scholarly journals Effect of heparin administration on plasma binding of benzodiazepines.

1980 ◽  
Vol 9 (2) ◽  
pp. 171-175 ◽  
Author(s):  
PV Desmond ◽  
RK Roberts ◽  
AJ Wood ◽  
GD Dunn ◽  
GR Wilkinson ◽  
...  
Keyword(s):  
Plasma Binding ◽  
Heparin Administration

Effects of Unfractionated and Low Molecular Weight Heparins on Platelet Thromboxane Biosynthesis “In Vivo”

1994 ◽  
Vol 72 (06) ◽  
pp. 942-946 ◽  
Author(s):  
Raffaele Landolfi ◽  
Erica De Candia ◽  
Bianca Rocca ◽  
Giovanni Ciabattoni ◽  
Armando Antinori ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Unfractionated Heparin ◽  
Low Molecular Weight Heparin ◽  
Primary Source ◽  
In Vivo Studies ◽  
Low Molecular Weight ◽  
Heparin Administration ◽  
To Receive

SummarySeveral “in vitro” and “in vivo” studies indicate that heparin administration may affect platelet function. In this study we investigated the effects of prophylactic heparin on thromboxane (Tx)A2 biosynthesis “in vivo”, as assessed by the urinary excretion of major enzymatic metabolites 11-dehydro-TxB2 and 2,3-dinor-TxB2. Twenty-four patients who were candidates for cholecystectomy because of uncomplicated lithiasis were randomly assigned to receive placebo, unfractionated heparin, low molecular weight heparin or unfractionaed heparin plus 100 mg aspirin. Measurements of daily excretion of Tx metabolites were performed before and during the treatment. In the groups assigned to placebo and to low molecular weight heparin there was no statistically significant modification of Tx metabolite excretion while patients receiving unfractionated heparin had a significant increase of both metabolites (11-dehydro-TxB2: 3844 ± 1388 vs 2092 ±777, p <0.05; 2,3-dinor-TxB2: 2737 ± 808 vs 1535 ± 771 pg/mg creatinine, p <0.05). In patients randomized to receive low-dose aspirin plus unfractionated heparin the excretion of the two metabolites was largely suppressed thus suggesting that platelets are the primary source of enhanced thromboxane biosynthesis associated with heparin administration. These data indicate that unfractionated heparin causes platelet activation “in vivo” and suggest that the use of low molecular weight heparin may avoid this complication.

High Fibrinopeptide A (FPA) Levels in Acute Non-Lymphocytic Leukemia Are Reduced by Heparin Administration

1984 ◽  
Vol 52 (03) ◽  
pp. 301-304 ◽  
Author(s):  
L Gugliotta ◽  
Silvana Viganò ◽  
A D’Angelo ◽  
Anna Guarini ◽  
S Tura ◽  
...  
Keyword(s):  
Body Temperature ◽  
Blast Cell ◽  
Lymphocytic Leukemia ◽  
Healthy Controls ◽  
Intravenous Bolus ◽  
Fibrinopeptide A ◽  
Cell Counts ◽  
Heparin Administration ◽  
Blast Cells ◽  
Baseline Values

SummaryPlasma levels of fibrinopeptide A (FPA) in 30 untreated patients with acute non-lymphocytic leukemia (ANLL) were significantly higher than in 30 healthy controls (p <0.001). Patients without laboratory signs of disseminated intravascular coagulation (DIC) had levels of FPA higher than controls (p <0.02) but markedly lower than patients with DIC (p <0.001). Five patients with M3 leukemia had a higher mean FPA level (p <0.02) and a lower peripheral blast cell count (p <0.05) than patients with other cytological subtypes of ANLL. When patients with M3 were excluded, a significant correlation was observed between the peripheral blast cell counts and the FPA levels (r = 0.66, p <0.001). FPA levels were similar with body temperature either above or below 38° C. After intravenous bolus of heparin FPA dropped to normal levels in 14 out of 17 patients who had high baseline values. These findings indicate that intravascular thrombin formation, which probably result from the expression of procoagulant activities of blast cells, is the main cause of high FPA in the majority of patients with acute non-lymphocytic leukemia.

scholarly journals Blood plasma binding of acebutolol and diacetolol in man.

1980 ◽  
Vol 9 (4) ◽  
pp. 395-397 ◽  
Author(s):  
TJ Coombs ◽  
CJ Coulson ◽  
VJ Smith
Keyword(s):  
Blood Plasma ◽  
Plasma Binding

Platelet count recovery and seroreversion in immune HIT despite continuation of heparin: further observations and literature review

2017 ◽  
Vol 117 (10) ◽  
pp. 1868-1874 ◽  
Author(s):  
Jo-Ann Sheppard ◽  
Theodore Warkentin ◽  
Andrew Shih
Keyword(s):  
Platelet Count ◽  
Additional Patient ◽  
Heparin Induced Thrombocytopenia ◽  
Prophylactic Dose ◽  
Heparin Administration ◽  
Immune Mediated ◽  
Antibody Levels ◽  
Count Recovery

SummaryOne of the standard distinctions between type 1 (non-immune) and type 2 (immune-mediated) heparin-induced thrombocytopenia (HIT) is the transience of thrombocytopenia: type 1 HIT is viewed as early-onset and transient thrombocytopenia, with platelet count recovery despite continuing heparin administration. In contrast, type 2 HIT is viewed as later-onset (i. e., 5 days or later) thrombocytopenia in which it is generally believed that platelet count recovery will not occur unless heparin is discontinued. However, older reports of type 2 HIT sometimes did include the unexpected observation that platelet counts could recover despite continued heparin administration, although without information provided regarding changes in HIT antibody levels in association with platelet count recovery. In recent years, some reports of type 2 HIT have confirmed the observation that platelet count recovery can occur despite continuing heparin administration, with serological evidence of waning levels of HIT antibodies (“seroreversion”). We now report two additional patient cases of type 2 HIT with platelet count recovery despite ongoing therapeutic-dose (1 case) or prophylactic-dose (1 case) heparin administration, in which we demonstrate concomitant waning of HIT antibody levels. We further review the literature describing this phenomenon of HIT antibody seroreversion and platelet count recovery despite continuing heparin administration. Our observations add to the concept that HIT represents a remarkably transient immune response, including sometimes even when heparin is continued.

Plasma clearance and tissue distribution of labelled insulin-like growth factor-I (IGF-I), IGF-II and des(1–3)IGF-I in rats

1991 ◽  
Vol 128 (2) ◽  
pp. 197-204 ◽  
Author(s):  
F. J. Ballard ◽  
S. E. Knowles ◽  
P. E. Walton ◽  
K. Edson ◽  
P. C. Owens ◽  
...  
Keyword(s):  
Growth Factor ◽  
Binding Proteins ◽  
Rank Order ◽  
Insulin Like Growth Factor ◽  
Plasma Binding ◽  
Factor I ◽  
Igf I ◽  
The Mean ◽  
Growth Factor I ◽  
Sites Of Action

ABSTRACT Incubation of 125I-labelled insulin-like growth factor-I (IGF-I) with rat plasma at 4 °C led to the transfer of approximately half the radioactivity to 150 kDa and smaller complexes with IGF-binding proteins. The extent of association was greater with labelled IGF-II and essentially absent with the truncated IGF-I analogue, des(1–3)IGF-I. A greater degree of binding of IGF peptides with binding proteins occurred after i.v. injection of the tracers into rats, but most of the des(1–3)IGF-I radioactivity remained free. Measurement of the total plasma clearances showed the rapid removal of des(1–3)IGF-I compared with IGF-I and IGF-II; the mean clearances were 4·59, 1·20 and 1·34 ml/min per kg respectively. The mean steadystate volume of distribution was larger for des(1–3)IGF-I than for IGF-I and IGF-II (461, 167 and 181 ml/kg respectively), probably because of the differences in plasma protein binding. With all tracers, radioactivity appeared in the kidneys to a greater extent than in other organs. The amount of radioactivity found in the adrenals, brain, skin, stomach, duodenum, ileum plus jejunum and colon was in rank order, des(1–3)IGF-I > IGF-I > IGF-II. Since this ranking is the opposite of the abilities of the three IGF peptides to form complexes with plasma binding proteins, we propose that the plasma binding proteins inhibit the transfer of the growth factors to their tissue sites of action. Moreover, we suggest that IGF analogues that are cleared rapidly from blood may have greater biological potencies in vivo. Journal of Endocrinology (1991) 128, 197–204

Abstract P65: Outpatient Atrial Fibrillation Ablation on Therapeutic Warfarin - Safety, Efficacy, and Cost Savings

2011 ◽  
Vol 4 (suppl_1) ◽  
Author(s):  
Michael C Giudici ◽  
Deborah L Paul ◽  
Caroline Sloane ◽  
Gisela Press ◽  
Ashley Petersen ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Cost Savings ◽  
Nerve Paralysis ◽  
Phrenic Nerve Paralysis ◽  
Outpatient Unit ◽  
Heparin Administration ◽  
Same Day Discharge ◽  
Procedural Time ◽  
Hospital Stays ◽  
Mean Time

Introduction: Catheter ablation for atrial fibrillation (PVI) is being performed with increasing frequency. This time and labor-intensive procedure is under increasing scrutiny as we look for means to decrease costs of delivering care. Performing these procedures on therapeutic warfarin could shorten hospital stays, eliminate costly low-molecular weight heparin (LMW) use, and decrease procedural heparin administration which could reduce hemorrhage from access sites. Methods: Over a six-year period, 180 patients, 138 M/42 F, mean age 43 yr (18-77 yr), underwent PVI for persistent - 99 pts., and paroxysmal - 81 pts. atrial fibrillation. Mean INR was 2.2 (1.5 - 4.2). Procedures were performed with standard radiofrequency (RF) catheters - 132, Cryoablation - 27, and Ablation Frontiers RF - 21. Procedural time, fluoroscopy time, hospital stays, outcomes, and complications were tracked. Results: 127 of 180 pts. were discharged the day of procedure (OP) from the outpatient unit, 51 pts. stayed one night post-procedure (IP), 2 patients stayed 4 days, one for pulmonary treatment and one for CVA. Mean procedural length was 3.3 hours, mean fluoro time was 52 min. Mean time from hospital admit to discharge was 17.3 hr. Mean time from procedure end to discharge was 11.0 hr. 77% of pts. were free from AF on follow-up on no meds or “pill-in-the-pocket”. 6 complications occurred - 1 phrenic nerve paralysis (resolved), 2 CVAs (one was 72 hrs post PVI), 1 perforation/tamponade, 1 groin bleed requiring evacuation, 1 PV stenosis. There was no difference in outcome for patients discharged OP vs IP. Cost savings by continuing warfarin were LMW = $205/dose X 6 doses - $1230/pt. Cost savings by same day discharge = $1330/day. Conclusions: PVI can be safely performed as an outpatient procedure on therapeutic warfarin with good clinical outcomes. Significant cost savings can be realized from OP PVI from reduced staff, medication, and facilities utilization.

Investigations of the Dose of Heparin and Whole Blood Coagulation Time during Endovascular Surgery

1997 ◽  
Vol 3 (2_suppl) ◽  
pp. 215-217 ◽  
Author(s):  
S. Nagai ◽  
A. Kurata ◽  
R. Tanaka ◽  
K. Irikura ◽  
Y. Miyasaka ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Whole Blood ◽  
Initial Level ◽  
Thrombus Formation ◽  
Constant Level ◽  
Bleeding Tendency ◽  
Coagulation Time ◽  
Continuous Administration ◽  
Heparin Administration ◽  
Whole Blood Coagulation Time

We chronologically determined whole blood coagulation time during continuous heparin administration, and investigated optimal doses of heparin in thirty-seven vascular surgery cases. ACT was determined with Hemochron 401. Heparin (2000 IU) was administered by bolus injection at the beginning of intravascular surgery, which was followed by continuous injection of 20 to 160 IU/kg/h. ACT determined before and 30 minutes after heparin administration were compared. There were no complications. ACT was maintained at a nearly constant level by continuous heparin administration. The dose of heparin required to maintain ACT at a level 1.5 to 2 times the initial level was 20 to 60 IU/kg/h. ACT was prolonged by more than three times in two of the ten subjects who were given heparin at a dose of 70 IU/kg/h or more. Continuous administration of heparin allowed maintenance of ACT at a nearly constant level during intravascular surgery. ACT was maintained within the range which is believed to be effective for prevention of thrombus formation (approximately 1.5 to 2.0 times larger than the initial level) by continuous administration of 20 to 60 IU/kg/h of heparin. ACT was, however, prolonged to more than three times the initial level in some subjects who were given 70 IU/kg/h or higher doses, suggesting the risk of a bleeding tendency. Accordingly, it is ideal to continue heparin administration at appropriate doses, while measuring ACT. The results of our study should serve as a useful standard for meeting this goal.

Plasma-Binding of Virginiamycin in vitro and in vivo

Chemotherapy ◽  
1969 ◽  
Vol 14 (2) ◽  
pp. 109-114
Author(s):  
P.J. Van Duck ◽  
G. Van Braekel
Keyword(s):  
Plasma Binding
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