muscles, or placenta. The increase in organ blood flow during hypoxemia was reduced in the VX group and even more in SAD fetuses, but in the latter group, blood flow was still increased in mid-brain, medulla, pons, skeletal muscles, and heart. Sleep states per se did not significantly affect the blood flow to any organs tested. However, the Biv. CO and blood flow to all organs except kidneys and adrenals was increased during fetal breathing in REM sleep. We conclude that 1) during moderate hypoxemia both aortic and carotid bodies plus an additional mechanism are involved in redistributing fetal blood flow, and 2) changes in organ perfusion during REM sleep are due to concomitant fetal breathing.

Animals↗
PubMed1988

The effect of chronic biphrenectomy on lung growth and maturation in fetal lambs. Morphologic and morphometric studies.

Three fetal lambs underwent phrenic nerve section between Days 99 and 104 of gestation, and 2 twins of the experimental animals underwent sham operation at the same time. When they were killed at 135 to 137 days of gestation, the experimental animals had lower specific lung weights (g/kg) and lung volumes (ml/kg) and had delayed lung development by subjective microscopy. Light microscopic morphometry showed significantly less volume proportion of potential gas-exchanging air spaces, less parenchyma, and more gas-exchanging wall. Scanning electron microscopy confirmed these findings and also showed that the transition zone between conducting and gas-exchanging areas was less sharp in the experimental animals, attributed to diminished alveolarization of distal conducting airways. Transmission electron microscopy, together with morphometry, showed a diminished maturation of alveolar Type II cells, with fewer osmiophilic lamellar bodies and more glycogen. The number of mesenchymal-Type II cell interconnections was not altered. Maturation of bronchiolar epithelium was not affected, and mesenchymal-epithelial connections were not observed. We conclude that bilateral phrenic nerve section not only diminishes lung growth, but also diminishes intrauterine maturation of the alveolar well. Maturation of bronchiolar epithelium may not be affected by fetal respiration.

Animals↗
PubMed1987

A novel analysis of fetal breathing.

We have analyzed a variety of approaches in assessing fetal breathing parameters (VT, TI, Ttot, VT/TI, VI) in eight fetal sheep during a control period and during stimulation with 6 and 9% CO2. By using conventional analysis of data blocks varying from 100 to 1500 breaths, several different conclusions could be reached regarding the respiratory response to hypercapnia: stimulation, depression, or no change in all parameters studied. A new analysis based on piecewise linear regression used as a data grouping technique indicated that a simple mean +/- SD of the individual parameters was an inappropriate description of normal or stimulated fetal breathing. Based on tests for homogeneity of regressions of VT on TI for a completely random design, it is concluded that an estimate of fetal respiratory drive is only described adequately by two to four regression regimes. These regimes, estimated from the regression technique, could be combined to give a weighted mean value based on the proportion of time they were present. Using this new approach and an analysis of variance, we found (i) that frequency and VI were similar between animals during control and hypercapnia, (ii) that breathing frequency decreased during hypercapnia, and (iii) a positive relationship between VT and TI.

Animals↗
PubMed1987

Maturation of spontaneous fetal diaphragmatic activity and fetal response to hypercapnia and hypoxemia.

The electromyogram (EMG) of the diaphragm, lateral rectus, and nuchal and hindlimb muscles were studied during spontaneous activity and during hypercapnia or hypoxemia in eight fetal sheep from 0.5 to 0.8 gestation (73-128 days). At the earliest gestational age, diaphragmatic EMG activity was mainly tonic and associated with tonic activity of somatic muscles. The stimulus for the diaphragmatic activity originated centrally. Brief periods of a rapid-eye-movement (REM) state characterized by phasic lateral rectus and diaphragmatic activity and absence of nuchal activity were recognized. Furthermore, from 0.5 to 0.7 gestation onward, activity of all muscles increased. Thereafter increased specificity of activity in relation to the apparent REM and non-rapid-eye-movement (NREM) state occurred. With maturation, phasic diaphragmatic activity increased at the expense of tonic activity. The most striking effect of maturation on apnea was a greater proportion of apnea lasting greater than 1 min, but the total duration of apnea as a percent of a total recording remained unchanged. The quantitative response to hypercapnia during maturation was independent of the pattern of spontaneous diaphragmatic activity. Hypercapnia at 0.5 gestation changed the pattern of diaphragmatic EMG activity from mainly tonic to phasic. Thus the central chemoreceptors and appropriate neuronal pathways are present and functional as early as 0.5 gestation. Hypercapnia at 0.5 gestation caused a shift in diaphragmatic EMG power to lower frequencies similar to that found during control conditions in the older fetus. This might suggest that during maturation there is increased recruitment of phrenic motoneurons. Hypoxemia abolished tonic somatic activity at 0.5 gestation and decreased phasic diaphragmatic activity at more advanced gestational ages. Therefore the central inhibitory mechanisms of hypoxemia are developed by 0.5 gestation.

Animals↗