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Am J Physiol Regul Integr Comp Physiol. 2000 Nov;279(5):R1841-8.
Testosterone receptor blockade after trauma and hemorrhage attenuates depressed adrenal function.
Ba ZF, Wang P, Koo DJ, Zhou M, Cioffi WG, Bland KI, Chaudry IH.
Center for Surgical Research and Department of Surgery, Brown University School of Medicine and Rhode Island Hospital, Providence, Rhode Island 02903, USA.
Although the testosterone receptor antagonist flutamide restores the depressed immune function in males after trauma and hemorrhage, it remains unknown whether this agent has any salutary effects on adrenal function. To study this, male rats underwent laparotomy and were bled to and maintained at a blood pressure of 40 mmHg until 40% of the shed blood volume was returned in the form of Ringer lactate. Animals were then resuscitated and flutamide (25 mg/kg body wt) was administered subcutaneously. Plasma adrenocorticotropic hormone (ACTH) and corticosterone, as well as adrenal corticosterone and cAMP were measured 20 h after resuscitation. In additional animals, ACTH was administered and ACTH-induced corticosterone release and adrenal cAMP were determined. The results indicate that adrenal contents of corticosterone and cAMP were significantly decreased and morphology was altered after hemorrhage. Administration of flutamide improved corticosterone content, restored cAMP content, and attenuated adrenal morphological alterations. Flutamide also improved the diminished ACTH-induced corticosterone release and adrenal cAMP response at 20 h after hemorrhage and resuscitation. Furthermore, the diminished corticosterone response to ACTH stimulation in the isolated adrenal preparation was improved with flutamide. These results suggest that flutamide is a useful adjunct for improving adrenal function in males following trauma and hemorrhage.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11049869&dopt=Abstract hemorrhage
Anesth Analg. 2000 Nov;91(5):1112-7.
Dexmedetomidine and hemodynamic responses to simulated hemorrhage in experimental heart failure.
Blake DW.
Department of Pharmacology, Anesthesia Research Unit, University of Melbourne, Victoria, Australia. d.blakharmacology.unimelb.edu.au
alpha(2)-Adrenoreceptor agonists may counteract the increased basal sympathetic nervous activity in patients with congestive heart failure (CHF), but they may also compromise reflex responses to hypovolemia. We have tested responses to simulated hemorrhage (central hypovolemia) after IV dexmedetomidine in normal animals and in experimental chronic CHF. Rabbits (n = 14) were treated with IV doxorubicin (or control saline) for 8 weeks inducing biventricular dilatation and myocardial damage. Cardiac output (CO) was measured continuously with a transit-time Doppler implanted on the ascending aorta. Progressive inflation of a cuff around the inferior vena cava (simulated hemorrhage) was used to reduce cardiac index at a constant rate. Arterial baroreceptor-mediated vasoconstrictor and heart rate responses were tested with repeated cuff inflations. Although resting CO was reduced in CHF, the blood pressure and heart rate changes with dexmedetomidine were not exaggerated. The slope of the vasoconstrictor response to graded hypovolemia was attenuated by dexmedetomidine with an earlier onset of decompensation. There was no added effect of CHF on the response until the dose of dexmedetomidine was sufficient to reduce resting CO in addition to arterial blood pressure and heart rate. Implications: As an adjunct to anesthesia, dexmedetomidine may be useful in reducing basal sympathetic nervous activity. This study in experimental animals suggests this may be achieved without compromising protective responses to decreased blood volume.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11049892&dopt=Abstract hemorrhage
Proc Natl Acad Sci U S A. 2000 Oct 24;97(22):12056-61.
Hematopoietic reconstitution of SLP-76 corrects hemostasis and platelet signaling through alpha IIb beta 3 and collagen receptors.
Judd BA, Myung PS, Leng L, Obergfell A, Pear WS, Shattil SJ, Koretzky GA.
University of Iowa Program in Molecular Biology, Iowa City, IA 52242, USA.
Mice deficient in the hematopoietic cell-specific adapter protein SLP-76 demonstrate a failure of T cell development and fetal hemorrhage. Although SLP-76-deficient platelets manifest defective collagen receptor signaling, this alone may not explain the observed bleeding diathesis. Because alpha IIb beta 3, the platelet fibrinogen receptor, is required for normal hemostasis, we explored a potential role for SLP-76 in alpha IIb beta 3 signaling. Interaction of soluble or immobilized fibrinogen with normal human or murine platelets triggers rapid tyrosine phosphorylation of SLP-76. Moreover, platelet adhesion to fibrinogen stimulates actin rearrangements, filopodial and lamellipodial extension, and localization of tyrosine phosphorylated proteins to the cell periphery. In contrast, SLP-76-deficient murine platelets bind fibrinogen normally, but spread poorly and exhibit reduced levels of phosphotyrosine. The in vivo bleeding diathesis as well as the defects in platelet responses to fibrinogen and collagen are reversed by retroviral transduction of SLP-76 into bone marrow derived from SLP-76-deficient mice. These studies establish that SLP-76 functions downstream of alpha IIb beta 3 and collagen receptors in platelets. Furthermore, expression of SLP-76 in hematopoietic cells, including platelets, plays a necessary role in hemostasis.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11050236&dopt=Abstract hemorrhage
Ophthal Plast Reconstr Surg. 2002 Nov;18(6):458-61.
Orbital and adnexal trauma associated with open-globe injuries.
Hatton MP, Thakker MM, Ray S.
Trauma Service, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, USA. m.hattonebox.com
PURPOSE: To describe the incidence and patterns of orbital and adnexal injuries in patients with open-globe injuries. METHODS: Charts of 300 consecutive patients with open-globe injuries presenting to the Massachusetts Eye and Ear Infirmary were retrospectively reviewed. The data were analyzed with respect to the type of open globe (penetrating, perforating, or rupture) and location (zone) of globe injury. Each of these subgroups was then evaluated for the absence (group 1) or presence (group 2) of coexisting orbital and/or adnexal injury. Visual acuity at presentation was compared between the two groups. RESULTS: Orbital and adnexal injuries were present in 25.7% of patients with open globes. The most common concurrent injuries were lacerations of the eyelid, orbital fracture, and retrobulbar hemorrhage. The mechanisms of globe injury differed significantly between groups 1 and 2. Penetrating injuries accounted for 82.1% of group 1 but only 49.3% of group 2 patients, whereas rupture occurred more frequently in group 2 (48.1%) than in group 1 (17.0%) patients. Orbital and adnexal injuries were associated with poorer visual acuity at presentation, probably because of the high incidence of posterior globe injuries in these patients. CONCLUSIONS: Orbital and adnexal injuries were observed in 25.7% of patients who sustained trauma that resulted in open globes. Concurrent injury to these extraocular structures is associated with worse visual acuity at presentation and an increased likelihood of posterior globe injuries.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12439061&dopt=Abstract hemorrhage
Am J Gastroenterol. 2000 Oct;95(10):2807-12.
Provocative angiography in patients with gastrointestinal hemorrhage of obscure origin.
Bloomfeld RS, Smith TP, Schneider AM, Rockey DC.
Department of Medicine and Radiology, Duke University Medical Center, Durham, North Carolina, USA.
OBJECTIVE: A standard diagnostic evaluation including upper and/or lower endoscopy, tagged red blood cell scintigraphy, and visceral angiography identifies the source of GI bleeding in the majority of patients who present with acute GI hemorrhage. However, in a small group of patients the source of bleeding remains obscure; this form of GI hemorrhage is uncommon but represents a considerable diagnostic challenge. Some investigators have advocated provocation of bleeding with vasodilators, anticoagulants, and/or thrombolytics in association with tagged red blood cell scans or angiography. Unfortunately, the available literature on this topic is limited. Therefore, the purpose of this study is to report our experience with provocative GI bleeding studies. METHODS: The radiology databases at Duke University Medical Center and the Durham Veterans Administration Medical Center were reviewed from 1994 to 1999. Any patient who received a vasodilator, anticoagulant, or thrombolytic to induce bleeding during a tagged red blood cell scan or visceral angiogram was included. RESULTS: Seven provocative bleeding studies were performed on seven patients. All patients underwent a visceral angiogram with intra-arterial administration of tolazoline (a vasodilator), heparin (an anticoagulant), and/or urokinase (a thrombolytic). Of the seven provocative studies, only two induced angiographically identifiable bleeding. Both of these patients underwent surgical therapy. There were no complications attributed to the provocative bleeding studies. CONCLUSIONS: These results suggest that provocative GI bleeding studies can be performed safely. However, because an active bleeding source was identified in only a small proportion of patients, we believe that further study is required to optimize patient selection and to clarify the cost-effectiveness of this approach in patients with GI hemorrhage of obscure origin.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11051352&dopt=Abstract hemorrhage
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