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H Nilsson

Publications and source records attributed to H Nilsson.

At least 37 records · Page 2Linked to original sources

Melanosome and erythrosome positioning regulates cAMP-induced movement in chromatophores from spotted triplefin, Grahamina capito.

This study investigated regulation of uniform positioning of melanosomes and erythrosomes in chromatophores from spotted triplefin Grahamina capito from New Zealand, by modulating levels of intracellular cAMP. Elevated cAMP levels, caused by forskolin treatment, inhibited aggregation and induced rapid dispersion of melanosomes and erythrosomes. The dispersing organelles moved to and accumulated at the cell periphery, leading to an abnormal hyperdispersed state with a melanosome- or erythrosome-depleted cell center. Minutes after hyperdispersion, these organelles reversed direction and moved towards the center again to finally distribute throughout the cells. When chromatophores with initially dispersed melanosomes or erythrosomes were treated with forskolin, no hyperdispersion was seen, but the erythrosomes aggregated slowly. Disassembly of actin by latrunculin resulted in a similar but constant hyperdispersed melanosome and erythrosome distribution. The results show that cAMP not only disperses but also aggregates melanosomes and erythrosomes, and that it is the intracellular position of these organelles that determine the directionality of the cAMP-induced movement. To ascertain the even distribution in the dispersed state, regulatory components associated with the actin cytoskeleton in the cell periphery might modify activity of cytoplasmic dynein or kinesin upon contact with dispersing melanosomes or erythrosomes.

Actins↗

Nitric oxide induces dose-dependent CA(2+) transients and causes temporal morphological hyperpolarization in human neutrophils.

We exposed adherent neutrophils to the nitric oxide (NO)-radical donors S-nitroso-N-acetylpenicillamine (SNAP), S-nitrosoglutathione (GSNO), and sodium nitroprusside (SNP) to study the role of NO in morphology and Ca(2+) signaling. Parallel to video imaging of cell morphology and migration in neutrophils, changes in intracellular free Ca(2+) ([Ca(2+)](i)) were assessed by ratio imaging of Fura-2. NO induced a rapid and persistent morphological hyperpolarization followed by migrational arrest that usually lasted throughout the 10-min experiments. Addition of 0.5-800 microM SNAP caused concentration-dependent elevation of [Ca(2+)](i) with an optimal effect at 50 microM. This was probably induced by NO itself, because no change in [Ca(2+)](i) was observed after treatment with NO donor byproducts, i.e. D-penicillamine, glutathione, or potassium cyanide. Increasing doses of SNAP (>/=200 microM) attenuated the Ca(2+) response to the soluble chemotactic stimulus formyl-methionyl-leucyl-phenylalanine (fMLP), and both NO- and fMLP-induced Ca(2+) transients were abolished at 800 microM SNAP or more. In kinetic studies of fluorescently labeled actin cytoskeleton, NO markedly reduced the F-actin content and profoundly increased cell area. Immunoblotting to investigate the formation of nitrotyrosine residues in cells exposed to NO donors did not imply nitrosylation, nor could we mimic the effects of NO with the cell permeant form of cGMP, i.e., 8-Br-cGMP. Hence these processes were probably not the principal NO targets. In summary, NO donors initially increased neutrophil morphological alterations, presumably due to an increase in [Ca(2+)](i), and thereafter inhibited such shape changes. Our observations demonstrate that the effects of NO donors are important for regulation of cellular signaling, i.e., Ca(2+) homeostasis, and also affect cell migration, e.g., through effects on F-actin turnover. Our results are discussed in relation to the complex mechanisms that govern basic cell shape changes, required for migration.

Actins↗

Neuropeptide Y regulates intracellular calcium through different signalling pathways linked to a Y(1)-receptor in rat mesenteric small arteries.

Simultaneous measurements of intracellular calcium concentration ([Ca(2+)](i)) and tension were performed to clarify whether the mechanisms which cause the neuropeptide Y (NPY)-elicited contraction and potentiation of noradrenaline contractions, and the NPY inhibition of forskolin responses are linked to a single or different NPY receptor(s) in rat mesenteric small arteries. In resting arteries, NPY moderately elevated [Ca(2+)](i) and tension. These effects were antagonized by the selective Y(1) receptor antagonist, (R)-N(2)-(diphenacetyl)-N-[(4-hydroxyphenyl)methyl]-D-argininea mide (BIBP 3226) (apparent pK(B) values of 8.54+/-0.25 and 8.27+/-0.17, respectively). NPY (0.1 microM) caused a near 3 fold increase in sensitivity to noradrenaline but did not significantly modify the tension-[Ca(2+)](i) relationship for this agonist. BIBP 3226 competitively antagonized the contractile response to NPY in arteries submaximally preconstricted with noradrenaline (pA(2) 7.87+/-0.20). In arteries activated by vasopressin, the adenylyl cyclase activator forskolin (3 microM) induced a maximum relaxation and a return of [Ca(2+)](i) to resting levels. NPY completely inhibited these effects. The contractile responses to NPY in arteries maximally relaxed with either sodium nitroprusside (SNP) or nifedipine were not significantly higher than those evoked by the peptide at resting tension, in contrast to the contractions to NPY in forskolin-relaxed arteries. BIBP 3226 competitively antagonized the contraction to NPY in forskolin-relaxed arteries with a pA(2) of 7.92+/-0.29. Electrical field stimulation (EFS) at 8-32 Hz caused large contractions in arteries relaxed with either forskolin or noradrenaline in the presence of phentolamine. These responses to EFS were inhibited by BIBP 3226. Similar EFS in resting, non-activated arteries did not produce any response. The present results suggest that different intracellular pathways are linked to a single NPY Y(1) receptor in intact rat mesenteric small arteries, and provide little support for involvement of other postjunctional NPY receptors in the contractile responses to NPY. Neurally released NPY also seems to act through Y(1) receptors, and may serve primarily as an inhibitor of vasodilatation.

Animals↗

Sorbitol and myo-inositol levels and morphology of sural nerve in relation to peripheral nerve function and clinical neuropathy in men with diabetic, impaired, and normal glucose tolerance.

AIMS: Sorbitol and myo-inositol levels and morphology of sural nerve were compared with nerve function and clinical neuropathy in men with diabetic, impaired (IGT), and normal glucose tolerance. METHODS: After neurography of sural nerve and determinations of sensory thresholds for vibration, warm and cold on the foot, whole nerve sural nerve biopsy was performed in 10 men with Type 1 diabetes mellitus, 10 with IGT, and 10 with normal glucose tolerance. Polyol levels were assessed by gas-liquid chromatography/mass spectrometry. RESULTS: Sural nerve amplitudes were significantly lower and sorbitol levels significantly higher in diabetic patients (median (interquartile range)) (3.7 (3.5) microV and 643 (412) pmol/mg protein, respectively) both compared with IGT (11.3 (10.6)microV; P = 0.04 and 286 (83) pmol/mg protein; P = 0.0032, respectively) and normally glucose tolerant (10.0 (11.6); P = 0.0142 and 296 (250) pmol/mg protein; P = 0.0191, respectively) subjects. There were no differences in nerve morphology between the three groups. Nerve myo-inositol levels correlated, however, positively with cluster density (rs = 0.56; P = 0.0054). In diabetic and IGT subjects, sural nerve amplitudes (2.6 (3.8) vs. 12.1 (10.6) microV; P = 0.0246) and myelinated nerve fibre density (MNFD; 4,076 (1091) vs. 5,219 (668) nerve fibres/mm2; P = 0.0021) were significantly lower in nine subjects with clinical neuropathy than in 10 without. CONCLUSIONS: Nerve degeneration (i.e. MNFD) correlated with clinical neuropathy but not with glucose tolerance status whereas nerve myo-inositol levels positively correlated with signs of nerve regeneration (i.e. increased cluster density).

Diabetes Mellitus, Type 1↗

Staphylococcal enterotoxin H displays unique MHC class II-binding properties.

Staphylococcal enterotoxin H (SEH) has been described as a superantigen by sequence homology with the SEA subfamily and briefly characterized for its in vivo activity. In this study, we demonstrate that SEH is a potent T cell mitogen and inducer of T cell cytotoxicity that possesses unique MHC class II-binding properties. The apparent affinity of SEH for MHC class II molecules is the highest affinity ever measured for a staphylococcal enterotoxin (Bmax1/2 approximately 0.5 nM for MHC class II expressed on Raji cells). An excess of SEA or SEAF47A, which has reduced binding to the MHC class II alpha-chain, is able to compete for binding of SEH to MHC class II, indicating an overlap in the binding sites at the MHC class II beta-chain. The binding of SEH to MHC class II is like SEA, SED, and SEE dependent on the presence of zinc ions. However, SEH, in contrast to SEA, binds to the alanine-substituted DR1 molecule, betaH81A, believed to have impaired zinc-bridging capacity. Furthermore, alanine substitution of residues D167, D203, and D208 in SEH decreases the affinity for MHC class II as well as its in vitro potency. Together, this indicates an MHC class II binding site on SEH with a different topology as compared with SEA. These unique binding properties will be beneficial for SEH to overcome MHC class II isotype variability and polymorphism as well as to allow an effective presentation on APCs also at low MHC class II surface expression.

Alanine↗

Clothing convective heat exchange--proposal for improved prediction in standards and models.

Convection is an important determinant for both sensible and evaporative heat exchange. Heat transfer by convection for normal boundary conditions is readily described by simple power functions. Clothing affects convection in various ways and existing characterisation of clothing by its static insulation values produces inaccurate prediction of sensible heat exchange, eventually leading to erroneous risk assessment. The present paper reviews various methods for evaluation of clothing convective (sensible) heat exchange. Based on available data, two equations are proposed for determination of the reduction of the total insulation values obtained under static, still wind conditions as a consequence of wind and walking effects. The equations apply from 0 to 1.84 clo, from 0.2 to 3 m/s and for walking speeds up to 1.2 m/s. The equations are incorporated in ISO 7933 to provide a more realistic and accurate prediction of sensible heat transfer through clothing.

Bias↗

Designed four-helix bundle catalysts--the engineering of reactive sites for hydrolysis and transesterification reactions of p-nitrophenyl esters.

Four-helix bundle proteins have been designed that catalyze the hydrolysis and transesterification reactions of p-nitrophenyl esters by a cooperative nucleophilic and general acid mechanism. The catalysts consist of two 42-residue peptides that fold into helix-loop-helix motifs and dimerise. They have previously been shown to recognize anionic and hydrophobic substrates and to follow saturation kinetics. The catalytic entity is a HisH(+)-His pair in a helical segment spaced i, i+4, which can be supplemented by arginines and lysines in the adjacent helix. The binding residues have now been optimized for the catalysis of mono-p-nitrophenyl fumarate hydrolysis and found to vary with the location of the site. The catalytic efficiency of the HisH(+)-His site in helix II in positions 30 and 34 is enhanced by the introduction of arginine and or lysine residues in positions 11 and 15, but not in 8 and 11 or in 15 and 19. The most efficient catalyst using this site, JNIIR11K15, catalyses the reaction with a second-order rate constant of 0.134 M(-1) s(-1) in aqueous solution at pH 5.1 and 290 K. The second-order rate constant is larger than those of the corresponding sites with 'longer' and 'shorter' binding residues. Similar experiments have shown that the efficiency and selectivity of catalysts based on a HisH(+)-11-His-15 site in helix I are enhanced the most by the introduction of Lys-30 and Arg-34.

Amino Acid Sequence↗

Evaluation of hand and finger heat loss with a heated hand model.

A heated full-scale hand model has been used to determine indirectly hand and finger heat losses of human subjects exposed to four ambient cold conditions (0, 4, 10 and 16 degrees C, air velocity approximately 0.3 m/s). Heat transfer coefficients determined with the hand model, were used to calculate heat flux based on measured skin to ambient temperature gradients. The responses of eight subjects from a previous study were used for the analysis. The measurements were carried out in a small climate chamber which was cooled by evaporating liquid carbon dioxide. The thermal hand was put into the chamber in a vertical position with the thumb up. The surface temperature of the thermal hand was controlled at 21, 25, 28, 31 and 34 degrees C under each of the four ambient cold conditions, in order to investigate possible temperature dependence of the calculated combined convective and radiate heat transfer coefficient (hCR). The value of hCR varied between approximately 9-13 W/m2 degree C for fingers and palm and back of hand, respectively. Calculated heat losses showed significant individual variation, corresponding to the maintained skin to ambient temperature gradient. Individual values from about 50 to more than 300 W/m2 were calculated. Several subjects showed CIVD and heat fluxes associated with this phenomenon were sometimes doubled. The measurement results showed realistic and comparable with literature date. The advantages of the thermal hand model can be counted as easy to use; directly measures the heat loss; highly reproducible and no interruption. It appears that a heated hand model provides a useful methods for analysis and quantification of hand heat loss.

Body Temperature Regulation↗

The effects of wind and human movement on the heat and vapour transfer properties of clothing.

This paper integrates the research presented in the papers in this special issue of Holmér et al. and Havenith et al. [Holmér, I., Nilsson, H., Havenith, G., Parsons, K. C. (1999) Clothing convective heat exchange: proposal for improved prediction in standards and models. Annals of Occupational Hygiene, in press; Havenith, G., Holmér, I., den Hartog, E. and Parsons, K. C. (1999) Clothing evaporative heat resistance: proposal for improved representation in standards and models. Annals of Occupational Hygiene, in press] to provide a practical suggestion for improving existing clothing models so that they can account for the effects of wind and human movement. The proposed method is presented and described in the form of a BASIC computer program. Analytical methods (for example ISO 7933) for the assessment of the thermal strain caused by human exposure to hot environments require a mathematical quantification of the thermal properties of clothing. These effects are usually considered in terms of 'dry' thermal insulation and vapour resistance. This simple 'model' of clothing can account for the insulation properties of clothing which reduce heat loss (or gain) between the body and the environment and, for example, the resistance to the transfer of evaporated sweat from the skin, which is important for cooling the body in a hot environment. When a clothed person is exposed to wind, however, and when the person is active, there is a potentially significant limitation in the simple model of clothing presented above. Heat and mass transfer can take place between the microclimate (within clothing and next to the skin surface) and the external environment. The method described in this paper 'corrects' static values of clothing properties to provide dynamic values that take account of wind and human movement. It therefore allows a more complete representation of the effects of clothing on the heat strain of workers.

Bias↗

Mechanisms of Ca2+ sensitization of force production by noradrenaline in rat mesenteric small arteries.

1. Mechanisms of Ca2+ sensitization of force production by noradrenaline were investigated by measuring contractile responses, intracellular Ca2+ concentration ([Ca2+]i) and phosphorylation of the myosin light chain (MLC) in intact and alpha-toxin-permeabilized rat mesenteric small arteries. 2. The effects of noradrenaline were investigated at constant membrane potential by comparing fully depolarized intact arteries in the absence and presence of noradrenaline. Contractile responses to K-PSS (125 mM K+) and NA-K-PSS (K-PSS + 10 microM noradrenaline) were titrated to 30 and 75%, respectively, of control force, by adjusting extracellular Ca2+ ([Ca2+]o). At both force levels, [Ca2+]i was substantially lower with NA-K-PSS than with K-PSS. With K-PSS, the proportion of MLC phosphorylated (approximately 30%) was similar at 30 and 75% of control force; with NA-K-PSS, MLC phosphorylation was greater at the higher force level (40 vs. 34%). 3. In alpha-toxin-permeabilized arteries, the force response to 1 microM Ca2+ was increased by 10 microM noradrenaline, and MLC phosphorylation was increased from 35 to 45%. The protein kinase C (PKC) inhibitor calphostin C (100 nM) abolished the noradrenaline-induced increase in MLC phosphorylation and contractile response, without affecting the contraction in response to Ca2+. Treatment with ATP gamma S in the presence of the MLC kinase inhibitor ML-9 increased the sensitivity to Ca2+ and abolished the response to noradrenaline. 4. The present results show that that in rat mesenteric small arteries noradrenaline-induced Ca2+ sensitization is associated with an increased proportion of phosphorylated MLC. The results are consistent with a decreased MLC phosphatase activity mediated through PKC. Furthermore, while MLC phosphorylation is a requirement for force production, the results show that other factors are also involved in force regulation.

Animals↗

Hydrophobic core substitutions in calbindin D9k: effects on Ca2+ binding and dissociation.

Hydrophobic core residues have a marked influence on the Ca2+-binding properties of calbindin D9k, even though there are no direct contacts between these residues and the bound Ca2+ ions. Eleven different mutants with substitutions in the hydrophobic core were produced, and their equilibrium Ca2+-binding constants measured from Ca2+ titrations in the presence of chromophoric chelators. The Ca2+-dissociation rate constants were estimated from Ca2+ titrations followed by 1H NMR1 and were measured more accurately using stopped-flow fluorescence. The parameters were measured at four KCl concentrations to assess the salt dependence of the perturbations. The high similarity between the NMR spectra of mutants and wild-type calbindin D9k suggests that the structure is largely unperturbed by the substitutions. More detailed NMR investigations of the mutant in which Val61 is substituted by Ala showed that the mutation causes only very minimal perturbations in the immediate vicinity of residue 61. Substitutions of alanines or glycines for bulky residues in the center of the core were found to have significant effects on both Ca2+ affinity and dissociation rates. These substitutions caused a reduction in affinity and an increase in off-rate. Small effects, both increases and decreases, were observed for substitutions involving residues far from the Ca2+ sites and toward the outer part of the hydrophobic core. The mutant with the substitution Phe66 --> Trp behaved differently from all other mutants, and displayed a 25-fold increase in overall affinity of binding two Ca2+ ions and a 6-fold reduction in calcium dissociation rate. A strong correlation (R = 0.94) was found between the observed Ca2+-dissociation rates and affinities, as well as between the salt dependence of the off-rate and the distance to the nearest Ca2+-coordinating atom. There was also a strong correlation (R = 0.95) between the Ca2+ affinity and stability of the Ca2+ state and a correlation (R = 0. 69) between the Ca2+ affinity and stability of the apo state, as calculated from the results in the present and preceding paper in this issue [Julenius, K., Thulin, E., Linse, S., and Finn, B. E. (1998) Biochemistry 37, 8915-8925]. The change in salt dependencies of koff and cooperativity were most pronounced for residues completely buried in the core of the protein (solvent accessible surface area approximately 0). Altogether, the results suggest that the hydrophobic core residues promote Ca2+ binding both by contributing to the preformation of the Ca2+ sites in the apo state and by preferentially stabilizing the Ca2+-bound state.

Amino Acid Substitution↗

Staphylococcal enterotoxin D is a promiscuous superantigen offering multiple modes of interactions with the MHC class II receptors.

Dimerization of MHC class II molecules on the cell surface of human THP-1 monocytic cell line is a requirement for staphylococcal superantigen (SAG)-induced cytokine gene expression. The capacities of various SAG to induce this response are governed by their modes of interaction with MHC class II molecules. Staphylococcal enterotoxin A (SEA), with its two binding sites, dimerizes MHC class II molecules and subsequently induces cytokine gene expression in THP-1 cells. Here, we demonstrate that staphylococcal enterotoxin D (SED) and staphylococcal enterotoxin E (SEE) induce, similarly, IL-1beta and TNF-alpha gene expression in these cells. Using mutated toxins that lost their binding site with the MHC class II alpha- or beta-chain, we demonstrate that this response is also mediated by the dimerization of MHC class II molecules through two binding sites. Furthermore, SED forms Zn2+-dependent homodimers that allow multiple modes of MHC class II clustering, including ligation of alpha-chains (alpha/alpha), beta-chains (beta/beta), or the alpha- and beta-chains of two different class II molecules. The beta/beta interaction following Zn2+-dependent SED/SED homodimer formation seems to be mediated by the appearance of a novel binding site on SED that interacts with histidine 81 of the MHC class II beta-chain. The different modes of SED interactions also influence SED-induced T cell activation where simultaneous ligation of the alpha- and beta-chains is essential for optimal response. These various modes of SED binding may be used to preserve bivalency regardless of variability in the MHC class II alpha/beta/peptide complexes.

Binding Sites↗

Microtubule aster formation by dynein-dependent organelle transport.

The interplay between microtubules and the motor enzyme, cytoplasmic dynein, is essential for organisation of the cytoplasm, organelle transport, and cell division in eukaryotic cells. During mitosis, cytoplasmic dynein organises microtubules into two spindle pole asters, as well as the comparable multiple cytoplasmic asters induced by the microtubule-stabilising agent taxol. The mechanisms behind this cell cycle-regulated organisation are, however, not fully understood. We report here that the unidirectional dynein-dependent pigment organelle aggregation in taxol-treated melanophores from Atlantic cod, induces multiple microtubule asters. Usually, the pigment aggregates to a central pigment mass in the cell center, but pigment aggregation in taxol-treated cells induces formation of several peripheral pigment clusters that each localise to the center of a microtubule aster formation. When a cell with previously formed peripheral pigment clusters redisperse pigment, the asters disappear. Upon a subsequent reaggregation of the pigment, the aster formations reappear. The results indicate that the pigment aggregation process organises the microtubules into these formations. Immuno-electron microscopy of isolated pigment organelles indicates the presence of several dynein molecules on each pigment organelle, making it possible for each organelle to interact with several microtubules and thereby focusing microtubule minus ends. The possibility of unidirectional dynein-dependent organelle movement for organising microtubules into asters during cell division, and similarities in signal transduction between mitosis and pigment movement, are discussed.

Animals↗

Dysphagia in stroke: a prospective study of quantitative aspects of swallowing in dysphagic patients.

This is a prospective study of 100 consecutive stroke patients. Within 24 h after stroke onset they were asked specifically about swallowing complaints and subjected to a clinical examination including neurologic examination, Mini-Mental test, and Barthel score. Dysphagic patients were examined with the repetitive oral suction swallow test (the ROSS test) for quantitative evaluation of oral and pharyngeal function at 24 h, after 1 week, and after 1 month. At 6 months, the patients were interviewed about persistent dysphagia. Seventy-two patients could respond reliably at 24 h after the stroke onset and 14 of these complained of dysphagia. Non-evaluable patients were either unconscious, aphasic, or demented. The presence of dysphagia was not influenced by age or other risk factors for stroke. Facial paresis, but no other clinical findings, were associated with dysphagia. Dysphagia 24 h after stroke increased the risk of pneumonia but did not influence the length of hospital stay, the manner of discharge from hospital, or the mortality. The initial ROSS test, during which the seated patient ingests water through a straw, was abnormal in all dysphagic stroke patients. One-third of the patients were unable to perform the test completely. Above all, dysfunction was disclosed during forced, repetitive swallow. All phases of the ingestion cycle were prolonged whereas the suction pressures, bolus volumes, and swallowing capacities were low. Abnormalities of quantitative swallowing variables decreased with time whereas the prevalences of swallowing incoordination and abnormal feeding-respiratory pattern became more frequent. After 6 months, 7 patients had persistent dysphagia. Five of these were initially non-evaluable because of unconsciousness, aphasia, or dementia.

Aged↗

Interactions between membrane potential and intracellular calcium concentration in vascular smooth muscle.

The intracellular calcium concentration is a major determinant of vascular tone. In the steady state it is regulated mainly by membrane potential. At the same time, several mechanisms regulating the calcium concentration, including the membrane potential, are influenced by the intracellular calcium concentration itself. There are thus multiple possible positive and negative feedback loops involved in calcium regulation. This review gives a brief overview of the different mechanisms involved, including calcium-dependent ion channels, exchangers, and ATPases, and discusses their role in agonist-mediated responses, in relation primarily to studies on the portal vein and mesenteric small arteries.

Animals↗

A 9-year longitudinal study of reported oral problems and dental and periodontal status in 70- and 79-year-old city cohorts in northern Sweden.

Before 1981 no representative studies of oral health in an elderly population in northern Sweden had been presented, and longitudinal studies of oral health in the aging person were in general rare. Thus the aim of this study was to investigate longitudinal changes in oral health in a representative sample of an elderly city population in northern Sweden. Reported oral problems and treatment needs were noted, and dental and periodontal status was registered in clinical examinations. The frequency of reported annual dental visits and of being called by the dentist increased in the younger but not in the older cohort during the 9-year period. In 1990 all the 79- and 88-year-olds with annual visits reported that they were recalled by the dentist. The clinical investigation showed an increasing amount of tooth loss, root caries, and periodontal disease with increasing age. Among dentulous persons 1.7 teeth per subject were lost from 1981 to 1990 in the younger cohort, compared with 2.6 teeth per subject in the older cohort. The number of sound teeth decreased very little in the younger cohort (from 3.44 to 3.34) but more evidently in the older cohort (from 3.47 to 2.65) during the 9-year period. The frequency of surfaces with attachment level > 3 mm increased statistically significantly from 1981 to 1990 in the older cohort. Subjects with annual visits had in general fewer oral problems.

Aged↗

Parasympathetic neuropathy associated with left ventricular diastolic dysfunction in patients with insulin-dependent diabetes mellitus.

Patients with insulin-dependent diabetes mellitus (IDDM) may develop autonomic neuropathy (AN) and cardiac complications. The association between AN and cardiac dysfunction was assessed in 34 IDDM patients (age 40 years, diabetes duration 21 years, 15 women) by echocardiography/Doppler and autonomic nerve function tests. The expiration/inspiration ratio (E/I) was used to assess parasympathetic damage, and the acceleration and brake indices for assessment of sympathetic impairment. AN was present in 21 patients. Patients with abnormal E/I (n = 11) had lower E/A ratios than patients without AN; early to atrial peak filling ratio (E/Amax) was median 1.1 (inter-quartile range 0.2) vs 1.4 (0.7), p = 0.022; early to atrial integral filling ratio (E/Aintegral) was 1.7 (0.3) vs 2.3 (1.2), p = 0.006. Patients with AN and normal E/I (sympathetic neuropathy, n = 10) and patients without AN had similar E/A ratios. E/Aintegral was also lower in patients with abnormal E/I compared with patients with AN and normal E/I; 1.7 (0.3) vs 2.2 (0.7), p = 0.008. Systolic function and cardiac dimensions were generally unaffected and similar in the three groups. In conclusion, diastolic dysfunction and parasympathetic neuropathy are related in IDDM patients.

Adolescent↗