Procaine HCl

Procaine is an inhibitor of sodium channel, NMDA receptor and nAChR with IC50 of 60 μM, 0.296 mM and 45.5 μM, which is also an inhibitor of 5-HT3 with K_D of 1.7 μM.

Basic science and clinical aspects of procaine HCl as a limbic system excitant.[Pubmed:4001428]

Prog Neuropsychopharmacol Biol Psychiatry. 1985;9(2):109-19.

The literature in animals and humans which indicate that systemic Procaine HCl activates limbic tissue is reviewed. Studies in cats which suggest that procaine excites limbic cells by reducing neural inhibition are then described. Evidence that power spectral analysis of high frequency EEG bands (omega or 31-55 cps) in the temporal cortical EEG reflects degree of limbic (amygdala) excitation in animals and humans is reviewed. Studies in cats are described which show that procaine selectively increases omega band activity in the amygdala and temporal cortex in a dose related fashion which parallels dose related increases in amygdaloid neural activity. Preliminary results of combining intravenous procaine and omega band analysis of scalp EEG in humans to predict therapeutic response to carbamazepine in borderline personality and affective disorder patients are then described. The effects of procaine on omega are compared to the effects of direct electrical stimulation of human limbic system in complex partial seizure patients undergoing assessment for temporal lobectomy. The results tentatively support the hypothesis that some psychiatric patients have hyperexcitable limbic systems, and those that do, show a positive behavioural response to carbamazepine.

Heat sensitization of G1 and S phase cells by procaine HCl. II: Toxicity and probability of dividing following treatment.[Pubmed:3171263]

Int J Hyperthermia. 1988 Nov-Dec;4(6):687-97.

Extended studies of the procaine sensitization of synchronous populations of CHO cells heated in monolayers were performed to help explain the mechanism for this sensitization. Cells were treated with 43.0, 45.5 and 43.0 degrees C + procaine, clonal survival of cells was determined, and time-lapse cinematography was used to monitor the time-dependent morphological changes and division delay of the various populations for up to 72 h following treatment. Procaine sensitized G1 and S phase populations to killing by 43.0 degrees C with thermal enhancement ratios of 7.4 +/- 0.5 and 7.9 +/- 1.1 (mean +/- SE), respectively. The division delays (39.2 +/- 3.5 h) of G1 cells exposed to 45.5 or 43.0 degrees C +/- procaine were longer than those (21.9 +/- 2.3 h) of S phase cells treated to comparable surviving fractions (SF). In these experiments the SF of the G1 populations was 0.50 +/- 0.17 versus 0.33 +/- 0.08 for the S phase populations. G1 populations heated with 43.0 degrees C alone (SF, 0.34 +/- 0.05) had division delays of 19.4 +/- 2.4 h. Colony formation correlated well with both G1 and S phase cells that had regular divisions subsequent to treatments; the heat-induced death of G1 and S phase cells correlated with interphase lysis and irregular divisions (including bipolar divisions yielding micronucleated progeny). Deaths due to both categories of lesions are increased by treatment with procaine; however, death due to interphase lysis is enhanced more by procaine. In summary, Procaine HCl sensitized G1 and S phase cells comparably to killing by 43.0 degrees C.

Effects of steroid with repetitive procaine HCl injection in the management of carpal tunnel syndrome: an ultrasonographic study.[Pubmed:22336701]

J Neurol Sci. 2012 May 15;316(1-2):76-8.

BACKGROUND AND AIM: With the use of musculoskeletal ultrasonography (MSUS), morphological changes in the median nerve have been recently reported in patients with carpal tunnel syndrome (CTS). On the other hand, the literature still lacks the information whether those changes are further altered with steroid and local anesthetic injection which is a widely used treatment in this group of patients. Therefore, the aim of our study was to explore in-vivo the effects of steroid with repetitive Procaine HCl injection on the median nerve of patients with CTS. MATERIALS AND METHOD: This prospective clinical trial followed-up patients for 2 months. 22 patients (37 median nerves) with clinical and electrophysiological evidence of CTS were included in the study. All patients received both 40 mg of triamcinolone acetonide once and 4 ml of 1% Procaine HCl twice a week for 2 weeks with the same technique. Clinical, functional, electrophysiological and ultrasonographic evaluations were performed at the study onset, and 2 months after the last injection. RESULTS: Electrophysiological, ultrasonographic findings (median nerve anterior-posterior diameter, transverse diameter and cross sectional area in the proximal carpal tunnel and volar bulging,) VAS scores, Boston carpal tunnel symptom and function assessment scale improved significantly (P<0.05). CONCLUSION: Steroid injection with repetitive Procaine HCl injection effectively reduced the symptoms of CTS, improved the Boston carpal tunnel symptom and function assessment scale and also electrophysiological and ultrasonographic findings. Long term effects remain to be studied. Indisputably, the use of MSUS seems to be promising in this regard.

The effects of procaine HCl on population cellular and evoked response activity within the limbic system of the cat. Evidence for differential excitatory action of procaine in a variety of limbic circuits.[Pubmed:3423267]

Prog Neuropsychopharmacol Biol Psychiatry. 1987;11(4):345-64.

1. The effects of intravenous injections of Procaine HCl on population cellular activity in limbic tissue and overlying cortex, and on transmission of evoked activity between limbic structures was investigated in awake cats. Clear dose-related increases in cellular activity were seen in amygdala and ventral hippocampus. Changes in cellular activity in the nucleus accumbens and temporal neocortex were also dose-related, but in a complex time-dependent manner. Changes in ventromedial hypothalamus only appeared at the second highest dose of procaine. 2. Procaine facilitated transmission of evoked excitatory activity from the amygdala to the ventromedial hypothalamus, but only after a considerable delay from the time of injection. On the other hand, procaine had no effect on activity evoked in the ventral hippocampus, nucleus accumbens or temporal cortex by amygdala stimulation. 3. It was concluded that intravenous procaine functions as an excitant of limbic system cells, and that procaine alters synaptic transmission in some, but not all, output pathways from the amygdala. The neuroexcitant effects of procaine appear to be idiosyncratic, however, varying over dose with limbic and cortical area examined.

Procaine is an inhibitor of sodium channel, NMDA receptor and nAChR with IC50 of 60 μM, 0.296 mM and 45.5 μM, which is also an inhibitor of 5-HT3 with KD of 1.7 μM.

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