PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “TETRACAINE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1994

Absorption of liposome-encapsulated tetracaine versus nonliposome-encapsulated tetracaine from open wounds in rabbits.

The plasma tetracaine concentration versus time profiles for liposome-encapsulated tetracaine (LET) versus nonliposome-encapsulated tetracaine (NLET) were determined after topical application to open wounds in six rabbits (three in LET and three in NLET). H3-tetracaine preparations of LET or NLET were applied randomly to uniform dermal lacerations in anesthetized rabbits. Plasma tetracaine concentrations (ng/mL) of arterial blood samples obtained were measured at predetermined intervals (0.25, 0.5, 1.0, 2.0, and 24 hours) by isotope tracer assay. Results (mean +/- standard deviation) showed the peak plasma tetracaine concentration (Cmax) and the time to Cmax were 40.8 +/- 5.1 ng/mL and 40.1 +/- 7.3 minutes for LET, and 117.8 +/- 9.7 ng/mL and 49.1 +/- 50.2 minutes for NLET. Plasma tetracaine concentrations at all samples times were significantly lower for LET versus NLET. Liposome encapsulation of topically applied tetracaine significantly decreases both the peak and overall plasma tetracaine concentrations compared with the nonencapsulated form. The data suggest that liposome encapsulation of topically applied local anesthetics such as a solution of tetracaine, adrenaline, and cocaine, might reduce the potential systemic toxicity caused by rapid absorption of these compounds.

Absorption↗
PubMed1982

Duration of the local anesthetic effect of tetracaine hydrochloride solutions and tetracaine in microspheres.

The local anesthetic effect of tetracaine in polylactic acid microspheres was compared with that of tetracaine hydrochloride solutions. As a first step, the local anesthetic effect of 0.1 ml tetracaine hydrochloride solutions was examined at four concentrations in vivo. Then, the local anesthetic effect of 0.2 ml tetracaine hydrochloride solutions was compared with that of 0.1 ml tetracaine hydrochloride solutions. The more the amount of tetracaine, the stronger and longer was the local anesthetic effect. The local anesthetic effect of tetracaine in microspheres was much longer and lasted over 100 h.

Anesthetics, Local↗
PubMed1986

Topical anesthesia for laceration repair: tetracaine versus TAC (tetracaine, adrenaline, and cocaine).

Topical anesthetics have always had a place in anesthetizing mucous membranes. The earliest writing in Greek medical literature makes reference to the use of these topical anesthetizing agents. Previous studies utilized a mixture of tetracaine, Adrenaline, and cocaine in the pediatric population with increased patient compliance. In contrast, another study cites the increased risk of infection in cases where topical anesthetics in combination with potent vasoconstrictors are used. To examine the efficacy and safety of a tetracaine and a tetracaine, Adrenalin, and cocaine mixture (TAC), a randomized, double-blind study was undertaken. A total of 68 patients participated in the study, with 36 receiving TAC and 32 receiving tetracaine. The results indicate that the most efficacious use of TAC is on facial lacerations, regardless of length or depth. Of the 46 participants available for follow-up, one patient in the tetracaine group reported a wound infection. A recommendation of increased use of TAC on facial lacerations, in both the adult and pediatric populations, is made based on the results of this study.

Administration, Topical↗
PubMed1998

Topical tetracaine versus topical tetracaine plus intracameral lidocaine for cataract surgery.

PURPOSE: To compare topical tetracaine 0.5% alone and with intracameral lidocaine 1% as a local anesthetic agent in phacoemulsification with intraocular lens (IOL) implantation. SETTING: The Toronto Hospital-Western Division, Toronto, Canada. METHODS: Fifty-nine consecutive patients (60 eyes) having phacoemulsification with implantation of a foldable acrylic IOL (AcrySof) were randomized into 1 of 2 groups: The intracameral balanced salt solution (BSS) group received topical tetracaine 0.5% plus intracameral BSS; the intracameral lidocaine group received topical tetracaine 0.5% with preservative-free intracameral lidocaine 1%. The patients' subjective experience of pain was measured at 4 points during surgery using a 4-point pain scale. Patient and surgeon satisfaction with the anesthesia used was measured using a 5-point satisfaction scale. Central endothelial cell counts were obtained preoperatively and 1 month postoperatively. Best corrected visual acuity (BCVA) was measured preoperatively and 1 hour, 1 day, 1 week, and 1 month postoperatively. RESULTS: The mean pain score after phacoemulsification was significantly higher in the intracameral BSS group than in the intracameral lidocaine group (0.63 +/- 0.7 [SD] and 0.23 +/- 0.4, respectively, P < .019). The mean pain score at the end of surgery was also significantly higher in the intracameral BSS group than in the intracameral lidocaine group (0.60 +/- 0.6 and 0.21 +/- 0.4, respectively; P < .014). The surgeon satisfaction score was significantly lower for the intracameral BSS group than for the intracameral lidocaine group (3.90 +/- 1.2 and 4.73 +/- 0.8, respectively; P < .0007). There was no difference in patient satisfaction between the intracameral BSS and intracameral lidocaine groups (4.60 +/- 0.6 and 4.70 +/- 0.8). Endothelial cell loss 1 month postoperatively was similar between the 2 groups (6.1% +/- 8% and 6.7% +/- 6%). Ninety-seven percent of patients (29/30) in each group noted BCVA improvement from preoperatively. The rate of potential visual acuity recovery was similar in both groups. CONCLUSION: Topical tetracaine 0.5% with intracameral lidocaine was safe and effective in patients having phacoemulsification with IOL implantation. The advantage of using intracameral lidocaine 1% over a placebo was a significant decrease in the patients' subjective experience of pain and in the surgeon's satisfaction with the anesthesia used. None of the other parameters measured in this study differed significantly between the 2 groups.

Administration, Topical↗
PubMed1990

Efficacy of tetracaine-adrenaline-cocaine topical anesthetic without tetracaine for facial laceration repair in children.

To determine whether the tetracaine component traditionally used in tetracaine-adrenaline-cocaine (TAC) is necessary to obtain effective topical anesthesia, a prospective study was performed to compare TAC and adrenaline-cocaine preparations for the repair of facial lacerations in children. Physicians were "blind" to which preparation was being used. Of 55 patients studied, 24 received TAC (103 sutures placed) and 31 received adrenaline-cocaine (151 sutures placed). The anesthetic efficacy of each preparation was approximately 95%; there were no adverse reactions related to administration of either medication or complications of wound healing noted in either group. The tetracaine component of TAC is superfluous for obtaining topical anesthesia of minor dermal lacerations of the face in children. The TAC formulation can be simplified by omitting tetracaine without compromising anesthetic efficacy.

Anesthetics, Local↗
PubMed1995

LAT (lidocaine-adrenaline-tetracaine) versus TAC (tetracaine-adrenaline-cocaine) for topical anesthesia in face and scalp lacerations.

The study objective was to compare the topical anesthetic LAT (4% lidocaine, 1:2,000 adrenaline, 1% tetracaine) to TAC (0.5% tetracaine, 1:2,000 adrenaline, 11.8% cocaine) for efficacy, adverse effects, and costs. The study design was a randomized, prospective, double blind clinical trial set in an inner-city emergency department with an emergency medicine residency program. Adults with linear lacerations of the face or scalp were eligible for inclusion in the study. Patients had lacerations anesthetized with topical TAC or LAT according to a random numbers table. A total of 95 patients were included in the study with 47 receiving TAC and 48 receiving LAT. Patients stated the number of sutures causing pain and patients and physicians rated the overall pain of suturing using a standard visual analog scale (VAS). The power of the study to determine a ranked sum difference of 15 was 0.8. Visual analog scale results and number and percentage of sutures causing pain were compared using Wilcoxon's Rank Sum Test. According to patients, the percentage of sutures causing pain was significantly fewer for LAT than TAC (P = .036, Interquartile Range 0.13 to 0.0 for LAT, 0.25 to 0 for TAC). Physicians found LAT statistically more effective than TAC (P = .0093, Interquartile Range 1 to 0 for LAT, 2 to 0 for TAC) but patients did not report a difference (P = .266, Interquartile Range 1 to 0 for both LAT and TAC). Our cost per application was $3.00 for LAT compared to $35.00 for TAC. Follow-up was accomplished in 91 of 95 patients (95%) with no reported complications for either medication.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Tetracaine, epinephrine (adrenalin), and cocaine (TAC) versus lidocaine, epinephrine, and tetracaine (LET) for anesthesia of lacerations in children.

STUDY OBJECTIVE: To compare the duration of anesthesia experienced with lidocaine, epinephrine, and tetracaine (LET) solution and that with tetracaine, epinephrine (Adrenalin), and cocaine (TAC) solution during suturing of uncomplicated lacerations on the face or scalp. DESIGN: Double-blind, randomized, controlled trial. SETTING: The emergency department of a university-affiliated private children's hospital. PARTICIPANTS: One hundred seventy-one children with lacerations on the face and scalp requiring suturing. INTERVENTIONS: After standard application of the anesthetic solution, patients were assessed for signs of discomfort before and during laceration repair. Duration of anesthesia during laceration repair was determined on the basis of the length of time after removal of the anesthetic solution to the first sign(s) of discomfort that required additional anesthesia. RESULTS: There was no statistical difference between TAC and LET in adequacy of anesthesia before suturing or in duration of anesthesia during suturing. CONCLUSION: LET is an effective alternative to TAC for topical anesthesia during suturing of uncomplicated lacerations on the face and scalp in children.

Adolescent↗
PubMed1995

Lidocaine adrenaline tetracaine gel versus tetracaine adrenaline cocaine gel for topical anesthesia in linear scalp and facial lacerations in children aged 5 to 17 years.

STUDY OBJECTIVE: The purpose of the present study is to compare LAT gel (4% lidocaine, 1:2000 adrenaline, 0.5% tetracaine) to TAC gel (0.5% tetracaine, 1:2000 adrenaline, 11.8% cocaine) for efficacy, side effects, and costs in children aged 5 to 17 years with facial or scalp lacerations. DESIGN: Randomized, prospective, double-blinded clinical trial. SETTING: Inner-city Emergency Department with an Emergency Medicine residency program. PATIENTS OR OTHER PARTICIPANTS: Children aged 5 to 17 years with linear lacerations of the face or scalp. INTERVENTION: After informed consent was obtained patients had lacerations anesthetized with topical TAC or LAT gel according to a random numbers table. MEASUREMENTS AND MAIN RESULTS: A total of 95 patients were included in the statistical analysis with 47 receiving TAC and 48 receiving LAT. Physicians and patients/parents separately rated the overall pain of suturing using a modified multidimensional scale for pain assessment specifically for children. Patients/parents also stated the number of sutures causing pain. The power of the study to determine a ranked sum difference of 15 was 0.8. Multidimensional rating scale results and number and percentage of sutures causing pain were compared using Wilcoxon's rank sum test. According to patients no difference could be detected in percent of sutures causing pain in the LAT versus TAC group (P = .51). Using the multidimensional scale, physicians and patients/parents found LAT statistically the same as TAC in effectiveness (P = .80 for physicians and P = .71 for patients). Cost per application was $3.00 for LAT compared to $35.00 for TAC. Follow-up was accomplished in 85 of 95 participants in the study with no reported complications for either medication. CONCLUSION: LAT gel worked as well as TAC gel for topical anesthesia in facial and scalp lacerations. Considering the advantages of a noncontrolled substance and less expense, LAT gel appears to be better suited than TAC gel for topical anesthesia in laceration repair in children.

Adolescent↗
PubMed1983

Effect of tetracaine and lidocaine on insulin release in isolated mouse pancreatic islets.

The effect of tetracaine and lidocaine on insulin secretion and glucose oxidation by islets of ob/ob-mice was measured. Tetracaine, at a concentration of 1 microM to 0.1 mM, did not markedly influence the basal (3 mM glucose) insulin secretion, whereas 0.5-3.5 mM induced a marked increase. At 7 mM glucose, there was a dose-dependent increase with 0.1-2.5 mM tetracaine. Insulin release induced by 20 mM glucose was potentiated by 0.1 mM and 0.5 mM tetracaine, but this effect disappeared at 1 mM tetracaine. The stimulatory effect of 0.5-1 mM tetracaine on basal insulin release was blocked by the secretory inhibitors, adrenaline (1 microM), clonidine (1 microM) and by Ca2+-deficiency, but the stimulation by 3.5 mM tetracaine was not reduced by 1 microM clonidine or Ca2+ deficiency. Atropine (10 microM) did not affect the stimulation by 0.5 mM tetracaine at 3 mM glucose or by 0.25 mM tetracaine at 20 mM glucose. Tetracaine, at 0.1 mM, potentiated the secretory stimulation of 20 mM L-leucine, 20 mM D-mannose, or 1 microM glibenclamide. Mannoheptulose, 10 mM, abolished the combined effects of 0.1 mM tetracaine and 10 mM glucose. Lidocaine, 1-5 mM, stimulated basal insulin release, but 1 microM-1 mM of the drug did not affect glucose-induced (20 mM glucose) insulin release and 5 mM lidocaine inhibited glucose stimulation. The oxidation of 10 mM D-[U-14C]glucose was slightly enhanced by 0.1 and 1 mM tetracaine. The results indicate that tetracaine and lidocaine, at certain concentrations, can induce insulin release and that tetracaine potentiates secretion induced by other secretagogues. It is concluded that these effects may be associated with beta-cell functions related to the adrenergic receptors but probably not to cholinergic receptors.

Animals↗
PubMed1999

Nitric oxide synthesis inhibition modifies the cardiotoxicity of tetracaine and lidocaine.

UNLABELLED: Suppression of nitric oxide (NO) production alters the toxicity of cocaine and bupivacaine. We undertook this study to determine whether the systemic toxicity of two other local anesthetics that differ in antiarrhythmic activity, plasma clearance, and biotransformation are similarly affected by nitric oxide synthase (NOS) inhibition. Sprague-Dawley rats anesthetized with 70% N2O and 0.5% halothane mixed with O2 were pretreated with saline (0.2 mL x kg(-1) x min(-1) i.v.) or N(omega)-nitro-L-arginine methyl ester (L-NAME; a competitive inhibitor of NOS) (2 mg x kg(-1) x min(-1) i.v.) for 30 min. The animals were then given tetracaine (3 mg x kg(-1) x min(-1) i.v.) or lidocaine (8 mg x kg(-1) x min(-1) i.v.) until cardiac arrest (asystole). Doses of lidocaine or tetracaine that produced arrhythmias, seizures, isoelectric encephalogram, and asystole were determined. Hemodynamic recordings were performed throughout the experiments, and plasma was collected to measure the concentration of lidocaine or tetracaine. L-NAME decreased tetracaine and lidocaine doses that produced arrhythmias (> or = 2 degrees atrioventricular conduction block) (tetracaine 14 +/- 2 mg/kg; lidocaine 102 +/- 9 mg/kg) versus saline treatment (tetracaine 28 +/- 2 mg/kg; lidocaine 136 +/- 9 mg/kg; P < 0.05). The tetracaine and lidocaine doses required to produce asystole were also smaller in animals with L-NAME pretreatment than those in saline-pretreated animals. L-NAME reduced the arrhythmia dose of tetracaine more than the arrhythmia dose of lidocaine (28 of 14 = 2.0 fold and 136 of 102 = 1.3-fold). The plasma concentration of lidocaine, but not tetracaine, was significantly higher at each sample time in L-NAME-pretreated animals than in saline-pretreated animals. Inhibition of NOS by L-NAME enhances the cardiotoxicity of lidocaine and tetracaine, with a greater effect on tetracaine than on lidocaine. Altered drug clearance by L-NAME was insufficient to explain these findings because L-NAME pretreatment increased the plasma levels of only lidocaine, not tetracaine. IMPLICATIONS: Inhibition of nitric oxide production in rats markedly enhances the cardiovascular toxicity of lidocaine and tetracaine. Altered drug clearance by N(omega)-nitro-L-arginine methyl ester was insufficient to explain these findings because N(omega)-nitro-L-arginine methyl ester pretreatment increased the plasma levels of only lidocaine, not tetracaine.

Anesthetics, Local↗
PubMed1998

Elucidation of biphasic alterations on acetylcholinesterase (AChE) activity and membrane fluidity in the structure-functional effects of tetracaine on AChE-associated membrane vesicles.

Tetracaine-induced biphasic structure-functional alterations were investigated in acetylcholinesterase (AChE)-associated membrane vesicles from the electric organ of Torpedo californica. Enzyme assays showed that tetracaine exhibits a biphasic effect on the activity of membrane-bound AChE: increasing it at low concentrations (< 12 mM) and decreasing it at high concentrations (> 12 mM). Fluorescence-polarization experiments demonstrated that tetracaine affects the fluidity of lipid hydrocarbon chains of these membranes in a biphasic manner: increasing it at < 20 mM and decreasing it at > 20 mM. This small molecule also alters the fluidity of the negatively charged lipid head group: increasing it at < 13 mM and remaining essentially at the same level at > 13 mM. The positively charged lipid head group is unaffected. Contrasting effects on AChE activity with changes in membrane fluidity showed that [tetracaine] for AChE activity is comparable to that for the fluidity of the negatively charged lipid head group (12 mM versus 13 mM), but lower than that for a biphasic effect on the fluidity of lipid hydrocarbon chains (12 mM versus 20 mM). Differential scanning microcalorimetry showed that, due to membrane protein-lipid interaction, the lipid-phase transition temperature (tml) is higher for AChE-associated membrane vesicles than for isolated lipids from these membranes. An overall disordering of the membranes by tetracaine, as inferred from the lowering of tml, was also demonstrated. These findings suggested that binding of tetracaine to the lipid polar head group and membrane protein-lipid interaction may contribute to a higher [tetracaine] in inducing a comparable biphasic effect on membrane fluidity. At high [tetracaine], charge interactions between the tetracaine cation and the negatively charged lipid head group may result in a new lipid phase in the membranes, which could reverse the increase in membrane fluidity, resulting in the observed biphasic effect. Although both tetracaine and alcohol are amphiphilic species, they exhibit distinctive structure-functional effects on the membranes, as shown by comparing the results obtained on tetracaine with those previously reported for alcohol. The present observations may have significant physiological implications and may be of importance in understanding the biochemical effects of tetracaine in correlation with its physiological impact.

1-Propanol↗
PubMed1997

Dual actions of tetracaine on intramembrane charge in amphibian striated muscle.

1. The effects of graded concentrations of tetracaine on the steady-state and kinetic properties of intramembrane charge were examined in intact voltage-clamped amphibian muscle fibres. 2. The micromolar tetracaine concentrations that were hitherto reported to abolish Ca2+ transients in skeletal muscle failed to affect significantly the steady-state charge. Maximal reductions of such intramembrane charge required relatively high, 1-2 mM, concentrations of tetracaine. 3. The plots of maximum charge against tetracaine concentration suggested a saturable 1:1 drug binding that spared a fixed amount of tetracaine-resistant (q beta) charge but inhibited a discrete fraction of susceptible (q gamma) charge with a KD between 0.1 and 0.2 mM. 4. The q beta charge thus isolated by 2 mM tetracaine was conserved through a wide range of applied test voltages and pulse durations and regardless of whether the imposed transition from the holding potential (-90 mV) to the test potential took place in one or more steps. 5. Similarly, 'on' and 'off' q beta currents that were elicited by voltage steps from fixed conditioning to varying test levels mapped onto non-linear phase-plane trajectories that nevertheless depended uniquely upon voltage. In contrast, the currents that followed voltage steps made from varying prepulse levels to fixed -90 or -20 mV test potentials mapped onto identical q beta phase-plane trajectories that were independent of the prepulse history. 6. The charge movements that followed strong depolarizing voltage clamp steps to test potentials in the range -50 to 0 mV approximated simple monotonic decays that could empirically be described by a single time constant. Nevertheless, a complete inhibition of a tetracaine-sensitive (q gamma) charge movement by 2 mM tetracaine that left only q beta charge, sharply altered both the magnitude and the voltage dependence of these time constants. This establishes a distinct contribution of the q gamma species to overall charge kinetics even at such test voltages. 7. Under such a criterion for the voltage dependence of charging kinetics, even the micromolar (0.05-0.2 mM) tetracaine concentrations that failed to markedly alter the steady-state charge consistently increased the charging time constants yet did not influence their voltage sensitivity. 8. These findings demonstrate the existence of separate kinetic and steady-state effects of tetracaine on intramembrane charge movements, at micromolar and millimolar anaesthetic concentrations, respectively. These parallel earlier effects of tetracaine that have been reported upon the transient and sustained components of sarcoplasmic reticular Ca2+ release. They also establish that maximally effective concentrations of tetracaine isolate a single distinct species of conserved (q beta) intramembrane charge.

Anesthetics, Local↗
PubMed1989

Effects of tetracaine and procaine on skinned muscle fibres depend on free calcium.

The local anaesthetics, tetracaine and procaine have previously been found to block, induce or potentiate Ca2+ release from the sarcoplasmic reticulum (SR) of skeletal muscle depending on the preparation, experimental conditions and design. We now show that low concentrations of tetracaine and procaine block SR Ca2+ release whereas high concentrations induce release from the SR of amphibian and mammalian skinned fibres. Both actions depend on pCa, such that a shift in pCa can alter their effect from blocking to releasing Ca2+. In skinned fibres with Ca2+-loaded SR, tetracaine (1 mM) produced a tonic contraction with a time to half-peak of 15-20 s and a magnitude reaching 80% of maximum force. Ca2+ release by tetracaine or procaine occurred at pCa less than or equal to 6.5 and was not blocked by Ruthenium Red (RR) (25 mM). This action of tetracaine was attributed to SR Ca2+ release rather than to a displacement of bound Ca2+ because fibres lacking a functional SR due to pre-treatment with quercetin (100 mM), A 23187 (100 micrograms ml-1) or Triton X-100 (1%) did not contract after additions of tetracaine. Lower concentrations of tetracaine (0.5 mM) and procaine (less than or equal to 10 mM) blocked contractions due to caffeine (at pCa greater than or equal to 6.73), sulphydryl oxidizing agents, or Ca2+-induced Ca2+ release (CICR). The inhibition of CICR as a function of pCa was difficult to measure quantitatively since lowering pCa to elicit CICR twitches was sufficient to initiate tetracaine-induced tonic contractions. Experiments with isolated SR vesicles showed that 1 mM tetracaine inhibited CICR, over a wide range of pCa but 3-5 mM tetracaine induced rapid Ca2+ release. The opposite effects of tetracaine and procaine depend mostly on their concentration in SR vesicles and/or pCa in skinned fibres. Blockade of release seems to occur via the CICR pathway, and induction of release through an increase in SR membrane permeability.

Animals↗
PubMed1997

Mechanism of tetracaine block of cyclic nucleotide-gated channels.

Local anesthetics are a diverse group of ion channel blockers that can be used to probe conformational changes in the pore. We examined the effects of the local anesthetic tetracaine on rod and olfactory cyclic nucleotide-gated channels expressed from subunit 1 in Xenopus oocytes. We found that 40 microM tetracaine effectively blocked the bovine rod channel but not the rat olfactory channel at saturating concentrations of cGMP. By testing chimeric channels containing regions of sequence from both rod and olfactory channels, we found that determinants of apparent affinity for tetracaine at saturating cGMP did not map to any one region of the channel sequence. Rather, the differences in apparent affinity could be explained by differences between the chimeras in the free energy of the opening allosteric transition. If a channel construct (such as the rod channel) spent appreciable time in the closed state at saturating cGMP, then it had a high apparent affinity for tetracaine. If, on the other hand, a channel construct (such as the olfactory channel) spent little time in the closed state at saturating cGMP, then it had a low apparent affinity for tetracaine. Furthermore, tetracaine became more effective at low concentrations of cGMP and at saturating concentrations of cAMP, conditions which permit the channels to spend more time in the closed configuration. These results were well fit by a model in which tetracaine binds more tightly to the closed channel than to the open channel. Dose-response curves for tetracaine in the presence of saturating cGMP are well fit with a Michaelis-Menten binding scheme indicating that a single tetracaine molecule is sufficient to produce block. In addition, tetracaine block is voltage dependent with an effective z delta of +0.56. These data are consistent with a pore-block hypothesis. The finding that tetracaine is a state-dependent pore blocker suggests that the inner mouth of the pore of cyclic nucleotide-gated channels undergoes a conformational change during channel opening.

Anesthetics, Local↗
PubMed1986

Clonidine prolongs canine tetracaine spinal anaesthesia.

Using a randomized blind cross-over design, the comparative efficacy of clonidine in prolonging tetracaine spinal anaesthesia was studied in six mongrel dogs. Lumbar subarachnoid injections (1 ml) of: tetracaine 4 mg with clonidine 150 micrograms, tetracaine 4 mg with epinephrine 200 micrograms, tetracaine 4 mg, clonidine 150 micrograms, epinephrine 200 micrograms, and five per cent dextrose in H2O (vehicle) were administered randomly to each animal at 5-7 day intervals. Subarachnoid tetracaine produced a motor blockade of 186 +/- 58 (mean +/- SEM) min. Both clonidine and epinephrine produced a similar prolongation of tetracaine motor blockade, 135 per cent (p less than 0.01) and 116 per cent (p less than 0.05) respectively, compared with tetracaine alone. No motor blockade was observed in dogs receiving clonidine, epinephrine or five per cent dextrose in H2O. The addition of clonidine to tetracaine spinal anaesthesia produced a significant increase in duration of sensory blockade, 56 per cent (p less than 0.01) and 107 per cent (p less than 0.01) respectively, when compared to tetracaine with and without epinephrine. Subarachnoid clonidine alone produced a sensory blockade of 76 +/- 17 minutes, while only one animal receiving subarachnoid epinephrine had a sensory blockade (40 minutes). No neurologic deficits were observed in any of the animals. The study concludes that during spinal anaesthesia with tetracaine in dogs, clonidine is as effective as epinephrine in prolonging motor blockade, but is more effective in prolonging sensory blockade.

Anesthesia, Spinal↗
PubMed1983

Tetracaine modifies the fragmentation mode of heated human erythrocytes and can induce heated cell fusion.

It is known that human erythrocytes in saline fragment by development of an unstable surface wave on the cell rim when cells are heated through the denaturation temperature of the structural protein, spectrin. Here the influence of tetracaine on the fragmentation process has been recorded and analysed by video microscopy of cells heated in rectangular glass microcapillaries. The number of waves per cell rim decreases with increasing tetracaine concentration until, at 0.5 mM tetracaine, wave growth on the cell rim is suppressed on most cells and the cells internalize membrane at the cell dimple. The rate constant for the change in the number of waves per cell with increasing tetracaine concentration is 9.6 mM-1 at a heating rate of 0.5 K/s. 50% of heated cells internalize membrane at 0.14 mM tetracaine. When cells are heated rapidly in suspension in test tubes the presence of tetracaine reduces the temperature for 50% haemolysis from 66 degrees C for washed control cells to 60.5 degrees C for cells in 2 mMs tetracaine. Cells heat in microcapillaries in tetracaine concentrations of 3 mM and higher begin to swell before the spectrin denaturation temperature is reached. Cell fusion was observed at and above the spectrin denaturation temperature in cells heated in 3 and 4 mM tetracaine. It was also noted that the morphology of erythrocytes maintained in 3.6 mM tetracaine for times up to 30 min at 37 degrees C or 20 degrees C was strongly dependent on temperature and time.

Cell Fusion↗