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Biomedical subjects

C P van der Grinten

Publications and source records attributed to C P van der Grinten.

16 recordsLinked to original sources
PubMed1999

Intrapulmonary gas mixing and the sloping alveolar plateau in COPD patients with macroscopic emphysema.

Chronic obstructive pulmonary disease patients, especially those with emphysema, show steep slopes of the alveolar plateau (S). This study tested the hypothesis that continued gas exchange between poorly and well-ventilated lung units by means of collateral ventilation would contribute to S in these patients. Nine young volunteers, nine older volunteers and 11 patients with macroscopic emphysema performed wash-out tests with helium (He) and sulphur hexafluoride (SF6). S was determined for breaths 1-5 (range 1), and for breaths between 95% and 98% of complete wash-out (range 2). An unequal ventilation index (UVI) was defined as the ratio between the estimated mean alveolar pressure and the end tidal pressure (PET) of each tracer gas, calculated over range 2. Over the same range, a phase III ratio was calculated by dividing PET by the estimated pressure at Fowler dead space. In all groups of subjects, the S for He and SF6 were greater for range 2 than for range 1 (p< or =0.012). In the emphysema patients, the correlations between S and UVI were 0.72 for He (p=0.012) and 0.81 for SF6 (p=0.002), while the mean phase III ratios were 1.7 for He and 2.4 for SF6, much less than their theoretical maxima. It was concluded that in patients collateral ventilation may account for only a small part of the increase in the alveolar plateau slope between ranges 1 and 2, and that this increase was mainly caused by unequal ventilation in combination with sequential emptying of lung units. The degree of sequential emptying, however, was modest compared with its full potential.

Adult↗
PubMed1998

Breathing efficiency during inspiratory threshold loading in patients with chronic obstructive pulmonary disease.

Patients with chronic obstructive pulmonary disease (COPD) demonstrate an increased oxygen cost of breathing. It is as yet unclear whether this is related to a decreased breathing efficiency. The aim of the present study was to compare breathing efficiency in 16 patients with COPD (11 men, five women) and 16 healthy elderly subjects (seven men, nine women), and to investigate a possible relationship between breathing efficiency and resting energy expenditure (REE). REE was measured using a ventilated hood system. Breathing efficiency was assessed by measuring oxygen consumption (V'O2), mean inspiratory mouth pressure (MIP) and flow during breathing at rest and subsequently during breathing against an inspiratory threshold (40% of maximal inspiratory pressure). During loaded breathing there was a significant increase in V'O2, MIP, and external work of breathing compared with unloaded breathing in both groups. As intended, ventilation did not increase significantly during the breathing efficiency test in the patients with COPD. The breathing efficiency (median, range) of the patients with COPD was similar (3.7%, 1.4-8.7%) to that of the healthy elderly subjects (3.2%, 1.7-8.3%). Breathing efficiency was not correlated with REE in either group. In the present study, in which dynamic hyperinflation was probably prevented, no difference in breathing efficiency was found between healthy elderly subjects and COPD patients when breathing against an external inspiratory threshold. Furthermore, breathing efficiency was not related to REE in both groups.

Adult↗
PubMed1998

Time to peak tidal expiratory flow and the neuromuscular control of expiration.

The ratio of the time needed to reach peak tidal expiratory flow (tPTEF) and the duration of expiration (tE) is used to detect airflow obstruction in young children. tPTEF is decreased in patients with asthma, but knowledge about the physiological determinants of this parameter is scarce. This study examined the relationship between tPTEF and postinspiratory activities of inspiratory muscles and evaluated the effects of changing sensory information from the lung. Airflow patterns and electromyographic (EMG) activity of inspiratory muscles were recorded in seven spontaneously breathing, anaesthetized cats. The trachea was cannulated and, as a result, the larynx and upper airways were bypassed. Changes in postinspiratory muscle activity were induced by changing afferent sensory nerve information (by cooling the vagus nerves, by administration of histamine and by additional application of continuous positive airway pressure (CPAP)). Durations of postinspiratory activities of the diaphragm and intercostal muscles (characterized by their time constants tau diaphr and tau interc) correlated strongly with tPTEF (r=0.85 and 0.77, respectively). Tau diaphr, tau interc and tPTEF were significantly increased during cooling of the vagus nerves (4-8 degrees C) compared with values at 22 and 37 degrees C (p<0.05). Conversely, administration of histamine and CPAP caused significant decreases in tau diaphr, tau interc and tPTEF, which were absent during cooling of the vagus nerves. In conclusion, the time needed to reach peak tidal expiratory flow is highly influenced by the activities of inspiratory muscles during the early phase of expiration which, in turn, depend on the activities of vagal receptors in the lung.

Animals↗
PubMed1997

Breathing pattern during bronchial challenge in humans.

Increases in minute ventilation (V'E) have been observed during exacerbations of asthma and in response to administration of histamine. However, it is not yet clear how the breathing pattern is affected, and whether the increase in V'E is found in general. In the present study, the effects of inhalation of histamine on respiratory frequency (fR), tidal volume (VT), V'E, and on functional residual capacity (FRC) were evaluated in 63 humans. Forty four subjects were hyperresponsive (BHR+). In each of these subjects, the doses of histamine applied for the present study (mean 3.5 mg x mL(-1)) caused a decrease in forced expiratory volume in one second (FEV1) that was greater than 20% of the control value. The dose of histamine applied in the 19 nonhyperresponsive subjects (BHR-) was substantially larger (8.0 mg x mL(-1)) whilst for this dose the decrease in FEV1 was less than 20% of control value. After histamine, fR was significantly increased in both subgroups of subjects, BHR+ and BHR-. The increase in V'E was significant in BHR- but not significant in BHR+. In general, the changes in V'E,fR and VT were not uniform; comparable numbers of subjects responded with increases (n=33) and decreases (n=30) in V'E. For fR 40 subjects responded with an increase and 23 with a decrease, and for VT these numbers were 26 and 37, respectively. The increase in FRC after histamine was significantly larger in BHR+ subjects than in BHR-. These findings may be interpreted to indicate that different mechanisms with opposite effects may be operating simultaneously, e.g. excitation of central inspiratory activity by stimulation of rapidly-adapting pulmonary stretch receptors, which will promote increases in respiratory frequency, tidal volume and minute ventilation, and bronchoconstriction with increased airway resistance, which will promote decreases in these parameters. As a consequence, depending on the net result of these opposite contributions to, e.g. minute ventilation, administration of histamine will cause an increase in minute ventilation in one subject and a decrease in another.

Adult↗
PubMed1996

Histamine induced bronchoconstriction and end tidal inspiratory activity in man.

BACKGROUND: End tidal inspiratory activity (ETIA) in diaphragm and parasternal intercostal muscles can be evoked in man and in animals by administration of histamine. Exacerbations of asthma and administration of histamine are often accompanied by hyperinflation. The aims of the study were to determine (1) the magnitude of ETIA in response to histamine in man, (2) the relative contributions of chemical and mechanical stimulation of airway receptors to ETIA, and (3) the importance of ETIA to hyperinflation. METHODS: The effects of inhalation of histamine on the electrical activities of the diaphragm and parasternal intercostal muscles measured with surface electrodes were studied in 21 subjects. The experiments were repeated after inhalation of 600 micrograms of salbutamol to prevent histamine induced bronchoconstriction and concomitant mechanical stimulation of airway receptors. Subjects were connected to a closed breathing circuit to measure the changes in functional residual capacity (FRC) for the different experiments. RESULTS: The mean values of histamine induced ETIA were 60.6% and 46.9% of peak inspiratory activities during control conditions for the diaphragm and intercostal muscles, respectively. After salbutamol histamine induced ETIA was reduced to about one quarter of pre-salbutamol values. FRC increased by 427 ml as a result of inhalation of histamine, but after salbutamol this increase was only 53 ml. The data for ETIA and FRC were interpreted as indicating that the contributions of airflow limitation and ETIA to histamine induced hyperinflation are comparable. CONCLUSIONS: Histamine is a forceful stimulus for inducing ETIA. Both chemical and mechanical stimulation of airway receptors contribute to evoke ETIA, of which the contribution of mechanical stimulation is the more important one. ETIA contributes substantially to histamine induced hyperinflation.

Adolescent↗
PubMed1995

Histamine-induced end-tidal inspiratory activity and lung receptors in cats.

Hyperinflation in acute asthma has been associated with inspiratory muscle activity, which persist during expiration. The main objective of the present study was to evaluate the role of rapidly adapting receptors (RARs), slowly adapting receptors (SARs) and C-fibre endings in generating end-tidal inspiratory activity (ETIA). ETIA was induced by intravenous administration of histamine and continuous negative airway pressure (CNAP) in anaesthetized, spontaneously breathing cats. To differentiate between reflex activities from the three types of lung receptors, both vagus nerves were cooled to eight different temperatures (Tvg) between 4 and 37 degrees C. It is known that CNAP stimulates RARs and inhibits SARs. Histamine was used to stimulate RARs, and this was combined with continuous positive airway pressure (CPAP) to further stimulate SARs. ETIA was evoked in the diaphragm and in parasternal intercostal muscles by both stimuli (histamine and CNAP) in 8 out of 18 cats. After vagotomy, neither histamine nor CNAP evoked ETIA any more. At Tvg = 37 degrees C, CPAP suppressed histamine-induced ETIA; whereas, this suppression was diminished at Tvg between 14 and 8 degrees C. ETIA sharply declined for Tvg between 8 degrees and 4 degrees C, and at Tvg = 4 degrees C ETIA had virtually disappeared. At Tvg = 37 degrees and 22 degrees C values of ETIA during CNAP were larger than those in response to histamine; whereas, at Tvg = 10 degrees C comparable ETIA values were obtained. It was shown that ETIA is a vagal reflex activity in which C-fibre endings are not involved. Histamine-induced ETIA originates from stimulation of RARs, and is inhibited by stimulation of SARs. Mechanical stimulation of RARs is a forceful stimulus to induce ETIA. This suggests that hyperinflation in acute asthma might be due, at least in part, to ETIA resulting from an imbalance between SAR and RAR activity.

Animals↗
PubMed1994

Continuous negative airway pressure increases tonic activity in diaphragm and intercostal muscles in humans.

The main objective of the present study was to quantify the increase in tonic inspiratory activity (delta TIA) in response to continuous negative airway pressure (CNAP) in humans. TIA represents the activity in inspiratory muscles at the end of expiration. In 20 subjects, electromyograms (EMGs) were recorded from the diaphragm and parasternal intercostal muscles (ICM) with surface electrodes during control and at three different levels of CNAP (-0.3, -0.6, and -0.9 kPa; 1 kPa approximately 10 cmH2O). From these recordings we determined delta TIA and the amplitudes of phasic EMG activities (EMGphas) during CNAP and control. To evaluate the effects of CNAP on functional residual capacity (FRC), respiratory frequency, tidal volume, and minute ventilation, the subjects were connected to a closed breathing circuit. When the pressure at the airway opening was -0.9 kPa, mean values of delta TIA were 53 and 49% of control EMGphas for the diaphragm and ICM, respectively. In addition, EMGphas at airway opening pressure of -0.9 kPa had increased to 195 and 162% of control EMGphas for the diaphragm and ICM, respectively. The concomitant decrease in FRC was on average 18.7% of predicted FRC. Minute ventilation had increased significantly (P < 0.05) at all levels of CNAP compared with control. We conclude that CNAP is a forceful stimulus to increase TIA in humans in both the diaphragm and the ICM.

Adolescent↗
PubMed1993

Tonic activity in inspiratory muscles during continuous negative airway pressure.

We studied tonic inspiratory activity (TIA) induced by continuous negative airway pressure (CNAP) in anaesthetized, spontaneously breathing cats. TIA in the diaphragm and parasternal intercostal muscles (ICM) was quantified in response to tracheal pressure (PTR) = -0.3 to -1.2 kPa. To differentiate between reflexes from rapidly adapting receptors (RARs), slowly adapting receptors (SARs) and C-fiber endings different temperatures of the vagus nerves (TVG) were used between 4 and 37 degrees C. At PTR = -1.2 kPa mean TIA values were 41% and 62% of peak inspiratory EMG activity of control breaths for the diaphragm and ICM, respectively. After vagotomy and for TVG < 6 degrees C CNAP did not induce TIA anymore. Changes in inspiratory and expiratory time during vagal cooling down to 4 degrees C confirmed the selective block of conductance in vagal afferents of the three types of lung receptors. We conclude that CNAP-induced TIA results from stimulation of RARs. Our data strongly indicate that stimulation of SARs suppresses TIA, whereas C-fiber endings are not involved in TIA at all. The results suggest that part of the hyperinflation in bronchial asthma may be caused by TIA in response to mechanical stimulation of RARs.

Airway Resistance↗
PubMed1992

Vagally mediated modification of inspiratory activity by changes in airway pressure.

The impact of varying the end-expiratory transpulmonary pressure (PE'tp) on phrenic (Phr) and parasternal intercostal (IC) activity early in inspiration was studied in 12 spontaneously breathing, anaesthetized cats. PE'tp was varied in a stepwise fashion by rapidly changing the tracheal pressure (Ptr) from ambient pressure to a pressure in the range between -1.2 and +1.2 kPa relative to ambient pressure, and vice versa. The amplitudes of integrated Phr and IC activity were determined in each breath at three particular points in time (t), corresponding to 0.1, 0.2 and 0.3 sec after the onset of Phr activity, respectively. For all three values of t, Phr and IC activity increased with a decrease in Ptr and decreased with an increase in Ptr. The relationships between Phr activity and PE'tp and between IC activity and PE'tp could be described satisfactorily by mono-exponential functions. An increase in PE'tp of 0.1 kPa resulted in a decrease in Phr activity of 16%, 13% and 12% for the 3 aforementioned values of t, respectively. For IC activity the corresponding values were 42%, 42% and 36%, respectively. After bilateral vagotomy no changes in Phr activity in response to changes in Ptr were observed any more, whereas the changes in IC activity had decreased to about one tenth of the corresponding values obtained before vagotomy. Apparently, extra-vagal mechanisms contribute for a small part to the effect of changes in PE'tp on IC activity. Our results indicate that relatively small changes in PE'tp may have a large impact on central inspiratory output.

Airway Resistance↗
PubMed1992

Conventional versus slug CO2 loading and the control of breathing in anaesthetized cats.

1. Conventional inspiratory CO2 loading (CCL) is accomplished by having the subject breathe CO2-enriched air. An alternative method of CO2 loading is to inject a bolus of CO2 at the start of each inspiration into the inspired air: slug CO2 loading (SCL). During SCL PCO2 in the conducting airways declines quickly towards 0 kPa in the course of inspiration, whereas PCO2 remains at a constant value equal to the inspiratory PCO2 during CCL. Therefore, CCL and SCL may stimulate the respiratory controller differently. 2. We compared the ventilatory responses to SCL and CCL in fourteen anaesthetized, spontaneously breathing cats. In each experimental animal we applied, in a fixed randomized order, five CCL experiments (fractional inspiratory CO2, FI,CO2 = 0.01-0.05), six SCL experiments (slugs of 50% CO2 ranging from 0.5 to 6 ml) and three control experiments in which no CO2 was loaded. Partial pressure of CO2 in arterial blood was determined from small blood samples (0.14 ml). In three cats we repeated the experiments after bilateral transection of the cervical vagi to evaluate the contribution of vagal receptors to the responses observed. 3. The average slope of the CO2 response curves for SCL was 2 times steeper than that for CCL (P less than 0.01). The larger minute ventilation for SCL for a particular value of arterial PCO2 (Pa,CO2) could not be attributed exclusively to the increased breathing frequency or the increased tidal volume (P greater than 0.10). Further, mean inspiratory flow (VI) was larger for SCL than for CCL at the same Pa,CO2 (P less than 0.01), also because the ratio TI/TE (inspiratory duration/expiratory duration) was smaller (P less than 0.01). After vagotomy the difference between SCL and CCL response curves was much reduced. 4. It is concluded that SCL and CCL affect the respiratory controller in a different way causing differences in breathing pattern and CO2 sensitivity between the two methods. Evidently, a mechanism based on CO2 sensitivity of pulmonary receptors is involved in the responses observed.

Anesthesia↗
PubMed1991

Vagal amplification of phrenic nerve activity at different levels of ventilation in spontaneously breathing cats.

The vagal amplification of phrenic nerve activity (APHR) was studied as a function of minute ventilation (VE) in 12 spontaneously breathing, anaesthetized cats. Increasing levels of VE were obtained by repeated venous administrations of 2,4-dinitrophenol. The APHR was obtained from the ratio of the phrenic nerve activities in a normal and in an occluded breath. The APHR is thought to be mediated by slowly and/or rapidly adapting stretch receptors. Because airway CO2 may inhibit the discharge of these receptors, we also investigated the influence on APHR of adding 1% and 2% by volume of CO2 to inspired gas. The results showed that an increase in VE had no influence on APHR. The values of APHR ranged from 0.95 to 1.31 and were on average 1.08. Low levels of CO2 in inspired gas did not influence APHR. Our findings suggest that the vagal amplification of central inspiratory output as determined from phrenic nerve activity has a constant gain and it seems to play a relatively unimportant role in sustaining hyperpnoeic breathing.

Animals↗
PubMed1987

Sleep in the domestic hen (Gallus domesticus).

Electrophysiological recordings were made of five closely observed hens, all permanently implanted with both EEG and EMG electrodes. Five behavioural postures were distinguished and percentages of wakefulness, sleep and presumably paradoxical sleep (PS) were determined during the third and sixth hour of the dark period. Substantial agreement was generally found between behaviour and sleep with the exception of sitting or standing motionless with at least one eye open. During two thirds of this behavioural posture, the EEG showed large amplitude slow waves undistinguishable from slow wave sleep. Characteristics of PS were determined: periods were short, whereas its percentage increased during the night. Furthermore, EMG atonia was never found. An all night recording was made, and delta activity (2-5 Hz) was filtered and plotted against time for three of the hens. A significant decrease in delta activity across the night was found. Differences and similarities between sleep in hens and in mammals are discussed. Although large similarities exist it is concluded that some properties of birds' sleep make it unique and are a challenge for further study.

Animals↗
PubMed1986

Immunocytochemical identification and localization of peptide hormones in the gastro-entero-pancreatic (GEP) endocrine system of the mouse and a stomachless fish, Barbus conchonius.

A large number of antisera mainly raised against mammalian hormones are tested immunocytochemically on the GEP-endocrine system of mouse and fish (Barbus conchonius). The endocrine pancreas of mouse and fish appeared to contain the same four endocrine cell types; insulin-, glucagon-, PP- and somatostatin-immunoreactive cells. In mouse about 13 GEP endocrine cell types are distinguished: 1. insulin-, 2. somatostatin-, 3. glucagon-, 4. PP-, 5. (entero)glucagon-/PP-like, 6. CCK-like, 7. substance P-, 8. neurotensin-, 9. VIP-, 10. gastrin-, 11. secretin-, 12. beta-endorphin-, 13. serotonin-immunoreactive cells. Based on this and a previous study at least 13 GEP endocrine cell types seems to be present in stomachless fish: 1-9 as described for mouse, 10. (entero)glucagon-like, 11. met-enkephalin, 12. VIP-like, 13. unspecific immunoreactive endocrine cells. Coexistence of glucagon and PP-like peptides is found in the gut and pancreas of mice and in the gut of B. conchonius. In mouse pancreas and fish gut, endocrine cells showing only PP- or glucagon-like immunoreactivity are found too. In mouse stomach some endocrine cells showing only PP-immunoreactivity are demonstrated. In the same region coexistence of C-t-gastrin- and FMRF-amide-immunoreactivity is found in endocrine cells. The importance of these phenomena are discussed. Enteric nerves immunoreactive with antisera raised against substance P and GRP are found in mouse, against somatostatin and met-enkephalin in both mouse and fish and against VIP in fish.

Animals↗
PubMed1986

Electrophysiological evidence for a sex difference in neural regulation of prolactin secretion in rats.

Prolactin (PRL) secretion patterns were determined in freely moving male and female rats chronically fitted with electrodes in the sexually dimorphic component of the medial preoptic area (MPOA) and the median eminence (ME), together with a chronic atrial blood sampling catheter. Electrodes made of stainless steel or platinum-iridium were implanted bilaterally. Female rats with 4 electrodes in the ME exhibited an attenuated surge of PRL secretion on proestrus (injured group), rats with 2 electrodes in the ME had a normal proestrous surge (intact group). Basal PRL levels were not different between the two groups. Stimulation (100-Hz voltage pulses, 0.2 ms width, 10 s on/5 s off, total duration 25 min) did not produce lesions. Evidence is presented that experimentation was performed without stress. Electrical stimulation applied to the MPOA increased PRL secretion in males, decreased PRL secretion in proestrous females and was without effect in conscious or anesthetized diestrous females. Electrical stimulation applied to different locations of the ME was without effect in male and diestrous female rats; it reduced PRL secretion in proestrous females. These data demonstrate that the MPOA has a sexually differentiated function in the regulation of PRL secretion. The data do not provide evidence for a sexual dimorphism in prolactin-inhibiting factor and prolactin-releasing factor activity in the ME.

Animals↗