scholarly journals The Effect of Gallium Nitrate on Arresting Blood Flow from a Wound

2011 ◽  
Vol 2011 ◽  
pp. 1-3 ◽  
Author(s):  
Paul H. Goodley ◽  
Moshe Rogosnitzky
Keyword(s):  
Blood Flow ◽  
Bleeding Time ◽  
Substantial Reduction ◽  
Treatment Modalities ◽  
Trauma Treatment ◽  
Gallium Nitrate ◽  
Open Wound

A novel application of gallium nitrate, hitherto unreported, in reducing bleeding time from an open wound is presented. Experiments performed using simple punctures in the forearm demonstrated a very substantial reduction in bleeding time when a solution of gallium nitrate was applied relative to a control. This outcome was shown to be unaffected by the anticoagulant properties of warfarin. The mechanism for such action of gallium nitrate is unknown and merits further investigation, as do the possibilities for such an application to improve both civilian and defense trauma treatment modalities.

scholarly journals WALANT–Epinephrine injection may lead to short term, reversible episodes of critical oxygen saturation in the fingertips

2021 ◽  
Vol 141 (3) ◽  
pp. 527-533
Author(s):  
P. Moog ◽  
M. Dozan ◽  
J. Betzl ◽  
I. Sukhova ◽  
H. Kükrek ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Substantial Reduction ◽  
Tissue Perfusion ◽  
Critical Levels ◽  
Short Term ◽  
Doppler Flowmetry ◽  
Epinephrine Injection ◽  
Venous Oxygen Saturation

Abstract Introduction Although the WALANT technique’s long-term safeness has been demonstrated in many studies, there are only few data investigating its short-term effects on tissue perfusion and oxygen levels. It was hypothesized that, temporarily, critical levels of tissue perfusion may occur. Methods Seventeen patients, who were scheduled for different procedures in WALANT technique, were injected with 5–7 ml of 1% Articain containing 1:200,000 epinephrine at the finger base. Capillary-venous oxygen saturation, hemoglobin volume in the capillaries, and relative blood flow in the fingertips were recorded once per second by white light spectrometry and laser Doppler flowmetry before, during and after injection for an average of 32 min. Results Clinically, no persistent tissue malperfusion was observed, and there were no postoperative complications. Capillary-venous oxygen saturation was reduced by ≥ 30% in seven patients. Critical levels of oxygen saturation were detected in four patients during 13 intervals, each lasting for 132.5 s on average. Oxygen saturation returned to noncritical values in all patients by the end of the observation period. Blood flow in the fingertips was reduced by more than 30% in nine patients, but no critical levels were observed, as with the hemoglobin. Three patients demonstrated a reactive increase in blood flow of more than 30% after injection. Conclusions Injection of tumescent local anesthesia containing epinephrine into finger base may temporarily cause a substantial reduction in blood flow and lead to critical levels of oxygen saturation in the fingertips. However, this was fully reversible within minutes and does not cause long-term complications.

Osteonecrosis of the Femoral Head of Laboratory Animals: The Lessons Learned from a Comparative Study of Osteonecrosis in Man and Experimental Animals

2003 ◽  
Vol 40 (4) ◽  
pp. 345-354 ◽  
Author(s):  
J. H. Boss ◽  
I. Misselevich
Keyword(s):  
Blood Flow ◽  
Femoral Head ◽  
Weight Bearing ◽  
Arterial Occlusion ◽  
Lessons Learned ◽  
Laboratory Animals ◽  
Treatment Modalities ◽  
Venous Stasis ◽  
Spontaneously Hypertensive ◽  
Bearing Loads

Animal models of osteonecrosis of the femoral head are indispensable to the understanding of successful treatment modalities for avascular necrosis of the femoral head in adults and in children with Legg-Calvé-Perthes disease. Many of these models adequately reflect the current “vascular deprivation” theory regarding the etiology of the disease. In addition to spontaneous occurrence, surgical- and corticosteroid-induced models are suitable, common experimental ones. Osteonecrosis of spontaneously hypertensive rats appears to be due to defective bone formation and compression of the arteries entering the femoral head at its lateral facets by daily weight-bearing loads. Successful modeling of surgical-induced femoral capital necrosis can be a challenge in animals with a dual epiphyseal blood supply. High doses of corticosteroids are a pivotal risk factor in the development of osteonecrosis. The pathogenesis of corticosteroid-induced osteonecrosis likely resides in reduced blood flow. Steroids may reduce blood flow by numerous mechanisms, including marrow adipocytic hypertrophy leading to sinusoidal compression, venous stasis and, eventually, obstruction of the arteries, and arterial occlusion by fat emboli and lipid-loaded fibrin-platelet thrombi. Other, less common varieties of osteonecrosis include those secondary to endotoxin-induced disseminated intravascular coagulation, immune reactions, immoderately low or high temperatures, and high-impact-related injuries. Common to these diverse forms of osteonecrosis are fibrin thrombi clogging arterioles and small arteries.

Naloxone infusion and drainage of cerebrospinal fluid as adjuncts to postoperative care after repair of thoracoabdominal aneurysms

1999 ◽  
Vol 19 (5) ◽  
pp. 37-47
Author(s):  
LA Iacono
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Critical Care ◽  
Postoperative Care ◽  
Regional Blood Flow ◽  
Neurological Complications ◽  
Critical Care Nurses ◽  
Treatment Modalities ◽  
Assessment Skills ◽  
New Treatment

The mechanisms that produce paraplegia in patients after TAA repair are complex and involve alterations in regional blood flow to the spinal cord, CSF dynamics, and reperfusion. Although neither the minimal level of blood flow nor the maximal spinal cord pressure that can be tolerated by the spinal cord is known, adjuncts such as CSF drainage and naloxone infusions may allow longer durations of aortic cross-clamping before irreversible ischemia occurs. Because paraplegia is multifactorial and none of the recommended adjuncts alone provides complete protection of the spinal cord, a combination of treatments may be necessary to reduce the prevalence of neurological complications after thoracoabdominal aortic reconstruction. Critical care nurses thus must be acquainted with the advanced monitoring techniques and the pathophysiology behind these new treatment modalities. Advanced assessment skills are also essential to recognize the potential neurological complications that may occur in these patients. Care of patients with TAA is a challenge. Critical care nurses must use multidimensional skills in the areas of hemodynamic monitoring, physical assessment, and psychological counseling to effectively manage postoperative care of these patients.

scholarly journals Duktus Arteriosus pada Bayi Prematur

2020 ◽  
Vol 1 (2) ◽  
pp. 89-97
Author(s):  
Agus Cahyono
Keyword(s):  
Blood Flow ◽  
Necrotizing Enterocolitis ◽  
Pulmonary Blood Flow ◽  
Ductus Arteriosus ◽  
Prostaglandin Synthesis ◽  
Treatment Modalities ◽  
Organ Blood Flow ◽  
Descending Aorta ◽  
Drug Adverse Event ◽  
Important Structure

Abstract—Ductus arteriosus (DA) is a connecting vessel between proximal descending aorta and pulmonary artery. This important structure normally close after birth. The opened ductus causes increasing of pulmonary blood flow and decreasing of certain organ blood flow (intestine, skin, muscle, and renal) causing complications such as heart failure, metabolic acidosis, necrotizing enterocolitis, and pulmonary edema/bleeding. Prevalence of DA is 0,2/1000 live birth. In under 1500 g babies the proportion of DA is 25%. Surgery and medicine are the treatment modalities of DA closure. Modalities of medicine are indometacine, ibuprofen, and paracetamol. These three modalities work by inhibiting cyclooxygenase enzime causing blockade of prostaglandin synthesis. Drug adverse event can be minimized by carefull in making treatment choice. Keywords: ductus arteriosus, complication, treatment Abstrak—Duktus arteriosus (DA) merupakan pembuluh darah yang menghubungkan aorta desendens proksimal dan arteri pulmonalis. Struktur yang penting pada janin tersebut secara normal menutup setelah lahir. Duktus yang masih terbuka tersebut mengakibatkan peningkatan aliran darah paru dan penurunan aliran darah ke organ usus, kulit, otot, dan ginjal sehingga menyebabkan komplikasi seperti gagal jantung, asidosis metabolik, necrotizing enterocolitis (NEC), serta edema paru/perdarahan. Prevalensi DA yang masih terbuka adalah 0,2 per 1000 kelahiran hidup. Proporsi bayi yang bergejala dengan DA yang masih terbuka kurang lebih 25% bayi dengan berat badan lahir di bawah 1500g. Pilihan terapi penutupan DA adalah cara bedah dan medis. Cara medis memiliki beberapa pilihan yaitu indometasin, ibuprofen, dan parasetamol. Ketiga modalitas terapi tersebut bekerja melalui penghambatan enzim siklooksigenase sehingga sintesis prostaglandin terhambat. Beberapa hal perlu diperhatikan dalam membuat pilihan terapi sehingga komplikasi yang berhubungan dengan efek samping obat dapat dihindari.. Kata kunci: ductus arteriosus, komplikasi, terapi

Novel Combination of Gallium Nitrate, Rituximab and Dexamethasone for the Treatment of Relapsed or Refractory Diffuse Large B-Cell Lymphoma, Mantle Cell Lymphoma or Transformed Follicular Lymphoma.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4755-4755
Author(s):  
Scott E. Smith ◽  
Patrick J. Stiff ◽  
Tulio Rodriguez ◽  
Amir Toor ◽  
Jared Klein
Keyword(s):  
Ribonucleotide Reductase ◽  
Transferrin Receptor ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
The United States ◽  
Treatment Modalities ◽  
High Dose ◽  
Gallium Nitrate ◽  
Hospitalization Costs ◽  
Grade 3

More than 56,000 new cases of non-Hodgkin’s lymphoma (NHL) will be diagnosed this year in the United States. Despite advances in treatment modalities such as radiation, biologic agents, and cytotoxic chemotherapeutic regimens, only 25–30% of these patients will be cured of their disease. Standard salvage regimens such as DHAP, ESHAP, ICE and EPOCH have proven efficacy at the cost of increasing toxicity and hospitalization costs. The reported response rates for these are on the order of 50–75% as first-line salvage regimens. However, as our aging patient population develops worsening performance status and co-morbidities, it seems appropriate to develop effective lymphoma treatments, which have fewer toxicities and lower costs for administration. One approach is to combine non-myelosuppressive therapies. One non-myelosuppressive agent, which has efficacy in lymphoma, is gallium nitrate. Investigation of gallium nitrate for cancer treatment dates back to the 1970’s. While it is currently approved for the treatment of bisphosphonate resistant hypercalcemia of malignancy, it has also been shown to inhibit ribonucleotide reductase and bind transferrin and potentially complex with the transferrin receptor, which is highly expressed in intermediate and aggressive histology lymphomas. It appears that the binding of the transferrin receptor on the lymphocyte as well as its inhibition of ribonucleotide reductase, eventually impairs iron metabolism, which is a necessary component of the intracellular cytochrome systems/mitochondrial function and ultimately oxidative phosphorylation. The current study is a phase II clinical trial investigating the combination of gallium nitrate, rituximab and dexamethasone (GaRD) for relapsed or refractory DLBCL, MCL or transformed follicular lymphomas. The gallium nitrate is given at 200mg/m2 CIV days 1–7, rituximab 375mg/m2 IVPB day 1 and dexamethasone 40 mg po days 1–4. Eligible patients must have proven relapsed or refractory disease and have a SWOG PS <3. Patients may have failed prior ASCT or allogeneic SCT. The accrual goal is 37 patients. We have enrolled 14 patients on study to date and have 12 evaluable patients; as part of the ongoing safety evaluation for this study, we have the following results: ORR 9/12 (75%); CR 2/12 (17%); PR 7/12 (58%); SD 2/12 (17%); and PD 1/12 (8%). Most of these patients were refractory to prior salvage regimens 8/12 (67%), including ESHAP, DHAP or high-dose cyclophosphamide. No patients developed grade 3 or 4 toxicities, with the exception of grade 4 lymphopenia and grade 3 anemia (most likely due to transferrin receptor binding). Conclusions: gallium nitrate, rituximab and dexamethasone (GaRD) appears to be an effective and relatively non-toxic salvage regimen for patients with relapsed DLBCL, MCL or transformed FL.

scholarly journals TCD Diastolic Velocity Decay and Pulsatility Index Increment in PVS Cases

2010 ◽  
Vol 37 (6) ◽  
pp. 831-836 ◽  
Author(s):  
Jesús Perez-Nellar ◽  
Calixto Machado ◽  
Claudio E. Scherle ◽  
Mauricio Chinchilla
Keyword(s):  
Blood Flow ◽  
Pulsatility Index ◽  
Functional Neuroimaging ◽  
Single Photon ◽  
Vegetative State ◽  
Photon Emission ◽  
Persistent Vegetative State ◽  
Substantial Reduction ◽  
Emission Tomography ◽  
Diastolic Velocity

AbstractBackground:Functional neuroimaging has provided new insights for assessing cerebral function in persistent vegetative state patients (PVS). Compared to controls, positron emission tomography and single photon emission tomography have shown a substantial reduction of global brain cerebral glucose metabolism and perfusion in PVS. Doppler ultrasonography (TCD) assesses local blood flow velocity and direction in the proximal portions of large intracranial arteries; it is a noninvasive technique, and it can be carried out at the bedside. To date, few studies have applied TCD to study PVS.Methods:We assessed intracranial circulation by TCD in five PVS patients. The cause of brain insult was hypoxic encephalopathy in four cases, and the other suffered an embolic cerebral infarct causing a top of the basilar artery syndrome. The sample volume was set at 12 mm; power output and gain settings were maximized as needed. The temporal bone acoustic window was not suitable for intracranial vessel insonation in all patients. As an alternative, the internal carotid artery siphon was assessed by orbital insonation between 55-70 mm.Results:Systolic velocity was within a normal range, between 44 and 62 cm/second in all cases. However, the diastolic amplitude was reduced, as well as the end diastolic velocity, and the pulsatility index was increased in all patients.Conclusions:We conclude that TCD diastolic velocity decrement and PI augmentation in our cases might be related to uncoupling of cerebral blood flow and cerebral metabolic rate, arising from reduced cerebral glucose consumption and oxygen uptake, after extensive brain injury.

In Vivo Relevance for Platelet Glycoprotein Ibα Residue Tyr276 in Thrombus Formation.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 216-216
Author(s):  
Jose A. Guerrero ◽  
Taisuke Kanaji ◽  
Junling Liu ◽  
Susan Russell ◽  
T.K. Gartner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Carotid Artery ◽  
Bleeding Time ◽  
Thrombus Formation ◽  
Type I ◽  
Complete Occlusion ◽  
Platelet Counts ◽  
Platelet Receptor

Abstract Background: GPIbα is a critically important platelet receptor best recognized for its ability to bind vWF and mediate platelet adhesion. In addition, a GP Ibα binding site for thrombin has been described and characterized for several decades. However, the physiologic relevance of GPIbα/thrombin binding has remained elusive. Site-directed mutagenesis has shown that a sulfated GP Ibα residue, Tyr276, is essential for thrombin binding to GP Ibα but not critical for vWF binding. The importance of Tyr276 was further substantiated in the crystal structure of a GP Ibα/thrombin complex confirming the sulfated Tyr276 GP Ibα residue directly participates with other neighboring negatively charged residues in establishing a first contact with the anion-binding exosite II of an α-thrombin molecule. To determine the physiologic relevance, if any, of the GP Ibα Tyr276 residue we generated mice with platelets containing a mutant human GP Ibα subunit containing a Tyr276 to Phe276 substitution (Y276F) and did comparative studies with mice expressing a normal human (WT) GP Ibα subunit. Methods: Mouse colonies expressing the normal or variant GP Ibα subunits were established by transgenic technology and bred into a mouse colony devoid of murine GP Ibα. Surface expression of WT or Y276F GP Ibα subunits was measured by flow cytometry. Relevant assays included platelet counts, FeCl3-induced thrombus formation, tail bleeding times, hemoglobin content following tail resection (measured as 575 nm absorbance of lysed erythrocytes), and washed platelet aggregation induced by different agonists (fibrillar type I collagen, thrombin, ristocetin, arachidonic acid, and PAR activating peptides). Results: Founder mice were selected with nearly identical levels of surface-expressed WT and Y276F GPIbα subunits. Circulating platelet counts were similar between the 2 colonies. Stirred platelet aggregation assays induced by 0.05, 0.1, 0.5 units/ml thrombin, 10 and 20 mg/ml fibrillar collagen, 1.25 mg/ml ristocetin, 0.25 mM arachidonic acid, 100 mM PAR3 activating peptide and 100 mM PAR4 activating peptide revealed no significant differences between WT and Y276F samples. No statistically significant values were obtained in tail bleeding time assays or hemoglobin loss comparing WT and Y276F animals. However, the time required for a reduction in carotid artery blood flow following FeCl3 injury was significantly prolonged in Y276F animals (10.6±1.6 min vs. 5.8±1.4 min). All WT animals displayed complete occlusion following the initial reduction in blood flow. In contrast, 3 out of 6 Y276F animals did not show complete occlusion and had evidence of fluctuating blood flow suggestive of embolization. Discussion: FeCl3 injury of the mouse carotid artery revealed an essential role for GP Ibα residue Tyr276. In contrast, no differences were seen in tail bleeding time assays or in any platelet aggregation assay. These results are suggestive that thrombin binding to human GPIbα may be relevant for the pathological development of a thrombus. This conclusion is based on both the failure of some carotid arteries from Y276F animals to fully occlude and our observation that all Y276F animals showed an increased length of time for the reduction of blood flow. The results suggest thrombin binding to GPIbα could be significant in terms of enhancing fibrinogen cleavage and therefore stabilizing the development of a platelet-rich thrombus.

Assessment of Bleeding for the Evaluation of Therapeutic Preparations in Small Animal Models of Antibody-Induced Hemophilia and von Willebrand Disease

1997 ◽  
Vol 77 (03) ◽  
pp. 591-599 ◽  
Author(s):  
P L Turecek ◽  
H Gritsch ◽  
G Richter ◽  
W Auer ◽  
L Pichler ◽  
...  
Keyword(s):  
Blood Flow ◽  
Animal Models ◽  
Blood Loss ◽  
Murine Model ◽  
Bleeding Time ◽  
Limit Of Detection ◽  
Small Animal ◽  
Von Willebrand Disease ◽  
Small Animal Models ◽  
Von Willebrand

SummaryThree small animal models of bleeding are described and used to evaluate the effects of preparations intended for therapy of human bleeding disorders. We modified techniques for the assessment of bleeding to be able to reproducibly quantify blood loss and rate of blood flow in addition to the measurement of bleeding time.Temporary hemophilia was induced in a rabbit model by injection of high titer human inhibitor plasma [>1000 Bethesda units (BU)/ml]. A decrease in rabbit FVIII from normal values to below the limit of detection was observed within 30 min, cuticle bleeding time changed from normal (approx. 10 min) to steady state bleeding (>30 min), and the rate of blood flow increased from 4 to >30 µl blood/min. Infusion of an activated prothrombin complex concentrate (FEIBA STIM4, Immuno) at doses between 75 and 150 U/kg normalized the rate of blood flow, while infusion of FVIII/vWF concentrate resulted in partial correction. Administration of FVIIa, both recombinant and plasma-derived, failed to correct bleeding, however. In an analogous murine model, FVIII/ vWF inhibitor plasma was obtained by immunizing goats with a purified human FVIII/vWF complex. This plasma cross-reacted with mouse vWF in vitro. Injection of the anti-FVIII/vWF inhibitor plasma into mice caused a decrease in vWF antigen, in some animals with a complete loss of vWF multimers comparable to severe von Willebrand disease. A specific anti-vWF inhibitor plasma obtained by immunization of goats with recombinant vWF was used in a further murine model, resulting in a gradual but substantial decrease in FVIII as well as in intensive bleeding. The infusion of a FVIII/vWF concentrate (IMMUNATE, IMMUNO) normalized the rate of blood flow in both murine models. The same assessment methods were used to characterize bleeding in a natural mouse model of von Willebrand disease (strain RIIIS/J). The use of quantitative techniques of assessment of blood loss and rate of blood flow appears to be a helpful tool for characterizing hemorrhagic situations and evaluating the capacity of therapeutic preparations to correct hemostatic defects.

Aspirin, Dipyridamole, Prostacyclin (PGI2) and Bleeding Time in Rats

1979 ◽  
Author(s):  
S. Villa ◽  
G. de Gaetano
Keyword(s):  
Blood Flow ◽  
Drug Treatment ◽  
Platelet Function ◽  
Bleeding Time ◽  
Physiological Role ◽  
Inhibitory Effect ◽  
Endogenous Substance ◽  
Prolonged Bleeding ◽  
Pharmacological Data

It has been suggested that dipyridamole (D) impairs platelet function by potentiating the inhibitory effect of endogenous circulating PGI2. Treatments combining D with aspirin - at doses inhibitine PGI2 synthesis - could therefore reduce its inhibitory effect on platelet function. We have tested this hypothesis on bleeding time in unanaesthetized male CD rats. Bleeding times were measured on the animal’s tails (immerged in saline at 37°C) by a standardized template technique, 5 min after drug treatment. Neither aspirin (5 - 200 mg/kg i.p.) nor D (30 mg/kg i.p.) significantly modified bleeding time. Pretreatment with aspirin from 5 min to 24 h before D resulted in marked lengthening (>10 min) of bleeding times. Aspirin pretreatment also potentiated - not reduced - the effect of two D congeners (SH-869 and VK-774) used at doses which themselves significantly prolonged bleeding times. D strongly potentiated the prolonging effect of exogenous PGI2 on bleeding time. These data indicate that the interactions between aspirin, D (or its derivatives) and PGI2 at the level of primary haemostasis mechanisms in the rat are complex and may involve factors other than platelets (such as blood flow in the micro-circulation). They also suggest that pharmacological data obtained with exogenous PGI2 does not necessarily reflect the physiological role of the endogenous substance.

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