[Neurologic diseases are common cause of dysphagia].
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Brain Diseases↗
Biomedical subjects
H Nilsson
Publications and source records attributed to H Nilsson.
Quantification of heat balance during work in three types of asbestos-protective clothing.
Three types of protective suits for asbestos removal work were tested in a climatic chamber at two ambient temperatures, 25 degrees and 36 degrees C. Four subjects performed 50 min of bicycle exercise at 90 W dressed in shorts, socks and sneakers (NoPS). The same test was carried out with three different types of asbestos-protective suits worn on top of NoPS. Suits were made of GoreTex (GT), polypropylene (PP) and Tyvek (TYV). At 25 degrees C, responses differed very little between suits and thermal strain was small. At 36 degrees C, strain was least with NoPS. TYV resulted in significantly higher physiological and thermal strain than did PP and GT. Evaporative heat loss was maintained at a similar level with less permeable ensembles, but at the expense of increased skin wetness and sweat rate. Measured values compared favourably with calculated values for skin wetness and sweat rate according to ISO 7933, when resultant, rather than standard, basic data for insulation and evaporative resistance of ensembles were used. Results indicate that differences between suits that may be of little importance at normal room temperature become significant at higher stress levels (increased activity and/or air temperature).
Asbestosis↗
Inositol phosphates and phosphoinositides in rat liver nodules.
Total amounts and turnover rates of phosphoinositides and inositol phosphates in normal rat liver and hepatocyte nodules were investigated. Male Wistar rats were injected i.p. with [3H]inositol 18-20 h before killing. The amount of phosphatidylinositol in a homogenate preparation was roughly doubled in the nodules, though levels of polyphosphoinositides were approximately the same. Basal levels of inositol phosphates were the same in nodules and in normal liver. Turnover rates of inositol tris- and tetrakisphosphates were studied after stimulation of intact cells with vasopressin for different periods of time (0-5 min). The initial rate of formation of inositol trisphosphate after agonist exposure was fast in both nodular and normal cells. Nodular cells reached peak amount of inositol trisphosphate at 2.5-fold basal levels after 20 s, while normal cells peaked after 40 s at 4.5 times the basal amount. The level of inositol tetrakisphosphate was enhanced very quickly in normal cells, but in the nodular cells there was no increase of this inositol phosphate after vasopressin stimulation. To investigate the mechanism of this difference, the activities of inositol 1,4,5-trisphosphate kinase and of inositol 1,4,5-trisphosphate phosphatase were studied. Both activities were rapid and equal in nodules and normal liver. The amount of cell surface receptors for vasopressin was shown to be one-third in the nodules, as compared to normal cells. This quantitative decrease in receptor number was reflected in lower formation of inositol trisphosphate when stimulated with vasopressin, but could not explain the loss of inositol tetrakisphosphate response in nodules. The significance of the reported alterations in second messenger traffic for the growth regulation of nodular cells and for their progression to carcinoma is not yet known, but could add to the nodules being less dependent on growth regulating signals.
Animals↗
Syncope--brain or heart? A case report.
A 44-year-old man suffered from recurrent episodes of unconsciousness, without any other concomitant manifestations. After routine workup, EEG and CT had proven nondiagnostic, prolonged Holter monitoring revealed a single episode of asystole, lasting 7.6 seconds. A pacemaker was inserted but did not abolish his episodic syncope. Subsequently, long-term EEG recording revealed epileptiform activity with independent foci in both temporal lobes. Antiepileptic treatment relieved the patient of his symptoms. This case illustrates the intimate relationship between the heart and the brain that sometimes lies behind syncope.
Adult↗
Effect of chronic ethanol consumption upon cardiovascular reactivity, heart rate and blood pressure in spontaneously hypertensive and Wistar-Kyoto rats.
OBJECTIVE: Clarification of the effect of chronic ethanol consumption upon cardiovascular reactivity in rats. DESIGN: Spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) normotensive rats were randomly allocated in groups of 10 to ethanol in tap water [20% (v:v) after the first week or tap water for 7-12 weeks]. METHODS: Intra-arterial blood pressure and heart rate were measured at rest and in response to vibration and noise stress. Vascular reactivity was assessed in isolated paired perfused hindquarters and in mesenteric arterioles in a Mulvany-Halpern myograph. RESULTS: Resting intra-arterial blood pressure but not heart rate was lower in both ethanol-treated groups. The ethanol treatment increased the SHR heart rate response to sudden noise but the WKY response did not increase. Pressor responses to noise were initially greater in the ethanol-treated SHR. The ethanol had no effect upon isolated perfused hindquarter resistance at maximal dilation, dose-response curves in response to noradrenaline or vasopressin, or maximal contractile strength. Isolated mesenteric arterioles showed that ethanol had no effect upon responses to nerve stimulation or upon the 50% effective dose required for a response to noradrenaline or vasopressin. CONCLUSIONS: Ethanol treatment heightened the heart rate reactivity to stress without substantially affecting vascular neuro-effector characteristics in SHR. This is likely to be a central effect, caused by suppression of the central nervous inhibitory systems that influence the heart rate and baroreflex activity in a strain of rat already showing evidence of an impaired ability to modulate the heart rate and blood pressure in response to stress. The small reduction in resting blood pressure may be a consequence of the lower weight in the ethanol-treated rats, and/or may reflect a direct depressing action by the alcohol on vascular and cardiac muscle. These findings are discussed in the context of ethanol-induced hypertension in humans and possible genetic variations in central nervous, cardiac and vascular effects.
Alcoholism↗
Incidence of work-related disorders and absenteeism as tools in the implementation of work environment improvements: the Sweden Post strategy.
In 1989, a comprehensive, five-year work environment project (Postal Work Environment [PWE] 2000) was launched by Sweden Post (SP). Its purpose was to identify the jobs and employees with the most exposed work environments and, in conjunction herewith, to initiate remedial programmes. Standardized interviews with a selection of employees and statistical and epidemiological evaluation of illness absenteeism and occupational injuries served as input data for devising different measures of work-related ill health (subjective complaints, symptoms, illness, illness absenteeism, and occupational injury). The results provided an incentive to regional action programmes, in which 'risk areas and risk occupations' were correlated with the load factors, primarily in ergonomic and work organization areas, cited in interview replies. In its regional efforts. PWE 2000 served as a stimulus/catalyst in the implementation of various regional action programmes.
Absenteeism↗
The effect of felodipine on cold-induced digital vasospasm.
Felodipine, a calcium antagonist with pronounced vascular selectivity, was given to 10 patients with cold-induced, digital vasospasm. Placebo and increasing doses of felodipine (2.5, 5, and 10 mg b.i.d.) were given for 2 weeks each. There was a significant decrease in systemic, but not in digital, blood pressure and a significant increase in heart rate during felodipine treatment. The subjective rating of symptoms improved significantly on all doses. No significant effect on cold-induced digital vasospasm during local cooling to 15 and 10 degrees C was registered. Typical side effects of calcium-entry blockers were reported. Moreover, two postmenopausal women reported recurrence of menstrual bleeding and one woman reported vaginal hemorrhagic discharge during treatment. In conclusion, felodipine, although causing a significant, symptomatic relief, had no significant effect on cold-induced digital vasospasm when objective measures were used.
Blood Pressure↗
Transmitter characteristics of small mesenteric arteries from the rat.
We have studied the neurogenic response of small mesenteric arteries from the rat to evaluate the involvement of possible co-transmitters under various modes of stimulation. Segments of small branches of the mesenteric artery were mounted in a myograph and the intramural nerves were activated with transmural electrical stimulation. A single stimulation of the nerves caused a contraction that was reduced by only 20% in the presence of adrenergic blocking agents (prazosin or phenoxybenzamine), whereas the steady-state response to continuous nerve stimulation of high frequency was reduced by 90-95%. In contrast, all responses to applied noradrenaline in doses up to at least 1 mM were eliminated by phenoxybenzamine treatment. The stable ATP analogue, alpha,beta-methylene ATP, reduced the response to a single nerve stimulation by 70%, but reduced the contraction caused by continuous high-frequency nerve stimulation by only 10%. None of these agents affected the response to applied neuropeptide Y (NPY). The response of relaxed vessels to nerve stimulation was totally blocked by the combination of an adrenoceptor-blocking agent and alpha,beta-methylene ATP, although even in this situation a further neurogenic response could be revealed in vessels precontracted with vasopressin. Responses to either single stimuli or brief burst stimulations were potentiated after high-frequency stimulation. Both the adrenergic and non-adrenergic components were enhanced to roughly the same extent. Also the potentiated response was eliminated by the combined application of prazosin and alpha,beta-methylene ATP. The non-adrenergic transmitter in the sympathetic nerves of small arteries thus appears to be the dominant transmitter during low-frequency nerve stimulation, causing rapid but phasic activation. Noradrenaline is the most important transmitter for higher frequencies, exerting slower but sustained contractions. The post-stimulatory potentiation affects both the adrenergic and the non-adrenergic part of the neurogenic response.
Adenosine Triphosphate↗
Endothelium-independent potentiation by neuropeptide Y of vasoconstrictor responses in isolated arteries from rat and rabbit.
An endothelium-dependent action of neuropeptide Y (NPY) has been implicated in studies on various vascular beds. In the present study, the requirement of an intact endothelium for NPY-evoked potentiation of the response to sympathetic nerve stimulation was determined in the small mesenteric arteries of the rat and in the central ear artery of the rabbit. Further, NPY-mediated inhibition of relaxing influences was determined in small mesenteric arteries of the rat. Vascular segments were mounted in a double myograph, where one of the two suspended vessels was denuded of endothelium by gently rubbing the intimal surface. Removal of endothelium was verified by en-face silver staining. In both species, the response to bursts of transmural field stimulation eliciting 10% of maximal contraction was potentiated 2-4 times in the presence of 10 nM NPY, whether the endothelium was present or not. In small mesenteric arteries precontracted with noradrenaline, addition of acetylcholine (I microM) caused relaxation only in vessels with an intact endothelium. Subsequent addition of 10 nM NPY enhanced vasoconstriction in both intact and endothelium-denuded vessels. The endothelium-independent beta-adrenergic agonist isoprenaline (I microM) relaxed both intact and denuded small mesenteric arteries, and in both further addition of 10 nM NPY increased the contraction to about the same extent. The results demonstrate that NPY potentiates the responses to sympathetic field stimulation in small mesenteric arteries from the rat and in central ear artery from rabbit whether the endothelium is present or not. NPY inhibits both endothelium-dependent and -independent relaxations in small mesenteric arteries from rat.
Animals↗
Sympathetic transmission in small mesenteric arteries from the rat: influence of impulse pattern.
We have previously studied the transmitters involved in, and the calcium dependency of, the neurogenic response to continuous, regular nerve stimulation in small mesenteric arteries from the rat. We have now studied responses to irregular nerve stimulation in these respects. Small mesenteric arteries from rat were mounted into a myograph and the intramural sympathetic nerves were activated by field stimulation. Irregular nerve stimulation was patterned after recorded activity in human cutaneous nerves. The response to irregular stimulation was reduced by only approximately 50% in the presence of the alpha 1-adrenoceptor antagonist prazosin. In particular, responses to low-frequency stimulation were resistant to prazosin. When the extracellular calcium concentration was reduced from 2.5 to 1.0 mM, approximately 50% of the response to irregular nerve stimulation remained. Responses to low-frequency stimulation were particularly reduced. Thus in these arteries the neurogenic response is caused by noradrenaline and a, perhaps purinergic, co-transmitter. The co-transmitter is important for the response to low-frequency stimulation and for the initial part of the contraction caused by high-frequency stimulation. Reducing the calcium concentration affects more strongly the response to low-frequency nerve stimulation.
Animals↗
Vascular adrenergic responses in morphine-dependent rats.
The circulatory effects of morphine abstinence have recently been found to involve decreased renal sympathetic nerve activity and increased mean arterial pressure, induced by vasoconstriction. A direct influence of morphine withdrawal on the peripheral vasculature could possibly contribute to the increased resistance. Therefore, contractile responses to transmural nerve stimulation and to applied noradrenaline of peripheral arteries from morphine-dependent and untreated rats were examined in vitro under paired conditions. No increase in contractile response was observed after chronic morphine treatment, either on nerve stimulation or on applied noradrenaline. Instead the smooth muscle sensitivity to adrenergic stimulation was reduced. Consequently, the present study does not support a peripheral adrenergic origin of the vasoconstriction during naloxone-precipitated morphine abstinence.
Animals↗
Induction of mRNA for HLA-DR beta in human keratinocytes cocultured with interferon-gamma.
Explanted human keratinocytes exposed in vitro to recombinant interferon-gamma (IFN-gamma) were investigated for the appearance of mRNA for HLA-DR. Using in situ hybridization with a (35S)UTP-labelled HLA-DR beta cRNA probe, mRNA-positive cells were detected already within 6 h with maximal numbers of positive cells as well as the amount of mRNA per cell after 48 h. The corresponding protein HLA-DR, as analysed by immunoperoxidase staining, was detected on 20%-40% of the cells after 24 h and on almost all cells within 48 h. The expression of HLA-DQ and -DP antigens were always exceeded by that of HLA-DR. Whereas an increase in the concentration of IFN-gamma above 50 U/ml did not affect the maximal level of HLA-DR reactive cells, there was a fourfold increase in the frequency of cells reactive with HLA-DQ and a twofold increase for HLA-DP when the IFN-gamma concentration was raised from 50 to 500 U/ml. When IFN-gamma was withdrawn from the cultures, HLA-DR mRNA and protein synthesis ceased--indicating the continuous need for IFN-gamma to maintain the HLA-DR synthesis in keratinocytes.
DNA↗
The effect of isradipine, a new calcium-channel antagonist, in patients with primary Raynaud's phenomenon: a single-blind dose-response study.
Isradipine is a new potent calcium-channel blocking agent with highly selective action on peripheral vessels. In this single-blind study, its dose-related effect on cold-induced changes in finger systolic pressure (FSP) was investigated in ten female patients with primary Raynaud's phenomenon, and the side effects of isradipine treatment were evaluated. The patients were studied during 9 weeks of treatment. After 3 weeks of placebo, isradipine was given in doses of 1.25 mg b.i.d. and 2.5 mg b.i.d. for 3 weeks each. FSP was measured on local finger cooling to 10 degrees C. FSP at 10 degrees C expressed in percent of the value of 30 degrees C increased from 21 +/- 16% (M +/- SD) after placebo to 42 +/- 28% (p less than 0.05) and 62 +/- 25% (p less than 0.001) after treatment with isradipine 1.25 mg and 2.5 mg b.i.d., respectively. The subjective efficacy of the treatment was assessed with a visual analogue scale (VAS). The VAS rating increased from 17 (range 0-66) after placebo to 39 (range 12-88) (NS) and 68 (range 25-99) (p less than 0.001) after isradipine treatment with 1.25 mg and 2.5 mg b.i.d., respectively. Adverse effects of isradipine therapy were few and did not differ from those reported after the placebo period. This single-blind, dose-response study showed that isradipine in doses of 1.25 mg and 2.5 mg b.i.d. had favorable objective and subjective effects in patients with primary Raynaud's phenomenon and had no serious side effects.
Adult↗
Thermal function of a clothing ensemble during work: dependency on inner clothing layer fit.
A tight-fitting crewneck undergarment (U) and a loose-fitting shirt (S) were studied as part of a commonly used clothing ensemble (Itot = 0.22 m2 K W-1). Ten clothed male subjects performed standardized packing work (VO2 = 0.761 min-1) at three climatic conditions, 20 degrees C and Va = 0.45 m s-1 (0-30 min), at 5 degrees C and Va = 0.39 m s-1 (30-60 min) and at 5 degrees C and Va = 1.23 m s-1 (76-90 min). From 60-75 min the subjects rested at 20 degrees C. The physiological and subjective responses varied with the environment from slightly warm to cool. U resulted in warmer responses than S: torso and upper arm skin temperatures were higher at both 5 degrees C and 20 degrees C, evaporation rate was higher at 20 degrees C, mean skin temperature was higher during work at 20 degrees C, sweating tended to begin earlier and skin wettedness to be higher with U than with S. No differences were observed in core temperature, heart rates, and subjective thermal evaluations. It was concluded that a tight-fitting inner layer (U) compared to a loose-fitting one (S) allows for less cooling of the skin in both a cool and a slightly warm environment.
Adult↗
Sympathetic transmission in small mesenteric arteries from the rat: highly calcium-dependent at low stimulation rates.
In the present study we examine the calcium requirements of the neurogenic response in vitro of small arteries (150-200 microns diameter) from the mesentery of Wistar rats. Intramural nerves were activated with electrical field stimulation. Responses to single impulses and to low-frequency repeated stimulation were reduced or abolished by reducing the Ca2+ concentration in the bathing solution from 2.5 to 1.0 mM. Responses to higher frequencies (16 Hz) were only slightly affected. Since calcium reduction had markedly less effect on responses to direct activation of the smooth muscle and on responses to any dose of exogenous noradrenaline, the calcium reduction had mainly pre-junctional effects. The data show that part of the neurogenic response is highly calcium-sensitive, perhaps more so than would be expected of a purely noradrenergic transmission.
Animals↗
Effects of pre-junctional alpha-receptor blockade on vascular neuro-effector characteristics in rats on high sodium intake.
Various in-vitro studies have indicated a direct attenuating effect of sodium on the affinity of adrenergic alpha 2-receptors. It has been suggested that ingested sodium in this way might increase blood pressure by reducing the activity of central alpha 2-receptors and thereby increasing sympathetic discharge. However, such an effect of sodium would also impair the function of peripheral alpha 2-receptors. In the present study we have therefore investigated the effect of high sodium intake on the alpha 2-receptor-mediated inhibition of the vascular neurogenic response. Male Wistar rats were given 2% NaCl in their drinking water from 4 to 9 weeks of age. Another group receiving plain tap water served as controls. Segments of small branches from the mesenteric artery were mounted in a myograph. Responses to transmural nerve stimulation were determined before and after alpha 2-receptor blockade with either yohimbine or idazoxan. The response to a continuous nerve stimulation that elicited 30% of maximal contraction was increased 2-3 times after addition of either idazoxan (0.1 microM) or yohimbine (0.3 microM), with no significant difference between sodium-treated and control rats; if anything the enhancement was slightly greater in the sodium-treated group. Also, responses to intermittent burst stimulation were increased from 30 to about 80% of maximal response in both rat groups. The results thus indicate that high sodium intake does not affect the inhibitory influence of pre-junctional alpha 2-receptors on the vascular neurogenic response.
Adrenergic alpha-Antagonists↗
Calcium dependency of the post-stimulatory potentiation of the neurogenic response in small mesenteric arteries from the rat.
We have previously shown that the contraction of small mesenteric arteries in response to nerve stimulation is enhanced by preceding high-frequency stimulation. We have now investigated the calcium dependency of this post-stimulatory potentiation. Small arteries (inner diameter 150-250 microns) from normotensive rats were dissected free from surrounding tissue, and segments were mounted in a myograph where the wall tension was measured at well-defined circumferences. Nerve stimulation was performed by field stimulation. A single stimulation of the nerve caused a contraction of 2.6 +/- 0.25% of maximal adrenergic response. After a high-frequency nerve stimulation with 16 Hz and 480 pulses the response to a single nerve stimulation was enhanced 6.6 +/- 1.3 times. The potentiation decayed with a time constant of 93.7 +/- 20.0 s. The amplitude of the post-stimulatory potentiation was dependent on the extracellular calcium concentration during the conditioning stimulation. In a solution containing 2.5 mM calcium the single twitch was enhanced 6.6 times while after exposure to reduced calcium (0.5 mM) it was only enhanced twice. The contraction caused by a short burst of high-frequency nerve stimulation (20 Hz and 10 pulses) was potentiated four times by a conditioning stimulation (16 Hz and 480 pulses), and this potentiation seemed to be independent of the extracellular calcium concentration during the conditioning stimulation. Thus the magnitude of the post-stimulatory potentiation of single nerve stimulations is linearly related to the extracellular calcium concentration during the conditioning nerve stimulation. For the potentiation of the response to burst stimulation no relation was found between the potentiation and extracellular calcium.
Animals↗
Neurogenic responses in resistance vessels: roles of alpha 1- and alpha 2-adrenoceptors, transmitter reuptake, ouabain, and plasma factors.
Experiments on the vasoconstrictor fiber control of isolated spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) resistance vessels, which is throughout more efficient in SHR, suggest that the presynaptic alpha 2-negative feedback mechanism and the reuptake pump are largely complementary in adjusting the effective transmitter concentrations in these narrow junctions, and first when both are blocked a marked leftward displacement of the nervous frequency-response curve ensues. Also, ouabain causes a marked leftward displacement of the frequency response curve in a way which suggests a considerable increase of transmitter release/impulse. Finally, normal rat plasma contains agent(s) which, even in very low concentrations, seems to cause a strong ouabain-like effect on the neurogenic responses. However, these various interferences with the neurogenic vascular effects influence SHR and WKY to largely equal extents, implying that the more efficient nervous control in SHR vessels is not merely due to an altered balance of the ordinary local mechanisms that influence the adrenergic transmitter release.
Animals↗