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K Addicks

Publications and source records attributed to K Addicks.

At least 91 records · Page 5Linked to original sources
PubMed1994

Nitric oxide modulates sympathetic neurotransmission at the prejunctional level.

In spite of accumulating evidence for a modulation of sympathetic neurotransmission by endogenously produced nitric oxide (NO), it remains unclear in which parts of the vascular system and at what level this interaction takes place. The aim of the present study was to investigate the distribution of endothelial and neuronal NO synthase (NOS) along the vascular tree of the heart at the light and electron microscopic level using NADPH-diaphorase (NADPH-d) staining as a marker for NOS. In addition, the functional effects of exogenous NO on coronary vascular resistance and cardiac adrenergic nerves was studied using the isolated perfused rat heart as a model. The intraaxonal catecholamine content of adrenergic nerve fibers was visualised and morphometrically assessed by applying glyoxylic acid-induced histofluorescence. The expression of endothelial NOS in the heart was found to depend on the diameter of the blood vessel. Arteries > 100 microns always showed intense staining, whereas staining in smaller arteries and veins was considerably weaker. Smooth-muscle free vessels were essentially devoid of NADPH-d activity. In atrial and ventricular myocardium, neuronal NOS localised in autonomic nerve fibers along the entire vascular tree. Ultrastructurally, NADPH-d staining revealed adjacent localisation of NOS-positive and -negative axons, suggesting and interaxonal modulation of adjacent autonomic nerve fibers by NO. In isolated perfused rat hearts, the intracoronary application of 10(-8) M NO produced a marked decrease of coronary perfusion pressure, which was accompanied by a distinct increase in intraaxonal catecholamine levels of intramural adrenergic nerve fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗
PubMed1994

Fine structural distinction between ganglia of the outer and inner submucosal plexus in porcine small intestine.

Ultrastructural differences between ganglia of the plexus submucosus internus (Meissner; PSI) and plexus submucosus externus (Schabadasch; PSE) are described. Comparison revealed a different glia index (ratio glia per neuron) between the PSE (3:1) and the PSI (1:1), the arrangement of PSI neurons in compartments and the appearance of broad membrane-to-membrane appositions inside the compartments of the PSI. Structural and immunohistochemical differences between the two plexuses are discussed. In general, PSE neurons show a wider variety in size and shape than most of the PSI neurons.

Animals↗
PubMed1994

A scleral shield for the application of mitomycin C during trabeculectomy: a rabbit model.

The use of mitomycin C during trabeculectomy is associated with a significant degree of persistent hypotony. To address this problem, we designed a scleral shield with a dry sponge glued on it for use in applying mitomycin C that reduces the penetration of the substance through the sclera. The effectiveness of the shield was tested in a rabbit model using regular sponges and sponges with the attached shield. Histopathologic examination of the eyes after 1 month revealed toxic changes in the eyes in which only a regular sponge had been used, but not in those in which the sponges with the attached scleral shield had been used. The scleral shield may help reduce the incidence of hypotony in eyes undergoing trabeculectomy with adjunctive mitomycin C.

Animals↗
PubMed1994

Extraocular application of mitomycin C in a rabbit model: cytotoxic effects on the ciliary body and epithelium.

Since prolonged postoperative hypotony has been a frequent complication of glaucomatous filtration surgery in which mitomycin C (MMC) was used, it is important to determine the intraocular toxic effects of the drug. We placed MMC, in concentrations of 0.05, 0.2, and 1.0 mg/mL on the intact sclera of rabbits and obtained the eyes after 1, 7, and 28 days. Examination of the ciliary epithelium by transmission electron microscopy revealed an electron-dense material near the endoplasmic reticulum. Large intracellular vacuoles were present, and the mitochondria appeared swollen. These findings suggest a toxic effect of MMC on the ciliary epithelium in rabbits after extraocular application, possibly decreasing aqueous production.

Animals↗
PubMed1993

Sympathetic autonomic neuropathy in the heart of the spontaneous diabetic BB rat.

There is evidence that autonomic nerves are disturbed in spontaneous diabetic BB rats indicating a peripheral diabetic autonomic neuropathy. For histofluorescent visualization of catecholamine containing nerve fibres in myocardium the method of De La Torre was applied. For electron microscopy, tissue specimens of ventricular and atrial myocardium were prepared. In myocardium of BB rats diabetic for 28 weeks morphometric quantification of catecholamine histofluorescence revealed a loss of fluorescent nerve fibres and varicosities of 57% from 1.18 +/- 0.17 to 0.51 +/- 0.18 per cent of the total field area (p < 0.009). Ultrastructurally, morphometric quantification of the density of axon profiles containing synaptic vesicles in transverse sectioned atrial myocardium showed a decrease of 42% (p < 0.021) in the diabetic group. In the diabetic nerves, axoplasmic lysis and a reduction in the Schwann cell envelope were prominent. Morphologic changes of nerves in ventricles were comparable to the findings in atrial tissue. It is concluded that a diabetic autonomic neuropathy of intramural sympathetic nervous tissue occurs in myocardium of spontaneous diabetic BB rats despite insulin substitution.

Animals↗
PubMed1992

[Diabetic cardiopathy. Pathophysiologic concepts and therapeutic approaches].

Epidemiological data reviewed suggest that diabetes itself increases the cardiac risk of diabetics (types I and II), independently from the development of coronary heart disease and in addition to other risk factors (hypertension, hypercholesterolemia, hypertriglyceridemia, smoking and others), presumably by a specific myocardial disease called "diabetic cardiopathy", or according to the recommendations of the WHO, "diabetic heart muscle disease." Disturbances of the left and right ventricular function as well as the autonomic function of the heart can be understood as signs of this specific cardiopathy. The pathophysiological mechanisms underlying this disease are not yet fully known; however, recent evidence is presented that diabetes leads to a facet of metabolic dysfunctions regarding glucose and energy metabolism, calcium homeostasis and the expression of specific proteins that diminish the ability of the heart to respond to increased workload and increase the vulnerability of the heart in diabetes. Since preliminary experimental data indicate that inhibitors of the angiotensin-converting enzyme can protect the heart in diabetes, it is intriguing to suggest that increased release of angiotensin II plays a significant role in the change from reduced adaptability to irreversible damage of the heart in diabetes.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Sialic acid removal modulates the myocardial and vascular activity of calcium channel ligands.

Selective removal of sialic acid from isolated guinea pig left atrial strips and rabbit thoracic aortic ring segments was performed by neuraminidase prepared from Clostridium perfringens and was controlled electron microscopically. Preincubation of these organs (2 units/mL; 2 hr) resulted in enzyme mediated hydrolysis of total tissue sialic acid; 55.2% for atria and 60.9% for aorta. Contractile force of atria and arterial diameter of thoracic aorta were measured isometrically and isotonically by means of a force displacement transducer. Pretreatment of both organs with neuraminidase (2 units/mL; 2 hr) in a carbogen saturated organ bath caused a moderate left-hand shift of the cumulative concentration response curves for the dihydropyridine type calcium antagonist nisoldipine, the phenylalkylamine derivative gallopamil and the benzothiazepine diltiazem. EC50 values were significantly lower (P less than 0.05), particularly in the atrial muscle, when compared to untreated preparations. There was no effect of neuraminidase on the negative inotropic and vasodilator potency of the calcium channel modulator fendiline. Conversely, neuraminidase induced a right-hand shift in the concentration response curves shown by the pure calcium agonist (-)-S-Bay K 8644 leading to significantly higher EC50 values in both organs. Similarly, the contractile potency of calcium chloride (atria) and potassium chloride (aorta) was attenuated upon neuraminidase treatment. From the results obtained it is concluded that sialic acid removal may modulate the action of calcium channel ligands through an inhibitory effect on transmembrane calcium fluxes and/or by decreasing the external calcium availability. Whether the present results suggest a functional role for sialic acid in the regulation of calcium channels warrants further investigation.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

[Neuropathy of the gingival autonomous nerve system in inflammatory diseases of the periodontium. Ultrastructural analysis].

In a comparative study the influence of periodontal disease on the autonomous nerve-system of human attached gingiva was analysed ultrastructurally in 20 gingiva specimens. The test group was formed by 10 patients with adult periodontitis (AP) and compared with 10 patients with clinically healthy gingiva. The specimens were prepared for ultrastructural evaluation. The autonomous nerve fibres near the epithelium, in the connective tissue, and at the blood vessels were qualified and quantified by means of electron microscopy. In the test group clear signs of neuropathy of the autonomous nerve system like lysis of axoplasm, evagination of axons from their Schwann's sheaths, de- and regeneration pistons and reduction of axons were found. The possible pathogenic significance of this neuropathy of the autonomous nerve system in periodontal disease is discussed.

Adult↗
PubMed1988

Effect of propranolol on early postischemia arrhythmias and noradrenaline and potassium release of ischemic myocardium in anesthetized pigs.

In anesthetized open-chest pigs, DL- or D-propranolol (1 mg/kg i.v.) was administered 15 min prior to ligation of the left anterior descending coronary artery (LAD) about halfway from its origin. Sequential myocardial tissue samples were obtained before and after LAD occlusion. The samples were analyzed histofluorimetrically to determine the density of catecholamine containing neurons (quantified morphometrically), and radioenzymatically for total tissue noradrenaline content. The extracellular K+ concentration was measured using K+-sensitive polyvinyl chloride (PVC)-membrane electrodes on the surface of the ischemic myocardium. Under control conditions, ventricular arrhythmias (VA) occurred in a typical 1a and 1b phase. Pretreatment with propranolol diminished the number of VA generated in the 1b phase but not those in the 1a phase; however, these differences were statistically not significant. Neither pretreatment with DL- nor D-propranolol influenced the time course or probability of development of ventricular fibrillation (VF). Coronary artery occlusion led to a significant reduction in noradrenaline concentration of the ischemic myocardium in control animals (from an initial concentration of 526 +/- 65 ng/g w/w to 368 +/- 75 ng/g w/w) within the first 5 min of ischemia, whereas noradrenaline concentration remained nearly unchanged in drug-treated animals (from 838 +/- 86 to 811 +/- 61 ng/g w/w in the DL group and from 701 +/- 36 to 709 +/- 31 ng/g w/w in animals that received D-propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1987

Effects of morphine on catecholamine release and arrhythmias evoked by myocardial ischaemia in rats.

The effects of morphine (10 mg kg-1 i.p.) on haemodynamics, arrhythmias and plasma and myocardial catecholamines (CA) were studied after coronary artery occlusion in anaesthetized rats. Myocardial intraneuronal CA were assessed histofluorimetrically and CA concentrations measured by high performance liquid chromatography. Morphine increased blood pressure, presumably due to higher plasma noradrenaline (NA) concentrations found in morphine-treated rats. Morphine increased the area of catecholamine-containing fluorescing neurones in the myocardium (as a percentage of total field area) 60 min after sham-operation (0.87 +/- 0.07%) or occlusion (0.57 +/- 0.05%) compared to untreated animals (0.67 +/- 0.06 and 0.38 +/- 0.03% respectively). Tissue NA content was not significantly affected by coronary occlusion and/or morphine within the first 60 min. Morphine had no effect on ischaemia-induced arrhythmias. Whether the higher intraneuronal NA content following morphine resulted from reduced central sympathetic outflow to the heart, presynaptic inhibition of NA release, or increased uptake due to higher plasma concentrations is unclear. Ischaemia-induced local NA release appears independent of these mechanisms, as it was unaffected by morphine.

Animals↗
PubMed1987

Effects of lidocaine on catecholamine release in the ischemic rat heart.

The effects of lidocaine (5 or 10 mg/kg bolus + 2.5 mg/kg/h) on arrhythmias and changes in myocardial and plasma catecholamines (CAs) after left coronary artery occlusion were investigated in anesthetized rats. Myocardial intraneuronal CAs were assessed histofluorimetrically and CA concentrations were measured using high-pressure liquid chromatography (HPLC). Both doses of lidocaine caused reductions in heart rate and blood pressure. The higher dose significantly reduced the number of ischemia-induced ventricular extrasystoles from 425 +/- 123 to 25 +/- 12 in the first 60 min of ischemia and abolished ventricular tachycardia and fibrillation. In the myocardium of untreated animals, the area of fluorescing adrenergic neurons (as percentage of total field area) was 0.42 +/- 0.02% after 60 min of ischemia as compared with 1.38 +/- 0.17% in sham-operated animals. Lidocaine pretreatment resulted in a dose-dependent inhibition of this ischemia-induced CA release from adrenergic neurons (0.96 +/- 0.06 and 1.30 +/- 0.05% for the lower and higher dose, respectively). Tissue and plasma CA concentrations were not significantly affected by lidocaine pretreatment and by coronary occlusion. It is concluded that lidocaine inhibits CA release from sympathetic nerve endings in the ischemic myocardium by its endoanesthetic and membrane-stabilizing properties. The reduction in CA release may also contribute to its antiarrhythmic effects.

Animals↗
PubMed1986

Testosterone application influences sympathetic activity of intracardiac nerves in non-trained and trained mice.

Application of testosterone and/or physical exercise causes degenerative and then regenerative patterns of intracardiac sympathetic neurons. Observations in 3 stages (1, 3 and 6 weeks) illustrate the adaptative changes of sympathetic neurons as a response to these stimuli and show that the effects following testosterone application or physical exercise are comparable. Ultrastructural investigations indicate that the sympathetic neurons are more sensitive to testosterone than to physical exercise. The combination of testosterone plus training indicates overlapping effects of these two stimuli. The system of adrenergic nerve fibers seems to be overstimulated. Its reaction pattern is found not only to depend on time but also on the intensity of the stimuli.

Adrenergic Fibers↗
PubMed1986

Quantitative studies of the aortic bodies of the cat. I. Point-counting analysis of tissue components.

Electron micrographs of cat aortic bodies were submitted to point-counting analysis to determine the volume/volume densities (vv%) of general tissue components. Paraganglia, enclosed by a perineural sheath (endoneural paraganglia), exhibit a significantly higher density of specific tissue elements (type-I cells, type-II cells, nerves) than those which covered by fibroblasts (exoneural paraganglia). Additional criteria which allowed distinction of these types of aortic bodies were not evident in this study. On average, type-I cells occupied 27.8 vv% if related to the entire organ, or 35.6 vv% if related to the blood vessel-free space. Comparing our data with those reported for the carotid body, we found an about twofold amount of type-I cells within aortic bodies. The relevance of this finding is discussed with respect to the known different electrophysiological properties of carotid and aortic body arterial chemoreceptors.

Animals↗
PubMed1985

Cholecystokinin-like immunoreactivity in cat extra-adrenal paraganglia.

In the cat peripheral dopaminergic organs such as the carotid body, subclavian bodies, aortico-pulmonary glomera and small intensively fluorescent cell (SIF cell) clusters of the superior cervical ganglion and the nodose ganglion were found to contain cholecystokinin (CCK)-immunoreactive paraganglionic cells. Thus, the extra-adrenal paraganglionic system may serve as a model for studying peripheral interactions of CCKergic and dopaminergic mechanisms.

Animals↗
PubMed1985

Vicious cycle of catecholamines and K+ in cardiac ischemia.

The distribution of catecholamine (CA)-containing neurones and tissue noradrenaline (NA) concentration was investigated in pig hearts with and without myocardial ischemia. All hearts were shock-frozen using a Wollenberger clamp, and tissue samples were obtained from the mid- and apical left ventricular wall (nonischemic and ischemic areas, respectively, in hearts with coronary artery occlusion). The distribution of CA-containing neurones was assessed morphometrically from histofluorescence sections, and the NA content measured using high pressure liquid chromatography (HPLC). In hearts without myocardial ischemia, both the density of CA-containing neurones (0.96 +/- 0.07 compared with 1.09 +/- 0.07% of total field area) and the NA content (738 +/- 63 compared with 884 +/- 84 ng/g wet weight, p less than 0.025) were less in apical samples compared with those obtained at the midventricular level. These differences were more pronounced in samples from hearts obtained following 5 min (fluorescence, 0.96 +/- 0.19 compared with 1.38 +/- 0.18%, p less than 0.01; NA content, 543 +/- 109 compared with 816 +/- 82 ng/g wet weight, p less than 0.01) or 15 min (fluorescence, 0.77 +/- 0.07 compared with 1.12 +/- 0.09%; NA content, 521 +/- 43 compared with 753 +/- 79 ng/g wet weight, p less than 0.01) of coronary artery occlusion, indicating a release of CA in the ischemic myocardium.

Animals↗