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Biomedical subjects

H Folgering

Publications and source records attributed to H Folgering.

At least 91 records · Page 5Linked to original sources
PubMed1983

Diving bradycardia is not correlated to the oculocardiac reflex.

Both facial immersion in cold water and pressure on the eyeball cause reflex bradycardia. These reflexes are called diving reflex and oculocardiac reflex, respectively. The latter is sometimes used in diving medicine to estimate the risk of severe diving bradycardia. The purpose of this study was to quantify the effects of both reflexes on heart rate in 15 subjects. All subjects performed four tests: (1) breath-holding (2) breath-holding and facial immersion in water of 10 degrees, 15 degrees, and 20 degrees C; (3) facial immersion in water and snorkeling; (4) application of pressure of 30, 50, and 70 mmHg on the eyeball. In seven subjects an additional test was done: (5) eyeball pressures during breath-holding. It was shown that the intensity of the oculocardiac reflex is not a good indication of the bradycardia that can be expected during diving. It is proposed that breath-holding with facial immersion in water of 20 degrees C or colder during at least 10 s is a more appropriate test to assess the possibility of severe diving bradycardia and cardiac arrhythmias.

Adult↗
PubMed1983

Time course of posthyperventilation breathing in humans depends on alveolar CO2 tension.

The time course of the decrease in ventilation immediately after 1 min of voluntary isocapnic hyperventilation was studied in eight healthy subjects. The hyperventilation tests were done at three different levels of alveolar CO2 tension (PACO2), and at each PACO2 level with a fixed respiratory frequency and with a freely chosen (increased) frequency. The time constant of the decrease in ventilation after free-frequency hyperventilation was inversely related to the PACO2, with a regression equation of tau 1 (s) = 78.6 - 1.2 PACO2. After the fixed-frequency hyperventilation, the time constant of the decrease in ventilation was virtually zero and independent of PACO2. These results do not agree with earlier findings in anesthetized animals. The fact that hypocapnia increases the excitability of neurons might explain the findings. The extreme respiratory afterdischarge phenomenon in hypocapnic patients suffering from the hyperventilation syndrome is consistent with the outcome of this study.

Adult↗
PubMed1983

Beta-blockade in the hyperventilation syndrome. A retrospective assessment of symptoms and complaints.

The effect of beta-adrenergic blockade on ventilatory parameters and on subjective complaints was studied in 73 patients suffering from hyperventilation syndrome. The beta-blockade made the PA,CO2 increase as much as tranquillizer therapy. No effect of any kind of therapy was found on the subjective complaints. A remarkable dissociation was found between the measured ventilatory parameters and the quantified subjective complaints. It is concluded that beta-blockade is an effective therapy for the basic problem of hypocapnia in the hyperventilation syndrome; in this respect it is to be preferred over other therapies such as tranquillizers.

Adult↗
PubMed1982

Arterial chemoreceptor inhibition by a single inspirate containing carbon monoxide is accounted for by raised arterial PO2.

Carbon monoxide (CO) slugs (10--100 ml) injected into the inspired air of 6 hypoxic, anaesthetized cats reduced carotid body chemoreceptor discharge. The inhibition was invariably associated with a sharp rise in Pa, O2 which was continuously recorded by a fast responding intravascular electrode. This suggests that CO in solution in the blood leaving the lungs displaces O2 from blood after it was left the exchange region and that the displaced O2 raises the Pa, O2 and inhibits chemoreceptor discharge. Our results provide no support for the idea that a haemoglobin-like pigment is involved in the mechanism of arterial chemoreceptor excitation.

Action Potentials↗
PubMed1982

Adrenergic mechanisms and chemoreception in the carotid body of the cat and rabbit.

1. The effect of beta-adrenergic and dopaminergic agonists and antagonists on the chemoreceptor response to graded hypoxia and hypercapnia was tested in nineteen cats and ten rabbits anaesthetized either with chloralose-urethane or pentobarbitone sodium, paralysed with pancuronium bromide and artificially ventilated.2. The inhibitory action of dopamine was confirmed. The inhibition following intra-arterial bolus injection was blocked by haloperidol; dopamine then excited and this excitation was blocked with propranolol. Adrenaline or noradrenaline caused a transient inhibition followed by a marked excitation. The inhibition was blocked with haloperidol and the excitation blocked with propranolol or metoprolol. Isoprenaline excited without inhibition and this was blocked with propranolol or metoprolol.3. A novel finding was that the chemoreceptor response to hypoxia was markedly reduced or even abolished with propranolol or metoprolol. The response was enhanced with a constant infusion of isoprenaline, adrenaline or noradrenaline in proportion to the degree of hypoxia, an effect mimicked by raising CO(2). The chemoreceptor response to hypoxia was similarly enhanced by haloperidol and depressed by a constant infusion of dopamine in proportion to the degree of hypoxia.4. The effect of these drugs on the chemoreceptor response to hypercapnia was less constant. In the majority of tests the aminergic agonists and antagonists caused a parallel shift of the CO(2) response curves in the same direction as the O(2) response curves and by amounts proportional to the degree of hypoxia. In some tests these drugs caused a change in the slope of the CO(2) response curves but only if P(a, O2) was less than 60 mmHg.5. One interpretation of these results is that hypoxia exerts a presynaptic action, causing the release of noradrenaline and dopamine from Type I cells, and that these substances act upon aminergic receptors on the sensory fibre, causing a change in potential and discharge frequency proportional to the rates of dopamine and noradrenaline release.6. An additional or alternative interpretation is that O(2) and CO(2) (the latter most probably acting on intracellular pH) alter the sensitivity of the aminergic receptors to their agonists.

Action Potentials↗
PubMed1981

Beta-adrenergic drugs do not affect phrenic nerve afterdischarge.

In anesthetized cats, a carotid sinus nerve was stimulated electrically. After this stimulation the time course of the afterdischarge in the phrenic nerve activity was studied in the control situation, during infusion of isoprenalin and after administration of metoprolol. The time courses were identical in all situations. It is concluded that in spite of the fact that the beta-adrenergic drugs change the steady state phrenic activity, the afterdischarge is unchanged and therefore probably mediated by a separate mechanism. A comparison is made with analogous findings in patients with a hyperventilation syndrome.

Adrenergic beta-Agonists↗
PubMed1981

Beta-blocker therapy with metoprolol in the hyperventilation syndrome.

16 patients suffering from a hyperventilation syndrome were treated with metoprolol 2dd 100 mg and an identical placebo in a double-blind, cross-over trial. Before therapy and after metoprolol and placebo therapy a ventilatory response to CO2 was taken, VC and FEV1, a hyperventilation provocation test, blood gas values, and the subjective experiences of the patients were documented. The ventilatory response to CO2 was described in terms of decrease or increase of ventilation: before therapy ventilation decreased in 10 out of 16 patients, after metoprolol ventilation decreased in 3 of 16 patients (p less than 0.01). The end tidal PCO2 increased with a mean of 3.86 mm Hg (p = 0.0005) after metoprolol as compared to placebo. No differences were found in respiratory frequency or depth, base excess, provocation test. It is concluded that the cardioselective beta-blocker metoprolol is a useful drug in the therapy of the hyperventilation syndrome.

Adult↗
PubMed1980

Maximal exercise power after a single dose of metoprolol and of slow-release metoprolol.

The treatment of hypertension with a single daily-dose of a beta-blocker gives rise to high peak-plasma concentrations 1.5 h after ingestion. After slow release-preparations of beta-blockers, the peak concentrations are half those produced by the conventional preparation at the same oral dose. A frequently occurring side-effect of beta-blocker therapy is fatigue. In this study the effect of a single dose of metoprolol 300 mg, 200 mg, 200 mg slow-release and a placebo on maximal exercise power was tested in 6 healthy subjects, 1.5 h and 24 h after ingestion. Maximal exercise power was significantly reduced 1.5 h after ingestion of metoprolol 300 mg and 200 mg. No change was found 1.5 h after 200 mg of a slow-release preparation. The possible reasons for reduced maximal exercise power are discussed. It is concluded that use of a beta-blocker for the treatment of hypertension in a single daily-dose regimen may be a reason to prefer a slow-release preparation.

Adult↗
PubMed1980

The dynamic effect of PETCO, on vertebral bloodflow in cats.

The central chemoreceptors are excited by the composition of the interstitial fluid of the brainstem. The concentration of the constituents is influenced by the perfusion ratio in that area and the composition of the arterial blood, in articular PaCO2. We assessed the perfusion ratio in cats by measuring the blood flow in one vertebral artery and its dependence on changes in PETCO2. Our findings support the theory that CBF is controlled by extravascular pH during CO2-loading. The mean time constant for dilatation (tau = 339.2 s) was found to be considerably greater than the mean time constant for constriction (tau = 40.9 s). Neither time constant depends on the initial flow rate.

Animals↗
PubMed1980

Clomipramine treatment of hyperventilation syndrome.

Six patients suffered from a hyperventilation syndrome for 3.4 +/- 1.2 years. They had a lowered PAco2 at rest and an abnormal CO2 response curve. During the entire period they had received unsuccessful treatment with anxiolytics, and had also undergone behaviour therapy for the last 1 -- 2 years without success. Both treatments were discontinued and the patients were placed on clomipramine, 25 mg t.i.d. for 9 months. Their anxiety and hyperventilation attacks diminished after one month of clomipramine, and their fear of attacks an their phobias subsided after two months. Eighteen months after clomipramine therapy had been initiated, they were feeling well without medication. The possible mode of action of clomipramine on the hyperventilation syndrome via central serotonergic mechanism is discussed.

Adult↗
PubMed1980

Central beta-adrenergic effects on the control of ventilation in cats.

beta-Adrenergic mimetics and blockers, as well as a local anesthetic (xylocaine) were infused into the vertebral artery of paralyzed and artificially ventilated cats. The effects of the drugs on the central control of ventilation was assessed by measuring the changes in phrenic nerve activity. beta-Mimetics [isoprenaline (1 and 2), metroprolol (1), oxprenolol (1 and 2)] decreased the phrenic nerve activity. beta 2-Mimetics (Salbutamol) and blockers (Butoxamine, H 35/35) had no clear effects. The mode of action of the beta-blockers is most probably not by their local anesthetic properties. It is concluded that beta-adrenergic mechanisms in the brain stem stimulate the ventilatory control system. The receptors are most probably beta 1-receptors.

Adrenergic beta-Agonists↗
PubMed1980

Ventilatory response to hypercapnia in normal subjects after propranolol, metoprolol and oxprenolol.

Steady state ventilatory response curves to CO2 were taken in 8 normal subjects in control situations and taking clinical doses of propranolol, oxprenolol and metoprolol in a double-blind crossover design. Furthermore, the expiratory peak flow was measured. No effect was found of any of the beta-blockers on the resting ventilatory parameters, the sensitivity to CO2 or the peak flow values.

Adult↗
PubMed1979

Stimulation of phrenic nerve activity by an acetylcholine releasing drug: 4-aminopyridine.

The effect of the acetylcholine releaser 4-aminopyridine on ventilation was studied by recording and quantifying the efferent phrenic nerve activity in 40 paralysed and vagotomized cats; with arterial Po2, PCO2 and pH kept constant. 4-Aminopyridine, given intravenously or in the vertebral artery, stimulates the phrenic nerve activity in a dose dependent manner. The stimulatory effects of 4-aminopyridine on the phrenic nerve activity could be abolished completely by administration of high doses of atropine. We conclude that 4-aminopyridine, which is used clinically for the reversal of a neuromuscular block, stimulates the phrenic nerve activity. Since the role of cholinergic mechanisms in the central chemoreception has been well established, the effect on the phrenic nerve activity is most probably by an increased release of acetylcholine at the site of the central chemoreceptors.

Aminopyrine↗
PubMed1979

The steady state response of brainstem respiratory neuron activity to various levels of PA,CO2 and PA,O2.

Extracellular recordings were made of 52 respiratory neurons in the brainstem of cats, anesthetized (chloralose-urethane), vagotomized and artificially ventilated. Phrenic nerve activity was recorded and quantified as an index of the output of the respiratory neuronal organization in the brainstem. The unit activity was quantified by using the modal spike frequency as a possible indication of the activating effect of one unit on other respiratory neurons (Smolders and Folgering, 1979). Inspiratory neurons showed the strongest reaction to changes in PA,CO2 and/or PA,O2. Expiratory neurons and frequency modulated neurons responded less to changes in chemical drive. Phase spanning neurons did not show any consistent response. Four out of ten continuously firing neurons without any respiratory rhytmicity increased their firing frequency when PA,CO2 was increased. Apart from the increase in modal spike frequency, the respiratory neuronal organization also reacted with an increase in active units (recruitment) when the chemical drive was increased. The relationship between quantified phrenic nerve activity and spike frequency was independent of the stimulus (hypercapnia or hypoxia). A model was developed in which the increase in modal frequency of a unit arouses other units: when the chemical drive increases, progressively more units tend to be recruited into the respiratory neuronal organization in the brainstem.

Action Potentials↗
PubMed1978

Respiratory oscillations of the arterial PO2 and their effects on the ventilatory controlling system in the cat.

The respiratory oscillations of the arterial PO2 were measured in paralyzed, artificially ventilated cats by a small (1.2 mm) fast-responding catheter oxygen electrode. The amplitude of these oscillations could be changed independently of the mean PA,O2n by a specially designed respirator circuit. deltaPaO2 was shown to increase with increasing tidal volume or decreasing frequency of the respirator, and with increasing mean PaO2. The amplitude of the oscillations was attenuated considerably from the left atrium to the aorta. No attenuation occurred from the aorta to the carotid artery, provided that the blood flow in the carotid artery was not impeded. The measured attenuation of the oscillations was compared to that calculated by Yokota and Kreuzer (1973) and found to be quite different. The output of the ventilatory controlling system of the cat was measured from the quantified phrenic nerve activity. When only deltaPaO2 was changed at a constant level mean PaO2, the quantified phrenic nerve activity did not change, indicating that the amplitude of the oscillations does not influence the ventilatory controlling system. In vagotomized animals, the periodicities of the oscillations and the phrenic nerve activity were completely dissociated. From the fact that no Cheyne-Stokes type of breathing occurred, it was concluded that the effect of timing is negligible.

Animals↗
PubMedDate not supplied

Occupational health and general practice: from opportunities lost to opportunities capitalised?

BACKGROUND AND AIM: Western populations are in the middle of the epidemiological transition of chronic diseases. Care of patients with chronic disease is directed at optimising life expectancy and quality of life. Daily and social functioning, including paid work are part of the treatment objectives. Yet, advice for and support in work related coping with chronic diseases, and collaboration with occupational health are not--yet--part of routine curative medical care procedures. This is also the case in general practice, where most patients with chronic conditions are treated. This 'blind spot' signals a generic lost opportunity in optimizing the care of patients with chronic disease. This paper analyses from empirical data the importance of integrating work-related advice and support in general practice and explores potential evidence of the benefits this provides for patients: the opportunities that can be capitalised through better interaction between occupational physicians (OP) and general practitioners (GP). METHODS: The paper is based on a review of three sources: (i) Epidemiology of chronic diseases: the Nijmegen Continuous Morbidity Registration; (ii) The relevant guidelines of the Dutch College of General Practitioners; (iii) Studies of work-related implications of asthma and COPD management of GPs of the Nijmegen centre of Evidence-Based Practice. RESULTS: Chronic diseases like cardiovascular disease, diabetes mellitus, COPD and asthma dominate general practice and lead annually to a large number of consultations. Although a majority of patients are 65 years or older--in particular for the first three diseases--GPs also care for a substantial number of under-65 years old. General practice guidelines for these disorders advocate care directed at normal functioning but do not systematically address functioning in the working place. Analysis of work-related functioning in case of chronic respiratory diseases, however, highlight that work-related factors and circumstances play an important role in patients' coping strategies. Patients tend to ignore negative effects of their workplace on their physical condition and as a consequence suffer undue limitations. Despite these work related risks, COPD patients who were in paid employement perceived higher quality of life than COPD patients who were disabled for work, but had similar disease severity (airway obstruction). Interestingly, a programme of patients' self-management of asthma resulted, in comparison to GP-supervised usual care in a substantial and lasting reduction of asthma related absence from work and other social-daily activities. CONCLUSIONS AND DISCUSSION: All consultations with employees with a chronic (respiratory) disease can be considered as opportunities to supervise work-related implications of the disease. Patients value their ability to work but frequently apply inefficient coping through ignoring the implications of their circumstances for their disease. A more efficient coping can probably be achieved through a more active involvement of patients in managing their own disease. Guidelines--like the Dutch College of General Practitioners'--have developed into a sophisticated and generally respected system of guidance of patient care. Explicit emphasis of management in relation to the workplace may present a logical opportunity to capitalise on.

Absenteeism↗
PubMedDate not supplied

Ventilatory function and continuous high thoracic epidural administration of bupivacaine with sufentanil intravenously or epidurally: a double-blind comparison.

Variables of ventilation were obtained preoperatively and during the first two postoperative days in 28 patients after thoracic surgery. All patients received 0.5% bupivacaine with epinephrine, 5 micrograms.ml-1 (5-10 ml), through an epidural catheter at the thoracic level supplemented by light general anesthesia. One hour after the initial dose of bupivacaine, patients were randomly allocated to one of two groups: an epidural (EP) sufentanil and an intravenous (IV) sufentanil group. Both groups received 0.125% bupivacaine via continuous epidural infusion postoperatively for three days. In addition, the EP group received 0.83 micrograms.ml-1 sufentanil added to the epidural infusion of 5-10 ml.hour-1, while the IV group received an identical dose of sufentanil via continuous intravenous infusion of 5-10 ml.hour-1. The ventilatory response to 5% CO2 was analyzed preoperatively and on postoperative Days 1 and 2. No significant depression in ventilatory response to CO2 could be detected by measurement of minute ventilation and mouth occlusion pressure at 100 milliseconds (P0.1). Pain measurement was assessed by blinded observers using the Inverse Visual Analog Scale, where 0 signifies most pain and 10 signifies least pain. The mean scores were above 7 in both groups and were attained at similar analgesic requirements. The incidence of side effects was not different. Only the initial mean sufentanil plasma levels in patients of the IV group were higher than those of the EP group. This study shows that the variables of ventilation were not affected by sufentanil administered via the epidural or the intravenous route, and that both techniques provided excellent pain relief when employed to supplement low-dose 0.125% bupivacaine epidurally.

Adult↗