Home About us Contact
|
Home About us Contact | ||
|
|
||
Mg/kg Bolus (kg + bolus)
Selected AbstractsDexmedetomidine during coronary artery bypass grafting surgery: is it neuroprotective?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2007A preliminary study Background:, In the present study, we aimed to determine whether during coronary artery bypass grafting (CABG) surgery, dexmedetomidine has protective effects against cerebral ischemic injury. Method:, Twenty-four patients, aged 50,70 years, undergoing CABG surgery were randomized into two groups of 12 patients each: those receiving dexmedetomidine (group D) and those not receiving it (group C). As basal blood samples from arterial and jugular bulb catheters were drawn, dexmedetomidine (1 ,g/kg bolus and infusion at a rate of 0.7 ,g/kg/h) was administered to patients in group D. Arterial and jugular venous blood gas analyses, serum S-100B protein (S-100B), neuron-specific enolase (NSE) and lactate measurements were performed after induction, 10 min after the initiation of cardiopulmonary bypass (CPB), 1 min after declamping, at the end of CPB, at the end of the operation and 24 h after surgery. Mann,Whitney U - and Wilcoxon's tests were used for statistical analyses. Results:, No significant between-group differences were found regarding arterial and jugular venous pH, PO2, PCO2 and O2 saturations. S-100B, NSE and lactate levels were also similar between groups D and C. During the post-operative period, there were no clinically overt neurological complications in any patient. Conclusion:, Cerebral ischemia marker (S-100B, NSE, lactate) patterns were as expected during CPB; however, there were no differences between the groups, which led us to believe that during CABG surgery dexmedetomidine has no neuroprotective effects. Future studies with larger populations are recommended to further establish the effects of this drug. [source] Acute Alcohol Intoxication During Hemorrhagic Shock: Impact on Host Defense From InfectionALCOHOLISM, Issue 4 2004K. L. Zambell Abstract: Background: Acute alcohol intoxication is a frequent underlying condition associated with traumatic injury. Our studies have demonstrated that acute alcohol intoxication significantly impairs the immediate hemodynamic, metabolic, and inflammatory responses to hemorrhagic shock. This study investigated whether acute alcohol intoxication during hemorrhagic shock would alter the outcome from an infectious challenge during the initial 24 hr recovery period. Methods: Chronically catheterized male Sprague Dawley® rats were randomized to acute alcohol intoxication (EtOH; 1.75 g/kg bolus followed by a constant 15 hr infusion at 250,300 mg/kg/hr) or isocaloric isovolemic dextrose infusion (dex; 3 ml + 0.375 ml/hr). EtOH and dex were assigned to either fixed-volume (50%) hemorrhagic shock followed by fluid resuscitation with Ringer's lactate (EtOH/hem, dex/hem) or sham hemorrhagic shock (EtOH/sham, dex/sham). Indexes of circulating neutrophil function (apoptosis, phagocytosis, oxidative burst) were obtained at baseline, at completion of hemorrhagic shock, and at the end of fluid resuscitation. Bacterial clearance, lung cytokine expression, and myeloperoxidase activity were determined at 6 and 18 hr after an intratracheal challenge with Klebsiella pneumoniae (107 colony-forming units). Results: Mean arterial blood pressure was significantly lower in acute alcohol intoxication-hemorrhagic shock animals throughout the hemorrhagic shock. In sham animals, acute alcohol intoxication alone did not produce significant changes in neutrophil apoptosis or phagocytic activity but significantly suppressed phorbol myristic acid (PMA)-stimulated oxidative burst. Hemorrhagic shock produced a modest increase in neutrophil apoptosis and suppression of neutrophil phagocytic capacity but significantly suppressed PMA-stimulated oxidative burst. Acute alcohol intoxication exacerbated the hemorrhagic shock-induced neutrophil apoptosis and the hemorrhagic shock-induced suppression of phagocytosis without further affecting PMA-stimulated oxidative burst. Fluid resuscitation did not restore neutrophil phagocytosis or oxidative burst. Acute alcohol intoxication decreased (,40%) 3-day survival from K. pneumoniae in hemorrhagic shock animals, impaired bacterial clearance during the first 18 hr postinfection, and prolonged lung proinflammatory cytokine expression. Conclusions: These results demonstrate that the early alterations in metabolic and inflammatory responses to hemorrhagic shock produced by acute alcohol intoxication are associated with neutrophil dysfunction and impaired host response to a secondary infectious challenge leading to increased morbidity and mortality. [source] Treatment of Acute Stroke with Recombinant Tissue Plasminogen Activator and AbciximabACADEMIC EMERGENCY MEDICINE, Issue 12 2003Daniel C. Morris MD Objectives: Preclinical data suggest that treatment of acute ischemic stroke (AIS) with the combination of recombinant tissue plasminogen activator (rt-PA) and abciximab may increase efficacy and decrease the rate of symptomatic intracranial hemorrhage (sICH). The authors report pilot data of five AIS patients with half-dose rt-PA and abciximab as part of an ongoing phase I safety trial with sICH as the primary outcome. Methods: Five patients with AIS were treated with the combination of half-dose rt-PA (0.45 mg/kg) and abciximab (0.25 mg/kg bolus followed by a 0.125 ,g/kg/min infusion over 12 hours). Head computed tomographic scan was obtained after 24 hours of treatment onset. Results: Four patients received the combination of half-dose abciximab and rt-PA without major complications. One patient experienced a parenchymal hematoma type-1 ICH without significant decline of his neurological status. The average National Institutes of Health Stroke Scale change at discharge in comparison with pretreatment was ,5.4 ± 7.0, and the median change was 6 points with a range of 4 points (worsening) to ,13 points (improvement) (p = 0.07) based on a one-sided t-test. Conclusions: Administration of rt-PA and abciximab to AIS patients was completed without difficulty. No sICH were observed; however, 20% (1 out of 5) experienced an asymptomatic ICH. Based on our observation of five patients, there was a trend of treatment efficacy; however, these results need to be confirmed in a larger-scale placebo-controlled clinical trial. [source] The Use of Bivalirudin for Cardiopulmonary Bypass Anticoagulation in Pediatric Heparin-Induced Thrombocytopenia PatientsARTIFICIAL ORGANS, Issue 8 2010Richard Gates Abstract Infants with heparin-induced thrombocytopenia (HIT) represent a challenging and high-risk group of patients when they require cardiopulmonary bypass (CPB). Bivalirudin offers many potential pharmacologic advantages over other nonheparin anticoagulants for such patients. We describe our protocol for the use of bivalirudin in a 5-month-old infant undergoing stage 2 Norwood for hypoplastic left heart syndrome. The patient was a 5- month-old, 6-kg infant who developed HIT after a bowel resection complicating initial Norwood stage 1. After sternotomy and dissection had been redone, the child received an initial dose of bivalirudin of 1.0 mg/kg and 0.5 mg/kg 5 min later. The CPB circuit was primed with 50 mg/kg bivalirudn/400 cc volume. With the initiation of CPB, a continuous infusion of 2.5 mg/kg bivalirudin was begun. Activated clotting time (ACT) was targeted for over 400 s, with an examination prior to bypass and each 15 min thereafter. Bivalirudin was discontinued with separation from bypass and during modified ultrafiltration (MUF). The ACT was 286 s after the initial 1 mg/kg bolus and 597 s after the second 0.5 mg/kg bolus and initiation of CPB. At a rate of 2.5 mg/kg/min, ACT ranged between 461 and 597 s. At the completion of MUF, the ACT was 316 s. The ACT was 214 s 20 min after MUF. No clots were noted in the CPB circuit, and good hemostasis was achieved within 10 min after MUF was completed. Incision to closure time was 160 min; time from completion of MUF to sternal closure was 30 min. Post-MUF, 60 cc of processed cell saver blood was reinfused, and no clotting factors were required. Chest tube output was 10, 10, 3, and 4 ccs, respectively, at hours 1,4 post operation. Bivalirudin provides effective anticoagulation in infants requiring CPB in the presence of HIT. Bivalirudin's efficacy is effectively monitored by ACT, and, after CPB, its short half-life and ability to be ultrafiltered facilitate the ability to achieve hemostasis in a timely fashion. [source] Effect of dose and input rate on the brain penetration of BMS-204352 following intravenous administration to ratsBIOPHARMACEUTICS AND DRUG DISPOSITION, Issue 6 2002Rajesh Krishna Abstract BMS-204352 is a novel maxi-K channel opener that is being developed for the treatment for stroke. The current study was designed to evaluate the plasma and brain pharmacokinetics of BMS-204352 in rats, in particular, assessing the effect of dose and input rate on brain penetration of BMS-204352. Rats (3 animals/group/time point) received a single intravenous dose of BMS-204352 as 5 mg/kg bolus, 5 mg/kg 30 min infusion, 5 mg/kg 60 min infusion, and 10 mg/kg bolus dose, into the jugular vein. Terminal blood (for plasma) and brain samples were collected for up to 9 h post-dose and samples were analyzed for the concentrations of intact BMS-204352 using a validated liquid chromatographic tandem mass spectrometric method (LC/MS/MS). As dose increased from 5 to 10 mg/kg, both BMS-204352 Cmax and AUC values increased in plasma and brain, somewhat greater in proportion to the increment in dose. Whereas the peak concentrations of BMS-204352 were affected by infusion time, overall AUCs were comparable across the bolus and infusion groups. Terminal disposition (T -half ranged from 1.6 to 2.7 h) of BMS-204352 was unaltered as a function of input rate. BMS-204352 crossed the blood,brain barrier with brain-to-plasma (B/P) ratios of approximately 7,11. Brain-to-plasma ratios appeared to be independent of dose and infusions produced somewhat higher brain penetration (B/P of ca. 11) as compared to bolus (B/P of ca. 7,8) dose. The decline of BMS-204352 in the brain paralleled that of plasma independent of the input rate and dose. Copyright © 2002 John Wiley & Sons, Ltd. [source] | ||||||||||