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Biomedical subjects

S Kazda

Publications and source records attributed to S Kazda.

At least 73 records · Page 4Linked to original sources
PubMed1985

[Mechanism of a genetically conditioned failure to thrive shown in a patient with ring chromosome 18].

The influence of genetic factors on growth is only partially understood. The assumed regulatory mechanism is an interplay of multiple genes, which are localized on various chromosomes. Numerical and unbalanced structural chromosome anomalies cause abundance or lack of genes and gene products. As a consequence the subtle, in their complexity hardly fully conceivable regulatory mechanisms for metabolism and growth of the single cells appear to be disturbed. This kind of model is supported by the occurrence of growth failure in most numerical and structural chromosome anomalies. Further evidence is the variability of the phenotype in cases of ringchromosome 18, which depends on the localization and degree of loss of chromosome material preceding ring formation: depending on the participation of one or several growth-regulating genes normal or impaired growth follows. Consequently we find some normally thrived proponents within the group of predominantly mal grown people with ringchromosome 18. Besides growth the phenotypical variability is concerned with a whole lot of body-functions and systems and virtually every case reported in the literature shows individual signs. This is also true for the patient reported in this paper, in whom we additionally describe the following hitherto not mentioned signs: rudimentary pair of first ribs, apical pulmonary hernias, submammilary dermal groove, hemangioma, meatal stenosis of the urethra, unilateral kidney aplasia, 6 lumber vertebral bodies, umbilical-, abdominal- and inguinal hernias.

Abnormalities, Multiple↗
PubMed1985

Healing of malignant hypertensive arteriopathy in Dahl rats by nifedipine.

Pathomorphological studies were undertaken to investigate the therapeutic effect of the Ca2+-antagonist nifedipine on malignant hypertensive arteriopathy in Dahl salt-sensitive rats. The individual course of disease was followed by comparing pre-treatment biopsies of the mesenteric arteries with post-treatment findings at necropsy. Within seven weeks, continuous therapy with nifedipine resulted in healing of early vascular lesions and in partial repair of the more advanced ones. Under normalization of blood pressure, vascular fibrinoid exacerbations were prevented and existing intramural fibrin insudates were completely or partially removed. Lamellar fibroelastosis of the intima occurred as a characteristic of repair.

Animals↗
PubMed1984

Stimulation by nifedipine of calcium transport by cardiac sarcolemmal vesicles from spontaneously hypertensive rats.

The effects of the calcium antagonist nifedipine on the binding and ATP-dependent accumulation of calcium by cardiac plasma membranes from spontaneously hypertensive rats (SHR) and from their normotensive controls (WKY) were studied at free calcium concentrations of 2 X 10(-8) M and 4 X 10(-7) M corresponding to very high affinity and high affinity binding sites respectively. Nifedipine did not significantly modify calcium binding to either class of sites in SHR or WKY membranes. In contrast, in a free calcium concentration of 2 X 10(-8) M, nifedipine enhanced ATP-dependent Ca2+ transport. The concentration of nifedipine required for significant stimulation was smaller in SHR than in WKY membranes (10(-7) M and 10(-5) M respectively). Another calcium antagonist, D600, did not modify ATP-dependent calcium accumulation by SHR or WKY vesicles. These results raise the question of the mechanism of action of nifedipine on the calcium pump and confirm the presence of abnormalities in cardiac plasma membranes from young SHR, rendering them more sensitive than WKY membranes to the calcium antagonist nifedipine.

Animals↗
PubMed1984

Mode of antihypertensive action of nitrendipine.

The antihypertensive effect of nitrendipine cannot be explained only by its reduction of the increased peripheral vascular resistance. In contrast to the antihypertensive vasodilators, nitrendipine improves impaired renal function and prevents generalized vasculopathy in hypertensive animals. Chronic treatment with nitrendipine prevents spontaneous (Okamoto rats) and salt-induced (Dahl rats) hypertension and cardiac hypertrophy. In rats with established hypertension, nitrendipine normalizes blood pressure, reduces cardiac hypertrophy, and improves renal ischaemia. In salt-induced malignant hypertension in stroke-prone spontaneously hypertensive rats, nitrendipine only slightly reduces blood pressure but dramatically improves survival and prevents vascular lesions in the heart, brain, and kidneys. Nitrendipine reduces the intracellular availability of calcium ions in vascular smooth muscle responsible for the increased peripheral and renovascular resistance in hypertension. Moreover, in preventing the deleterious calcium overload, nitrendipine preserves tissue integrity and increases life span in malignant hypertension.

Aging↗
PubMed1984

'Calcium agonist' in salt-dependent hypertension: hints at calcium-mediated blood pressure increase.

To substantiate further the hypothesized importance of increased calcium influx into vascular smooth muscle, salt-sensitive Dahl rats (DS/JR, John Rapp), on either a low or a high salt diet, were treated with 100 or 300 ppm (i.e. mg/kg food) BAY k 8644, a calcium agonist. Simultaneously, salt-resistant Dahl rats (DR/JR) on a high salt diet received 300 ppm BAY k 8644. Blood pressure rose more rapidly in the agonist-treated DS/JR rats than in the untreated DS/JR controls on high salt diet. On the low salt diet, blood pressure was only slightly higher in the agonist-treated DS/JR. Although an increased calcium influx seems to be involved in salt-induced hypertension, the presence of high sodium chloride is apparently essential for its development. In addition, since DR/JR rats remained resistant to the effect of the calcium agonist, calcium per se is not the decisive factor responsible for the sensitivity or resistance of Dahl rats to salt load.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1983

alpha 1-Antitrypsin (Pi) types and subtypes in the Tyrolean population.

Since nine patients with infantile liver cirrhosis or hepatopathy associated with the Pi ZZ phenotype had been observed in recent years in the Children's Hospital of the University of Innsbruck, Tyrol, the distribution of the Pi types and the PiM subtypes was determined in the Tyrolean population. Apparently healthy blood donors (868) from different regions of Tyrol were examined. Isoelectricfocusing was used for classification of Pi types. The frequency of the allele PiZ was 0.0138, which corresponded to the range observed in other Middle European populations. The frequencies for the suballeles of PiM were PiM1 = 0.7062, PiM2 = 0.1480, and PiM3 = 0.1037. PiS had a frequency of 0.0225, the other rare alleles occurred with a combined frequency of 0.0058.

Alleles↗
PubMed1983

Correlation between the inhibitory activities of calcium entry blockers on vascular smooth muscle constriction in vitro after K+-depolarisation and in vivo after alpha 2-adrenoceptor stimulation.

Calcium entry blockers are known to depress the maximal increase in diastolic pressure induced in pithed rats by selective alpha 2-adrenoceptor stimulation. In order to substantiate the relevance of calcium fluxes in this interaction, a correlation between the potency of calcium entry blockers in pithed rats and their calcium antagonistic potency in vitro was investigated. Accordingly, the inhibition of calcium entry blockers with respect to alpha 2-adrenoceptor-mediated vasoconstriction was quantified in terms of -log ID50 values. As a measure of calcium antagonistic potency, the inhibitory activity of a number of calcium entry blockers on K+-induced contractions of rabbit thoracic aorta strips was determined and the negative logarithms of the 50% inhibitory concentrations, -log IC50, were calculated. A highly significant linear relationship was found between the in vitro, -log IC50, and the in vivo parameter, -log ID50, of the calcium entry blockers. This result suggests a similar type of interaction for the calcium entry blockers in vivo and in vitro, i.e. inhibition of a transmembrane influx of extracellular calcium.

Animals↗
PubMed1983

Nitrendipine and other calcium entry blockers (calcium antagonists) in hypertension.

Nitrendipine is a calcium antagonistic 1,4-dihydropyridine derivative with a pronounced antihypertensive activity in animal experiment. Similar to other calcium entry blockers, nitrendipine decreases blood pressure by lowering the elevated peripheral vascular resistance. However, its long-term effect differs from that of vasodilators such as hydralazine and minoxidil. In contrast to vasodilators, nitrendipine reduces heart hypertrophy in various forms of experimental hypertension in rats. Nitrendipine is highly effective in normalizing blood pressure, reducing heart hypertrophy, and preventing mortality in salt-related hypertension (two-kidney renal hypertension, salt-induced hypertension in Dahl rats), which are rather refractory to the effect of vasodilators. Nitrendipine reduces renovascular resistance in spontaneously hypertensive rats but has no effect on that of normotensive rats. In conscious renal hypertensive dogs, nitrendipine decreases blood pressure more than does hydralazine. The reflex tachycardia is more pronounced after hydralazine than after nitrendipine; blood pressure decrease is greater and the duration of the effect is longer than that of nifedipine. Nitrendipine is thus predicted as an effective drug for antihypertensive monotherapy.

Animals↗
PubMed1982

Nimodipine: a new calcium antagonistic drug with a preferential cerebrovascular action.

Nimodipine, isopropyl (2-methoxy-ethyl) 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate, is a new calcium antagonistic vasodilator with a preferential effect on brain vessels. Nimodipine prevents spasm of the isolated rabbit basilar artery produced both by depolarization and by receptor stimulation. In peripheral vessels nimodipine does not inhibit agonistically induced contractions. In vivo nimodipine also dilates predominantly cerebral vessels; peripheral vasodilation resulting in a decrease in blood pressure is much less pronounced. Nimodipine prevents the impaired reperfusion of the brain caused by a transitory global cerebral ischaemia. Nimodipine is predicted to be useful in the prophylaxis and treatment of cerebral vasospasm in humans.

Animals↗
PubMed1982

Prevention of malignant hypertension in salt loaded "S" Dahl rats with the calcium antagonist nifedipine.

Female "S" Dahl rats, fed an 8% NaCl diet from the 6th week of age developed malignant hypertension and heart hypertrophy in the course of 6 weeks on the salt regimen. Simultaneous treatment with nifedipine (300 ppm in diet additional to 8% NaCl) prevented the increase in blood pressure, reduced heart hypertrophy and mortality and improved the impaired renal function in "S" rats. The decrease in hematocrit in salt loaded "S" rats was prevented by nifedipine. The prophylactic effect of the calcium antagonist nifedipine is only partly due to the prevention of increase in systemic vascular resistance. In addition an improvement of failed intrarenal hemodynamics by nifedipine can be postulated. This enables the kidney of "S" rats to excrete the salt load without increasing blood pressure and plasma volume.

Animals↗
PubMed1982

[Hereditary alpha 1-antitrypsin deficiency and infantile cirrhosis of the liver].

A report on 9 cases of infantile hepatopathy and cirrhosis of the liver respectively in cases of hereditary autosome-recessive alpha 1-antitrypsin deficiency (alpha 1-ATM). The genetic variants of the serum-protease-inhibitor (Pi) alpha 1-antitrypsin (alpha 1-AT) were examined by means of iso-electric focusing (Polyacrylamidgelen). The gene incidence was of the allel PiZ 0,0138 in the 868 blood donors from the Tyrol and was therefore within the range of the PiZ-frequencies seen in other Central-European populations. The other alleles PiM1, PiM2, PiM3, and PiS, point to the incidence of 0.7062, 0.1480, 0.1037, and 0.0225. The patients under observation (9) are homozygote PiZZ, the clinically healthy parents heterozygote PiZM. Risk of repetition in siblings of the patients is 25%. Early indicative symptoms are prolonged jaundice, acholic stools and hepatomegaly. Further developments are the fading of the hyperbilirubinaemia, temporary improvement in the pathological liver values, a freedom of symptoms for different lengths of time in each case, in the case of two patients, finally, decompensated cirrhosis of the liver and death in hepatic coma. The histological picture of the liver tissue shows PAS-positive storage granula in hepatozytes, intrahepatic hypoplasia of the bile duct, cholestasis as well as early cell necrobiosis, fibrosis and cirrhotic transformation. Course and severity of the liver complaint differ greatly, and are independent of the quantitative alpha 1-antitrypsin deficiency revealed, treatment is purely symptomatic.

Child↗
PubMed1982

Prevention of hypertensive vasculopathy by nifedipine in salt-loaded Dahl rats.

In female "salt-sensitive" (S) Dahl rats, with hypertension induced by 8% sodium chloride (NaCl) in the diet for six weeks, a severe generalized arteriopathy was observed histopathologically. Fibrinoid degeneration, medial hyperplasia and periarteritis were especially pronounced in the preglomerular arterial system of the kidneys. Necrosis of afferent glomerular arterioles led to regressive changes in the renal corpuscles. Numerous dilated renal tubules were filled with protein casts. In the heart, arterial lesions were predominantly localized in the outer wall of the right ventricle. Occlusion of intracardiac arteries was accompanied by focal myocardial necrosis and fibrous replacement of the myocardial fibres. A left ventricular hypertrophy was found. The degree of renal arteriopathy inversely correlated with the magnitude of the hematocrit. S rats treated with nifedipine, 300 ppm in addition to 8% NaCl in the diet remained normotensive. No changes in vessels, tissues or in the hematocrit were seen in any of the nifedipine-treated rats. The same picture was observed in "salt-resistant" (R) rats on a high (8%) and on a low (0.4%) NaCl diet. S rats fed a low NaCl diet showed only dilated renal tubules containing protein casts. It is assumed that nifedipine primarily decreases the renovascular resistance in S rats under salt load, enabling the kidney to eliminate excess sodium without inducing pressure natriuresis. Organ damage in salt-loaded S rats is thus due to a fulminant increase in blood pressure, compensating for the sluggish natriuresis.

Animals↗
PubMed1982

Cerebrovascular effects of the calcium antagonistic dihydropyridine derivative nimodipine in animal experiments.

Isopropyl(2-methoxy-ethyl) 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate (Bay e 9736, nimodipine) is a calcium antagonistic dihydropyridine derivative with a preferential effect on cerebral vessels. It dilates cerebral vessels in several species after intraarterial, intravenous, perlingual, and oral administration in low dosage. Its effect on the peripheral blood vessels is less pronounced so that nimodipine increases cerebral blood flow without substantial decrease of blood pressure. Nimodipine does not inhibit carbonic anhydrase and does not stimulate the oxygen consumption of brain tissue in vitro. Its effect is not influenced by propranolol. Therefore its cerebral vasodilating effect is due to its direct relaxing effect on vascular smooth muscle. Nimodipine prevents the postischaemic impaired cerebral reperfusion in cats. Transient global cerebral ischaemia increases the cerebrovascular resistance to flow by means of the increase in extracellular concentration of potassium ions. Such depolarization produces sustained cerebral vasoconstriction presumably by enhancing transmembrane influx of calcium. Nimodipine does not influence the ischaemic increase in Ko+ ions but effectively prevents the postischaemic cerebrovascular spasm. From its pharmacological properties nimodipine is predicted to be effective in the prevention and therapy of cerebrovascular spasm of various origins and especially in the treatment of postischaemic brain damage.

Administration, Oral↗