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Biomedical subjects

G Hansmann

Publications and source records attributed to G Hansmann.

9 recordsLinked to original sources
PubMed2004

[Neonatal-emergencies: basics in cardiopulmonary resuscitation].

The international guidelines for neonatal resuscitation were recently updated by the American Academy of Pediatrics (AAP), the American Heart Association (AHA) and the International Liaison Committee on Resuscitation (ILCOR). The most important steps in resuscitation of the newly born infant are oxygenation and ventilation, including endotracheal intubation. These fundamental techniques will be emphasized and discussed in a problem-oriented approach. The clinical assessment of the newly born infant is based on a triad of respiration, heart rate and color. If indicated, resuscitation has to be initiated approximately 30 s after birth, i. e. prior to determination of the 1 min. Apgar score and umbilical artery pH. The key to successful neonatal resuscitation is establishment of adequate ventilation; it should commence - after oropharyngeal suctioning and ineffective tactile stimulation - when the heart rate drops < 100 bpm. Clinical evidence supporting the hypothesis that ventilation with room air versus 50 or 100 % oxygen is preferable in terms of neurological outcome is still preliminary and requires further investigation. Chest compressions should be administered if the heart rate remains < 60 bpm (or heart rate 60 to 80 bpm and not rising) despite adequate assisted ventilation. There should be a 3 : 1 ratio of compressions to ventilations to achieve approximately 120 events per minute. Moreover, the international guidelines recommend crystalloid volume expanders (normal saline or Ringer's lactate), red blood cells, sodium bicarbonate and naloxone for cardiopulmonary resuscitation of the newly born infant.

Cardiopulmonary Resuscitation↗
PubMed2001

The impact of chemotherapy on Leydig cell function in long term survivors of germ cell tumors.

BACKGROUND: Because patients with germ cell tumors expect an additional life span of around 50 years after successful treatment, attention is now focused on potential long term toxicity. Limited data are available on Leydig cell function in long term survivors. METHODS: The authors measured testosterone, sex hormone binding-globulin (SHBG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels in 244 patients with germ cell tumors. Patients were divided into three groups: Group 1 had received no chemotherapy (n = 58 patients), Group 2 had received cumulative doses of cisplatin < or = 400 mg/m(2) (n = 117 patients), and Group 3 had received cumulative doses of cisplatin > 400 mg/m(2) (n = 69 patients). The median times from chemotherapy were 74 months and 75 months in Groups 2 and 3, respectively. RESULTS: Subnormal testosterone levels (< 10 nmol/L) were found in 5%, 11%, and 20% in Groups 1, 2, and 3, respectively (Group 1 vs. Group 3; P = 0.02). The mean testosterone level and the testosterone/SHBG ratio did not differ significantly between Groups 1 and 2; however, they did differ between Groups 1 and 3 (testosterone: 17.0 nmol/L vs. 14.9 nmol/L, respectively; P = 0.02; testosterone/SHBG ratio: 0.70 vs. 0.59; P < 0.05). There was a significant inverse correlation between the testosterone/SHBG ratio and LH (correlation coefficient [r] = -0.25; P = 0.0002). A significant positive correlation was found for LH and FSH (r = 0.78; P < 0.0001), indicating a strong association between Leydig cell dysfunction and germinal epithelial damage. CONCLUSIONS: Standard doses of cisplatin-based chemotherapy do not lead to a significant deterioration of Leydig cell function in long term survivors of germ cell tumors. In contrast, high cumulative doses of chemotherapy cause a significant and persistent impairment of Leydig cell function. More data are needed regarding the clinical relevance of moderate testosterone deficiency. Further research is necessary to determine whether some patients may benefit from testosterone replacement.

Adolescent↗
PubMed1998

Nucleotide-evoked relaxation of human coronary artery.

Endothelium-dependent dilation of coronary blood vessels in response to ATP and related nucleotides has been demonstrated in various animal species. The aim of the present study was to investigate a possible relaxant effect of ATP, the adenine nucleotides 2-methylthio ATP (MeSATP) and adenosine 5'-O-(2-thiodiphosphate) (ADPbetaS), and the pyrimidine nucleotide UTP in isolated human coronary artery. In endothelium-intact rings of human coronary artery precontracted with K+ (20-40 mM), the nucleotides caused relaxation. Average maximal percentage relaxations and average EC50 values (concentrations causing half-maximal relaxation) were 89% and 47.1 microM for ATP, 28% and 0.3 microM for MeSATP, 35% and 0.6 microM for ADPbetaS, and 49% and 1.6 microM for UTP. For each of the four agonists, the potency to elicit relaxation varied greatly between individual rings, so that equi-relaxing concentrations spanned several orders of magnitude. Moreover, the sensitivities to ATP and UTP, when tested in the same ring, were not correlated. Mechanical removal of the endothelium as well as NG-nitro-L-arginine methyl ester (L-NAME; 30 microM), an inhibitor of nitric oxide synthase, abolished the relaxation caused by MeSATP, ADPbetaS and UTP and greatly attenuated the response to lower concentrations of ATP (3.2-320 microM), but high concentrations of ATP (320 and 1000 microM) caused relaxation also in endothelium-denuded preparations and in the presence of L-NAME. High concentrations of ADPbetaS (32 and 100 microM) and UTP (320 and 1000 microM) caused contraction of endothelium-denuded preparations. Thus, extracellular nucleotides cause endothelium-dependent, primarily nitric oxide-mediated relaxation of human coronary artery. ATP in addition causes endothelium-independent relaxation. The receptors activated by the nucleotides appear to be unevenly distributed on the coronary endothelium.

Adenosine Diphosphate↗
PubMed1997

Characterization by antagonists of P2-receptors mediating endothelium-dependent relaxation in the rat aorta.

The receptors through which 2-methylthio ATP (MeSATP), adenosine 5'-O-(2-thiodiphosphate) (ADP beta S), UTP and ATP elicit endothelium-dependent relaxation of noradrenaline-precontracted rings of the rat aorta were characterized by means of a series of antagonists. The acetylcholine-induced relaxation and the degradation of MeSATP, UTP and ATP were also studied. The potency of the nucleotides at producing relaxation decreased in the order MeSATP (EC50 0.24 microM) > ADP beta S (0.43 microM) > UTP (1.09 microM) > ATP (3.53 microM). MeSATP, ADP beta S and UTP did not cause relaxation when the endothelium had been destroyed; high concentrations of ATP still caused some relaxation. The relaxation by MeSATP, ADP beta S and UTP became very small after treatment of the rings with NG-nitro-L-arginine methyl ester; the relaxation by ATP was less affected. Pre-exposure to MeSATP (100 microM) abolished or almost abolished the relaxation normally elicited by MeSATP and ADP beta S, did not change that elicited by UTP and slightly enhanced the relaxation elicited by ATP. Of nine compounds examined as antagonists, six attenuated selectively the effect of some or all of the nucleotides (as compared to acetylcholine): suramin, reactive blue 2, pyridoxalphosphate-6-azophenyl-2',5'-disulphonate (iso-PPADS), pyridoxalphosphate-6-azophenyl-2',4'-disulphonate (PPADS), reactive red 2 and 5,5'-(1,1'-biphenyl-4,4'-diylbisazo)-bis-7-amino -6-hydroxy-naphthalene-1,4-disulphonate (NH05). Decreases of maximal relaxations and slopes different from unity in Schild plots often indicated non-competitive kinetics of the antagonism. For each of the six 'selective' antagonist, the apparent Kd values against MeSATP and against ADP beta S were similar: none of the six differentiated between MeSATP and ADP beta S. Also, for each of four 'selective' antagonists, the apparent Kd values against UTP and against ATP were similar: none of the four differentiated between these two nucleotides (two antagonists did not act against UTP and ATP in the 'selective' concentration range). On the other hand, for five of the six 'selective' antagonists (the exception being NH05), the apparent Kd values against MeSATP and ADP beta S were considerably lower than those against UTP and ATP. At the highest concentrations tested against agonist-evoked relaxations, the antagonists did not alter the removal from the incubation medium, by pieces of rat aorta, of MeSATP, UTP and ATP. It is concluded that nucleotides cause endothelium-dependent relaxation of the rat aorta through two sites: a P2Y-receptor and a P2U-receptor. The receptors may be pharmacologically similar to a bovine endothelial P2Y (P2Y1) and a cloned rat P2U (P2Y2) receptor, respectively. ATP acts mainly through the P2U-receptor. Suramin, reactive blue 2, iso-PPADS, PPADS and reactive red 2 are more potent at the P2Y- than the P2U-receptor. NH05 does not discriminate between the two receptors but is the most potent P2U antagonist so far described.

Acetylcholine↗
PubMed1997

Vasoconstrictor and vasodilator effects of guanine nucleotides in the rat aorta.

Although GTP, like ATP and UTP, is stored in platelet dense granules, little is known about its vascular effects. The present study was carried out in order to characterize the effects of GTP and related compounds in the rat aorta. Contractions were examined in aortic rings at resting tension. In rings with intact endothelium, GTP, GDP, guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) and guanosine 5'-O-(2-thiodiphosphate) (GDP beta S) caused small contractions. In endothelium-denuded rings, the contractions were unchanged or increased and persisted after desensitization of P2X-receptors by alpha,beta-methylene ATP. Relaxations were examined in aortic rings precontracted with noradrenaline. In rings with intact endothelium, GTP (EC50 131 microM), GDP (no maximal effect obtained), GTP gamma S (EC50 6.8 microM) and guanosine (EC50 822 microM) caused prominent relaxation, whereas GDP beta S caused further contraction. In endothelium-denuded rings, the relaxant effect of GTP was greatly reduced, that of GDP and guanosine was unchanged, and that of GTP gamma S was abolished. Relaxations by GTP and GTP gamma S in endothelium-intact rings were studied in more detail. The relaxation by GTP was slightly and the relaxation by GTP gamma S greatly reduced after treatment with NG-nitro-L-arginine methyl ester. Pre-exposure to a high concentration of the P2Y-receptor agonist 2-methylthio ATP (MeSATP) did not attenuate the effects of GTP and GTP gamma S. Four compounds previously identified as antagonists at the P2Y- and P2U-receptors of rat aortic endothelium--suramin, reactive blue 2, pyridoxalphosphate-6-azophenyl-2',5'-disulphonate (iso-PPADS) and 5,5'-(1,1'-biphenyl-4,4'-diylbisazo)-bis-7-amino-6- hydroxynaphthalene-1,4-disulphonate (NH05)--were tested against GTP and GTP gamma S. Suramin, reactive blue 2 and iso-PPADS were much less potent against GTP and GTP gamma S than previously found against (the P2Y effect of) MeSATP. Suramin, iso-PPADS and NH05 were about as potent against GTP and GTP gamma S as previously found against (the P2U effect of) UTP and in particular ATP. It is concluded that guanine nucleotides can cause both contraction and relaxation of the rat aorta. The high concentrations of GTP and GDP required, and in the case of contraction the small size of the response, make a physiological role of the vascular effects of these nucleotides unlikely. GTP and GTP gamma S elicit endothelium-dependent relaxation through P2U-receptors. GTP in addition relaxes the aorta through smooth muscle receptors, possibly by way of its degradation product guanosine. The stable analog GTP gamma S is a relatively potent and selective agonist for the endothelial P2U-receptor.

Animals↗
PubMed1988

The pigmented epithelium sustains cell growth and tissue differentiation of chicken retinal explants in vitro.

Embryonic retinae from 5-6-day-old chicks (E5-E6) were cut into stripes either in close contact with (RPE stripes) or in absence of the neighboring retinal pigmented epithelium (R stripes). The stripes were explanted and cultivated in vitro for up to 6 days, during which time they show the following differences in their characteristics of growth and differentiation. Compared with R stripes, RPE stripes morphologically showed a significant increase in size during the first 2 days in culture. Using E5 tissue, this is also demonstrated by a higher rate of cell proliferation (as measured by uptake of radioactive thymidine as well as by DNA contents). In contrast, R stripes after two days in culture show a much stronger neurite growth. After longer periods of culturing (5-6 days) we can show by cholinesterase histochemistry (AChE and BChE) and by PNA-lectin binding that the RPE stripes have started to form all major layers of the in vivo retina, whereas R stripes remain unstratified and start to degenerate earlier. We conclude that the pigment epithelium might exert a specific stimulus on growth and tissue differentiation of the neural retina not only during in vitro, but possibly also during in vivo development. The in vitro methods introduced here could become useful model systems to further investigate the significance of the RPE for developmental, regenerative and even adult processes of the neural retina. Their future applicability in ophthalmologic research is briefly discussed.

Animals↗
PubMed1983

Self-renewal of stem cells and differentiation of nerve cells in the developing chick retina.

Data on proliferation and self-renewal of stem cells in the developing chick retina were obtained on the basis of measurements of cells labeled by [3H]thymidine pulses in conjunction with the rate of increase in total cell number. Duration of S-phase was found to be about 4 h between stages 4 and 9 days. Self-renewal drops below the critical value of 50% (implying a transition from increase to depletion of absolute number of stem cells in the tissue) around day 7.6. The spatial order of cell proliferation was studied by measurements taken on subregions of retinas at various stages of development. Proliferating cells forming the ventricular layer increase in all regions of the retina up to day 7, though the proportion of proliferating cells is lowest in the center. From day 5 on it is higher in the nasal as compared to the temporal part of the tissue. After day 7 self-renewal of stem cells drops below 50%, stem cells become depleted and withdraw gradually from mitosis. The process is initiated in the center slightly temporal to the dorsal end of the optic fissure and then spreads rapidly towards the periphery, reaching the temporal margin first. The findings imply that while cells at the periphery are younger on the average, those cells which have become postmitotic at an early stage are not confined to a small central core of the fully developed retina, because the tissue continues to grow and produce postmitotic cells in all regions of the retina up to day 7.

Animals↗