Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Articles: DFG German National Licenses  (3)
  • Angiotensin II  (1)
  • Cardiomyopathy  (1)
  • Clotting inhibitors  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Deterioration of metabolic coronary regulation in hemorrhagic shock (1985)
    Springer
    Research in experimental medicine 185 (1985), S. 429-443 
    Details
    ISSN: 1433-8580
    Keywords: Myocardial blood flow ; Angiotensin II ; Saralasin ; Nephrectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of hypoxia and the renin-angiotensin system on metabolic coronary regulation in hemorrhagic shock was studied in 22 anesthetized open-chest dogs. Left circumflex coronary blood flow was measured with an electromagnetic flowmeter. Dogs were ventilated with room air (n = 8) or 100% oxygen (n = 7). A third group of dogs was ventilated with room air and bilaterally nephrectomized 5 h prior to starting the experimental protocol (n = 7). After control data had been obtained, dogs were bled from the femoral arteries into a pressurized reservoir which maintained blood pressure at 45 ± 1 mm Hg. The angiotensin II receptor blocker, saralasin, was then infused i.v. (0.1, 1.0, 10.0 µg/kg per min). Coronary blood flow was reduced by hemorrhage, and no significant difference existed in coronary flow during hemorrhage among the three groups. Coronary sinus oxygen saturation was diminished in control animals during hemorrhage from 26% ± 1% to 17% ± 1% (P 〈 0.05) but normal in 100% oxygen ventilated animals (30% ± 3%) and in nephrectomized dogs (34% ± 4%). Coronary oxygen extraction was reduced by saralasin in intact but not in nephrectomized dogs. In six additional experiments, in which blood pressure was not artificially held constant during saralasin infusion, saralasin still significantly improved coronary sinus oxygen saturation and thus reduced coronary oxygen extraction. The data suggest that both hypoxia and the reninangiotensin system participate in the restriction of metabolic coronary regulation in hemorrhagic shock.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01851849
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Effects of long-term treatment with lovastatin on the clotting system and blood platelets (1992)
    Springer
    Annals of hematology 64 (1992), S. 196-201 
    Details
    ISSN: 1432-0584
    Keywords: Type-IIa hypercholesteremia ; Lovastatin ; Platelet function ; Fibrinogen ; Clotting inhibitors ; Fibrinolytic activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a study of 20 patients with hypercholesterolemia (type IIa) the effects of lovastatin (20–80 mg/ day) on various clotting and thrombosis parameters were monitored for 12 months. On 11 occasions various cholesterol fractions and clotting parameters were determined in each patient. In additon, the clotting inhibitors AT III, protein C, protein S, and C1-esterase inhibitor and the fibrinolysis parameters plasminogen and α2-antiplasmin were examined. Platelet function was monitored on the basis of spontaneous and induced (collagen, ADP, epinephrine, ristocetin) aggregation. Lovastatin in the above dosage brought about a 66 mg/dl (from 320 ± 12.6 to 254 ± 12.0 mg/dl) reduction in the total cholesterol level and a 56 mg/dl (from 244 ± 11.4 to 188 ± 12.1 mg/dl) reduction in LDL cholesterol at the end of the study. Fibrinogen showed a significance decrease during the study period, whereas PT and aPTT remained unaffected. The initial slopes of the ADP-induced platelet aggregation revealed a significant decrease. C-reactive protein and platelet count remained within the normal range, indicating no significant change. Thrombin clotting time, AT III, Cl-esterase inhibitor, plasminogen, and α2-antiplasmin were not modified. Protein C and S behaved in a contradictory way, but remained within the normal range. Long-term treatment with lovastatin was associated with a significant reduction of fibrinogen levels and platelet aggregation induced by ADP in type-IIa hypercholesterolemic patients. These alterations, as well as their role in cardiovascular disease, should be the subject of further investigations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01696223
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Absoluter TBG-Mangel (Athyropexinämie) und hypertrophische obstruktive Kardiomyopathie (1978)
    Springer
    Journal of molecular medicine 56 (1978), S. 1213-1216 
    Details
    ISSN: 1432-1440
    Keywords: Athyropexinemia ; Cardiomyopathy ; Hypertrophic ; Heart defects ; Congenital ; Hereditary diseases ; Combined thyroxine-binding protein thyropexin deficiency ; Athyropexinämie ; Erbgang ; Erbanomalien, kombinierte ; Kardiomyopathien, hypertrophische, kongenitale ; Erbgang ; Thyropexinmangel, erblicher ; Thyroxin-bindendes Globulin ; Kombinierter Erbgang Thyropexinmangel und Kardiomyopathien
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei einem Patienten mit hereditärer hypertrophischer obstruktiver Kardiomyopathie (HOCM) fehlt das thyroxinbindende Globulin („Thyropexin“) völlig. Obwohl der Thyroxinspiegel extrem niedrig ist und die Schilddrüse eine erhöhte Jodavidität aufweist, erscheint der Patient klinisch euthyreot. Ein ähnliches Syndrom hat Ingbar 1961 beschrieben. Bei einem Onkel des Patienten und bei zwei Neffen, von denen einer eine asymmetrische Septumhypertrophie (ASH) aufweist, besteht eine Athyropexinämie; bei der Mutter, bei einer Schwester und einer Kusine ist das Thyropexin vermindert. Die Mutter leidet an einer hypertrophischen Kardiomyopathie (HCM).
    Notes: Summary A twenty-five years old man was found to have simultaneous total deficiency of thyroxine-binding globulin (“thyropexin”) and hereditary hypertrophic obstructive cardiomyopathy (HOCM). The thyroxine-binding capacity (RT3U), thyroid hormone levels, PB127I, PB131I and TBG (RIA) in serum were very low and TBG cap was zero. Trapping of radioiodine in the thyroid was enhanced. Clinically, the patient appeared euthyroid. The case seems to be similar to another one described earlier by Ingbar. An investigation of the family showed that in one uncle and two nephews of the patient thyropexin was absent whilst the mother, one sister and one female cousin had partial thyropexin deficiencies. One of these nephews also suffers from asymmetric septal hypertrophy (ASH), the mother of the propositus has a non-obstructive hypertrophic cardiomyopathy (HCM).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01477077
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...