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PubMed1990

Reversal of lethal citrate intoxication by intravenous infusion of calcium. An experimental study in pigs.

Intravenous infusions of 750 and 1000 ml 2.2% sodium citrate were given over a 60 min period to 17 pigs to study its effect on aortic pressure, electrocardiogram, ionised calcium, and citrate clearance. In group 1 (seven pigs) the animals did not receive calcium and the median survival time was 30 min (range 20-70 min). In groups 2 and 3 (five in each group) the pigs were treated with calcium chloride infusions (1 ml 10% calcium chloride to 10 ml citrate) and they all survived. In group 1 the ionised calcium concentrations in blood fell to values below 0.4 mmol/l, after which the blood pressure dropped abruptly. In the animals treated with calcium the mean ionised calcium concentration fell to 0.6 mmol/l, whereas total calcium increased to more than 7 mmol/l. The aortic pressure was consistently within normal values in the groups treated with calcium, but in the group that was not treated the blood pressure fell dramatically. There was no correlation between electrocardiographic changes and ionised calcium concentrations. In summary, calcium was an effective antidote to lethal citrate intoxication, and the only reliable method of determining the necessary dose of calcium was monitoring of ionised calcium concentrations.

Animals↗
PubMed1994

An evaluation of the quality of nursing care rendered to patients with intravenous infusions in the Windhoek Hospital Complex.

Patients on intravenous infusions are commonly seen in the Windhoek Hospital Complex. There was concern regarding the type of nursing care these patients received which led to a survey on the quality of care rendered to these patients. The findings showed that care delivered ranged from very poor to good. Some startling information became evident in that legal aspects were often ignored and that basic things such as calculating and charting the daily intake and output, were omitted. Most of these problems can be rectified through in-service education.

Female↗
PubMed1997

Pharmacokinetics of isepamicin following a single administration by intravenous infusion or intramuscular injections.

The pharmacokinetics of isepamicin following administration of a 1-g dose were evaluated for 18 healthy male volunteers between the ages of 26 and 38. In a randomized crossover fashion, each volunteer received doses of isepamicin by a 30-min intravenous infusion and as an intramuscular injection. Blood samples were collected at specified times after dosing and assayed for isepamicin by a validated radioimmunoassay method. The individual plasma concentration-time curves were analyzed by noncompartmental methods. In general, the pharmacokinetics after intravenous infusion and intramuscular injection were similar. As expected, the maximum concentration of isepamicin in serum following intramuscular injection (37.2 microg/ml) was lower than the observed concentration at the end of infusion (66.7 microg/ml). The areas under the concentration-time curves from 0 h to infinity following intramuscular and intravenous administration were 164.8 and 154.5 microg x hr/ml, respectively, indicating complete absorption following intramuscular administration. The respective mean terminal-phase half-life (t1/2) values were 2.6 and 3.6 h. Although t1/2 was slightly longer following intravenous infusion, the small difference in the observed t1/2 values was not considered to be clinically significant. Total body clearances following intramuscular injection and intravenous infusion were 1.3 and 1.4 ml/min/kg, respectively, which were similar to renal serum creatinine clearances in healthy volunteers (> 1.14 ml/min/kg). The drug was safe and well tolerated. The results of the present study clearly show complete absorption of isepamicin following intramuscular administration. The similarity in the pharmacokinetics after intravenous infusion and intramuscular dosing would permit interchangeable administration of isepamicin by either route without compromising clinical efficacy.

Adult↗
PubMed1999

Pharmacokinetics and pharmacodynamics of aztreonam administered by continuous intravenous infusion.

The pharmacodynamic parameter that appears to correlate best with a successful therapeutic outcome with beta-lactam antibiotics is the length of time the serum antibiotic concentration remains above the minimum inhibitory concentration (MIC) for the infecting pathogen. By maximizing this parameter, continuous administration of beta-lactam and related antibiotics by intravenous infusion could represent the optimal mode of drug administration. The pharmacokinetic and pharmacodynamic properties of ceftazidime administered by continuous intravenous infusion have been evaluated previously. Aztreonam is a monobactam antibiotic with similar pharmacokinetic and microbiologic activity to that of ceftazidime. This study evaluated the pharmacokinetic and pharmacodynamic characteristics of aztreonam administered as a continuous intravenous infusion in healthy volunteers against multiple clinical isolates. Five men and 3 women received 6 g of aztreonam administered by continuous intravenous infusion over 24 hours. Blood samples were collected before the infusion and at 0.5, 1 through 8, 12, 18, and 24 hours after the start of the infusion. Pharmacokinetic parameters were determined by standard equations. In vitro susceptibility testing was performed using National Committee for Clinical Laboratory Standards guidelines for 4 clinical isolates of gram-negative bacteria (2 each of Escherichia coli and Pseudomonas aeruginosa). Serum inhibitory titers (SITs) were determined in duplicate for each clinical isolate at 0 and 24 hours. The subjects' mean (+/- SD) age was 29.3+/-4.4 years; mean weight, 74.6+/-14.0 kg; and calculated mean creatinine clearance, 107+/-13 mL/min. For the pharmacokinetic parameters, mean (+/- SD) values were as follows: steady-state serum concentration, 40.9+/-8.8 microg/L; half-life, 1.5+/-0.4 hours; elimination rate constant, 0.50+/-0.13 hours(-1); steady-state volume of distribution, 0.18+/-0.04 L/kg; and total body clearance, 6.1+/-1.2 L/h. The MICs were 0.0625 and 0.125 microg/mL against the 2 E coli isolates and 4 microg/mL against both P aeruginosa isolates. The median SITs against the E. coli isolates were 1:256 and 1:512, and against the P. aeruginosa isolates were 1:8 and 1:16. At steady state, II subjects had serum concentrations of aztreonam > or =4 times the MIC for each organism. These findings suggest that further clinical study of the administration of aztreonam by continuous intravenous infusion is warranted.

Adolescent↗
PubMed1988

A comparison of two ranitidine intravenous infusion regimens in critically ill patients.

The effect of two ranitidine intravenous infusion regimens on intragastric pH was studied in 134 critically ill patients admitted to 15 intensive care units. Intragastric pH was determined hourly for 30 hours. Those patients whose intragastric acidity fell below pH 4.0 for 3 or more of the first 6 hours were considered 'at risk' of developing stress-related gastric lesions and randomized to receive a 50 mg bolus of ranitidine together with a continuous intravenous infusion of either 0.125 or 0.25 mg kg-1 h-1 ranitidine for 24 hours. The maximal elevation in intragastric pH was achieved within 12 hours. The median intragastric pH for the last 20 hours of the infusion period was 5.9 for the higher dose group and 5.6 for the lower dose group. The increase in intragastric pH achieved by the two dosage regimens did not differ significantly throughout the 24 hour period. Patients having two or more of five major risk factors (head injury, major trauma, sepsis, respiratory failure/insufficiency and major surgery) had better overall control of intragastric pH on the higher dose of ranitidine than those receiving the lower dose. The majority of intensive care patients are likely to receive satisfactory treatment with the lower dosage regimen that was tested (0.125 mg kg-1 h-1). Those with multiple risk factors may, however, require treatment with higher doses of ranitidine (0.25 mg kg-1 h-1).

Adolescent↗
PubMed2000

A preliminary study on intravenous infusion of sodium eicosapentaenoate.

Eicosapentaenoic acid (EPA) and arachidonic acid (AA), made into sodium salt solution (50 micrograms/ml), were used for intravenous infusion. In a preclinical study in dogs, Na-EPA lowered the activity of transminases (glutamic pyruvic transaminase [GPT], glytamic oxaloacetic transaminase [GOT]); however, Na-AA increased the activity of GPT and GOT. In the clinical study, the numbers of leukocytes and lymphocytes of volunteers increased and remained at that level for 3 to 5 days after intravenous infusion. The study indicated that an intravenous infusion of Na-EPA may have anti-inflammatory and immunomodulatory effects.

Animals↗
PubMed2002

[Combination chemotherapy with Taxol and cisplatin for 57 patients with non-small cell lung cancer by intraartery and intravenous infusion].

BACKGROUND & OBJECTIVE: Although previous studies showed that intravenous infusion chemotherapy combined with Taxol and cisplatin (DDP) can improve the effects of the treatment of advanced non-small cell lung cancer (NSCLC), the results remained unsatisfactory because of the lower concentration of local chemotherapeutic agent. This study was designed to administrate the chemotherapeutic agents through the local artery and to evaluate the efficacy of the intraartery (IA) and the intravenous (i.v.) infusion chemotherapy combined Taxol with cisplatin (DDP) in the treatment of NSCLC. METHODS: Fifty-seven patients with advanced NSCLC were enrolled and randomized into two groups. Group A (27 patients) was given by IA chemotherapy consisting of Taxol 135 mg/m2 and DDP 80 mg/m2 within 3 hours in the first day. Group B (30 patients) was given by i.v. chemotherapy consisting of Taxol 135 mg/m2 and DDP 80 mg/m2 within 3 hours in the first day. The patients in two groups were repeatedly treated every 3-4 weeks for at least 2 cycles. RESULTS: The recent effect was evaluated by the CT or X-ray results. Of the 57 patients, 1 case acquired complete response, 29 partial response. The overall response rate was 52.63% with 66.67% (18/27) in group A and 40.00% (12/30) in group B. The median TTP was 5.5 months in group A and 4.0 months in group B. The median survival time was 13.5 months in group A and 10.5 months in group B. The 0.5, 1, 2, and 3-year survival rates were 85.18%, 66.67%, 48.15%, and 18.51% months in group A, respectively. The 0.5, 1, 2, and 3-year survival rates were 70.00%, 53.33%, 30.00%, and 6.67% months in group B, respectively. The main side effects were myelosuppression, gastrointestinal reactions and peripheral neuropathy. They could be effectively treated with large amount of vitamines, antacid, guastil, white blood cell stimulating drugs and liquid compensation. CONCLUSION: The artery infusion Taxol and DDP chemotherapy is one of the useful methods in the treatment of NSCLC patients. The local response rate in the patients treated by IA may be higher than those treated by i.v.

Adult↗
PubMed1966

Mechanisms of endotoxin tolerance. IV. Specificity of the pyrogenic refractory state during continuous intravenous infusions of endotoxin.

The mechanisms underlying the pyrogenic refractory state which develops rapidly during a continuous intravenous infusion of bacterial endotoxin have been further explored. The findings demonstrate that: (a) rabbits rendered refractory to a continuous intravenous infusion of E. coli endotoxin at a standard rate (18 x 10(-4) microg/min) become highly refractory to a single intravenous test bolus of endotoxin, but remain fully responsive to preformed endogenous pyrogen and to substances known to release endogenous pyrogen, i.e. influenza virus, old tuberculin in specifically sensitized rabbits, and staphylococcal enterotoxin; (b) administration of fresh whole blood from normal donors containing an average of 1.6 - 10(8) granulocytes fails to restore febrile responsiveness to the continuing E. coli endotoxin infusion; (c) refractory phase plasma and liver homogenates exhibit no enhanced capacity to inactivate E. coli endotoxin pyrogenicity; (d) splenectomized animals readily develop the pyrogenic refractory state during E. coli endotoxin infusions and exhibit diminished, rather than the increased inflammatory responses to intradermal endotoxin seen in sham-operated controls; (e) continuous intravenous infusions of gelatin-stabilized, heat-killed pneumococci produce sustained fevers; and (f) continuous intravenous infusions of old tuberculin into specifically sensitized animals rapidly elicit a pyrogenic refractory state. The present observations, considered together with those of other investigators, support the hypothesis that pyrogenic unresponsiveness to endotoxin involves two distinct immunologic mechanisms. In terms of this hypothesis, the rapid reduction in febrile responsiveness to endotoxin is mediated by desensitization at the cellular level. With small doses of endotoxin, such as those employed in the present studies, this desensitization is primarily specific; with larger doses, nonspecific mechanisms are superimposed. So long as the subsequent doses of endotoxin are closely spaced or continuously infused, optimal conditions are provided for cellular desensitization and pyrogenic unresponsiveness to a given quantity of endotoxin can be induced rapidly and maintained without the requirement for antibody. However, as the interval between endotoxin challenge is lengthened, cellular desensitization wanes and tolerance becomes increasingly dependent upon those antibodies directed against the common toxophore groupings responsible for endotoxin pyrogenicity which assist the reticuloendothelial system in the clearance and destruction of this molecule.

Animals↗
PubMed1983

Intravenous infusion device artifact in the EEG-confusion in the diagnosis of electrocerebral silence.

Intravenous infusion devices are routinely used in the intensive care unit to accurately regulate the delivery of various intravenous fluids and vasoactive drugs. These devices have been well described in the literature as the cause of various electrocardiographic artifacts. There has been little documentation in the literature implicating these devices as the etiology of artifacts in the electroencephalogram. The association of intravenous infusion devices with electroencephalographic artifacts became relevant during the brain death evaluation of two patients. The electroencephalograms, which were done for documentation of electrocerebral silence clearly showed activity in both patients which disappeared when the intravenous infusion devices were stopped. Possible mechanisms responsible for producing these artifacts include piezoelectric current, poor electrode contact, inadequate skin preparation, current leakage, static charges and electromagnetic activity. In the evaluation of patients for electrocerebral silence, it is important to both recognize and eliminate this artifact so that it is not confused with true electrocerebral activity.

Brain Death↗
PubMedDate not supplied

Histologic lesions associated with intravenous infusions of large volumes of isotonic saline solution in rats for 30 days.

The objective of this study was to characterize the changes associated with intravenous infusions of large volumes of isotonic saline solution in rats so that effects of the infusion process could be more easily distinguished from effects of test articles. Male Sprague-Dawley rats weighing approximately 225-275 g at the beginning of the study were given intravenous infusions of isotonic saline solution once daily for 30 consecutive days at dosages of 40 or 80 ml/kg body weight. Saline solution was administered through catheters placed in the caudal veins of the tail according to one of the following regimens: 80 ml/kg at 0.25 ml/min; 80 ml/kg at 0.5 ml/min; 80 ml/kg at 1.0 ml/min; and 40 ml/kg at 1.0 ml/min. Control rats were catheterized but not administered intravenous fluids. One day following the last treatment, all rats were necropsied and major organs were collected in 10% formalin. Histologic lesions associated with treatment included increased incidence and severity of pulmonary periarterial infiltrates of eosinophils, multifocal pulmonary inflammation, pulmonary granulomas that often contained hairshaft fragments, endothelial hypertrophy and hyperplasia within pulmonary arterial vessels, and pulmonary arterial medial thickening. Infiltrates of eosinophils around small pulmonary arteries were more severe in rats given intravenous infusions than in untreated rats and were more severe in rats given isotonic saline at the 80-ml/kg dosage than at the 40-ml/kg dosage. The severity of periarterial infiltrates of eosinophils increased with increasing infusion rates in rats that received 80 ml/kg isotonic saline. Pulmonary granulomas and multifocal pulmonary inflammation were observed in more rats that received intravenous saline than in control rats, but their incidences did not appear to vary with the volume or rate of infusion. Multifocal endothelial hypertrophy and hyperplasia occurred in most rats given isotonic saline solution at all volumes and rates, but not in untreated control rats. Inflammatory lesions in the tail near the injection site were considered sequellae of catheter insertion that, in some instances, may have been exacerbated by intravenous saline infusion. There were no lesions in other organs that were attributable to intravenous infusions of isotonic saline solution.

Animals↗
PubMed1981

[Pharmacokinetic studies of tobramycin using the continuous intravenous infusion method (author's transl)].

Tobramycin (TOB) was administered to 4 healthy adult volunteers (mean body weight 63.5 kg, surface area 1.71 m2) as one time 90 mg dose by intramuscular injection or by intravenous infusion (30 or 60 minutes) in a crossover study. Serum and urinary concentrations were assayed by bioassay and radioimmunoassay (RIA). Pharmacokinetic analysis was done with a one-compartment open model in the case of intramuscular injection and a two-compartment open model in the case of intravenous infusion. The correlation constant was 0.92, and the relation formula was y = 0.81x+0.13 between bioassay and RIA. In the case of intramuscular injection, the peak serum concentration was 5.1 approximately 6.3 mcg/ml (mean 5.3 mcg/ml), and values calculated with pharmacokinetic parameters from the mean serum concentration were Tmax = 0.745 hour, Cmax = 5.34 mcg/ml and half life (T1/2) = 89.6 minutes. With 60 minutes intravenous infusion, the peak serum concentration was 6.7 approximately 9.1 mcg/ml (mean 7.5 mcg/ml), and the calculated value was 7.63 mcg/ml. The value after 2 hours was nearly equal to those for intramuscular injection. T 1/2 of beta-phase was 95.8 minutes. With 30 minutes intravenous infusion, the peak serum concentration was 8.4 approximately 11.8 mcg/ml (mean 10.2 mcg/ml), and the calculated value was 9.81 mcg/ml. T 1/2 of beta-phase was 105.3 minutes and the serum concentration of the beta-phase was same as that for intramuscular injection administration after 6 hours. We concluded that 60 minutes intravenous infusion of TOB 90 mg is more effective and safe than the 30 minutes method from the standpoint of toxicity, and the serum concentration of the beta-phase is similar to that with intramuscular injection. With each administration method, urinary recovery was 70 approximately 80% for 8 hours.

Adult↗
PubMedDate not supplied

Effect of continuous intravenous infusion of carteolol chloride on tissue blood flow in rabbit optic nerve head.

PURPOSE: To investigate the effect of an intravenous infusion of carteolol on tissue blood flow in the optic nerve head (ONH) of rabbits. METHODS: Rabbits received either a 3-week topical instillation, or a single intravenous injection (10, 20, 30 microg/kg) or a continuous intravenous injection (2.5, 5, 20, 40, 80 microg/kg per hour) of carteolol. The plasma carteolol level was determined by the gas chromatography negative-ion chemical ionization mass spectrometric method. The ONH blood flow was determined by the hydrogen clearance method. RESULTS: The plasma level of carteolol after a 3-week instillation was 5.55 ng/mL, and a continuous intravenous injection (5 microg/kg per hour) led to approximately the same plasma level. The continuous intravenous infusion of 5 microg/kg per hour of carteolol significantly increased the ONH blood flow compared to the controls from 30 minutes to 2 hours after the beginning of the infusion (n = 10). The mean blood pressure and intraocular pressure (n = 6) were not significantly changed during the continuous intravenous infusion of carteolol. CONCLUSIONS: These results suggest that the plasma carteolol level in rabbits after long-term instillation can increase the ONH blood flow. We conclude that the increase resulted from a reduction in the vascular resistance in the ONH.

Adrenergic beta-Antagonists↗
PubMed1975

Effect of intravenous infusion of corticosteroids on blood pressure, electrolytes, and water metabolism in sheep.

ACTH administration (80 IU/day for 5 days), which produces hypertension and charateristic metabolic effects in sheep (38), has been compared with the effect of intravenous infusion of cortisol (5 mg/h), corticosterone (0.5 mg/h), deoxycorticosterone (50 mug/h), and 11-deoxycortisol (1 mg/h), each given singly for 5 days. Further, a mixture consisting of aldosterone (3 mug/h), cortisol (5 mg/h), deoxycorticosterone (25 mug/h), corticosterone (0.5 mg/h), and 11-deoxycortisol (1 mg/h), was also infused intravenously for 5 days. In another series of experiments, 18-hydroxydeoxycorticosterone (100 mg/h) was also included in the combined-steroid solution. With the exception of 18-hydroxydeoxycorticosterone, which was not measured, the rates of infusionproduced peripheral arterial blood levels of the steroids similiar to those seen with ACTH stimulation. Blood pressure,water intake, urine output, and plasma and urinary electrolytes were measured: individual steroids had little effect on these, but manyof the metabolic changes produced by ATCH (hypokalemia and increased water intake andurine output) were produced by the combined-steroid infusion. However, the combined-steroid infusion failed to induce an increase in blood pressure similiar to that seen inthe ACTH experiments. Thus the findings are against a major role in ACTH hypertension for any steroid used, either singly or in combination. As yet unrecgnized factor/s may be involved in the ACTH-induced hypertension.

18-Hydroxydesoxycorticosterone↗
PubMed1990

[Combined pharmacokinetic--pharmacodynamic model analysis of N-acetyl procainamids following intravenous infusion in rabbits].

The pharmacokinetic and pharmacodynamic profiles of N-acetyl procainamide were analyzed by integrated PK-PD model following intravenous infusion to rabbits. No significant differences between the PK parameters estimated from iv administration and intravenous infusion were found. However, two of the PD parameters were shown to be significantly different. The values of Emax, Keo, S, EC50 were found to be 120 +/- 13.2 ms, 0.0182 +/- 0.007 min-1, 2.26 +/- 0.93, 6.31 +/- 0.71 microgram/ml respectively following intravenous infusion; the corresponding values following iv administration were 53.6 +/- 2.5 ms, 0.061 +/- 0.017 min-1, 2.19 +/- 0.39, 6.21 +/- 1.74 micrograms/ml respectively.

Acecainide↗
PubMed1983

[Effects of intravenous infusion of isosorbide dinitrate (ISDN) on acute experimental congestive heart failure].

Experiments were undertaken to examine whether and how intravenous infusion of ISDN ameliorated hemodynamics of anesthetized dogs with congestive heart failure. A model of acute congestive heart failure with markedly high left ventricular end-diastolic pressure (LVEDP) and low cardiac index (CI) was induced by occlusion of the left anterior descending coronary artery (LAD) following 30-min infusion of dextran solution containing propranolol in halothane anesthetized open-chest dogs. Five minutes after occlusion of LAD, intravenous infusion of ISDN (100 and 500 micrograms/kg/min for 5 min) decreased the elevated LVEDP, aortic pressure and systemic vascular resistance, and enhanced the reduced CI. These changes produced by ISDN were significant (P less than 0.05 or P less than 0.01) as compared with values just before infusion of ISDN. ISDN at the same doses slightly reduced LVEDP, but did not increase CI in normal dogs which were not subjected to the coronary occlusion and dextran infusion. These results indicate that intravenous infusion of ISDN reduces both pre- and after-load and increases CI in dogs with heart failure, demonstrating that ISDN is useful for the vasodilator therapy of heart failure.

Animals↗
PubMed1965

MECHANISMS OF ENDOTOXIN TOLERANCE. 3. THE REFRACTORY STATE DURING CONTINUOUS INTRAVENOUS INFUSIONS OF ENDOTOXIN.

Bacterial endotoxins were administered by continuous intravenous infusions at constant rates to normal man and rabbits. An initial progressive febrile reaction was followed by progressive defervescence to baseline. The resulting pyrogenic refractory state was characterized as follows: (a) reticuloendothelial blockade with thorotrast neither prevented nor reversed its course; (b) passive transfer was unsuccessful with refractory phase plasma; (c) infusions of normal plasma or fresh whole blood failed to restore responsiveness; (d) a minimum of 4 hours of continuous endotoxin infusion was required for full development of unresponsiveness; (e) circulating antibody titers to endotoxin remained unaltered; (f) peripheral leukocytosis appeared; (g) infusion of febrile phase plasma reevoked an immediate, monophasic fever; (h) endotoxinemia could be demonstrated by pyrogen bioassay; (i) 10-fold increases in endotoxin infusion rates reevoked fever; (j) impaired responsiveness extended to heterologous endotoxins; (k) dermal inflammatory responses to endotoxin were suppressed in man while tuberculin reactivity remained unimpaired; dermal inflammatory responses to endotoxin were enhanced in rabbits; and (l) pyrogenic reactivity to endotoxin reappeared within 24 hours in man; refractoriness persisted in rabbits. It is concluded that the pyrogenic refractory state reflects an inability of the host to continue to mobilize endogenous pyrogen during sustained endotoxinemia. Such observations, together with previous studies, are consistent with two distinct immunologic mechanisms of resistance to endotoxin pyrogenicity: (a) desensitization at the cellular level; and (b) elaboration of circulating antibodies which assist reticuloendothelial clearance and destruction of endotoxin. Whereas both such mechanisms may contribute to pyrogenic tolerance, the characteristics of the pyrogenic refractory state suggest the participation only of the former.

Allergy and Immunology↗
PubMed2006

The disposition of lidocaine during a 12-hour intravenous infusion to postoperative horses.

Lidocaine is administered as an intravenous infusion to horses for a variety of reasons, but no study has assessed plasma lidocaine concentrations during a 12-h infusion to horses. The purpose of this study was to evaluate the plasma concentrations and pharmacokinetics of lidocaine during a 12-h infusion to postoperative horses. A second purpose of the study was to evaluate the in vitro plasma protein binding of lidocaine in equine plasma. Lidocaine hydrochloride was administered as a loading dose, 1.3 mg/kg over 15 min, then by a constant rate IV infusion, 50 microg/kg/min to six postoperative horses. Lidocaine plasma concentrations were measured by a validated high-pressure liquid chromatography method. One horse experienced tremors and collapsed 5.5 h into the study. The range of plasma concentrations during the infusion was 1.21-3.13 microg/mL. Lidocaine plasma concentrations were significantly increased at 0.5, 4, 6, 8, 10 and 12 h compared with 1, 2 and 3 h. The in vitro protein binding of lidocaine in equine plasma at 2 microg/mL was 53.06+/-10.28% and decreased to 27.33+/-9.72% and 29.52+/-6.44% when in combination with ceftiofur or the combination of ceftiofur and flunixin, respectively. In conclusion, a lower lidocaine infusion rate may need to be administered to horses on long-term lidocaine infusions. The in vitro protein binding of lidocaine is moderate in equine plasma, but highly protein bound drugs may displace lidocaine increasing unbound concentrations and the risk of lidocaine toxicity.

Anesthesia↗