Comparison of Sodium Lactate Infusion and Carbon Dioxide Inhalation Panic Provocation Tests: A Meta-analysis

Background Sodium lactate (NaL) infusion and carbon dioxide (CO2) inhalation are proven to provoke acute panic attacks (PAs) in patients with panic disorder (PD). A systematic literature search and meta-analysis were performed to compare the effect sizes of these methods. Methods Odds ratios were calculated for each of the original studies and were pooled using the random-effects model. Results Either NaL or CO2 provocations significantly increased the rates of PAs in individuals with PD compared to those in healthy controls. However, the effect size of NaL infusion (OR=25.13, 95% CI=15.48–40.80) was significantly greater than that of CO2 inhalation (OR=10.58, 95%CI=7.88–14.21). Conclusion The evidence for the efficacy of the two panic provocation tests is very strong. Yet, the results support the superiority of NaL infusion over CO2 inhalation challenge as a panic provocation test. Thus, lactate seems a much stronger stimulus than CO2 for the brain suffocation detector.

Ventromedial Hypothalamic Nucleus Glycogen Regulation of Metabolic-Sensory Neuron AMPK and Neurotransmitter Expression: Role of Lactate

Astrocyte glycogen is dynamically remodeled during metabolic stability and provides oxidizable L-lactate equivalents during neuro-glucopenia. Current research investigated the hypothesis that ventromedial hypothalamic nucleus (VMN) glycogen metabolism controls gluco-stimulatory nitric oxide (NO) and/or gluco-inhibitory gamma-aminobutyric acid (GABA) neuron 5'-AMP-activated protein kinase (AMPK) and transmitter marker, e.g. neuronal nitric oxide synthase (nNOS), glutamate decarboxylase65/67 (GAD) protein expression. Adult ovariectomized estradiol-implanted female rats were injected into the VMN with the glycogen phosphorylase inhibitor 1,4-dideoxy-1,4-imino-D-arabinitol (DAB) before vehicle or L-lactate infusion. Western blot analysis of laser-catapult-microdissected nitrergic and GABAergic neurons showed that DAB caused lactate-reversible up-regulation of nNOS and GAD proteins. DAB suppressed or increased total AMPK content of NO and GABA neurons, respectively, by lactate-independent mechanisms, but lactate prevented drug enhancement of pAMPK expression in nitrergic neurons. Inhibition of VMN glycogen disassembly caused divergent changes in counter-regulatory hormone, e.g. corticosterone (increased) and glucagon (decreased) secretion. Outcomes show that VMN glycogen metabolism controls local gluco-regulatory transmission by means of lactate signal volume. Results implicate glycogen-derived lactate deficiency as a physiological stimulus of corticosterone release. Concurrent normalization of nitrergic neuron nNOS and pAMPK protein and corticosterone secretory response to DAB by lactate infers that the hypothalamic-pituitary-adrenal axis may be activated by VMN NO-mediated signals of cellular energy imbalance.

A STUDY ON ANALGESIA PROVIDED BY ULTRASOUND GUIDED FASCIA ILIACA COMPARTMENT BLOCK WITH AND WITHOUT PARACETAMOL: EFFECT ON HEMODYNAMICS DURING INTUBATION

Introduction: Paracetamol acts by the inhibition of Cyclooxygenase (COX) mediated production of Prostaglandin unlike the non steroidal anti inflammatory agents, so it was found that tissue inflammation was not reduced. Methodology: A detailed pre-anaesthetic checkup carried out in each patient. Patient is kept nil per orally 6 hours prior to surgery, i.v line secured, pre medicated with Inj Ranitidine 50mg iv, Inj Ondansetron 4mg iv and IVF Ringer Lactate infusion at 100ml/hr 3 hours prior to surgery. Results: Among the patients undergoing spinal anaesthesia in fracture femur surgery, there was no statistically significant difference in Blood pressure, Mean arterial pressure (MAP) between the groups. Conclusion: Among the patients undergoing spinal anaesthesia in fracture femur surgery, there was no statistically significant difference in Oxygen saturation (SpO2) between the groups

Lactate and BDNF: Key Mediators of Exercise Induced Neuroplasticity?

Accumulating evidence from animal and human studies supports the notion that physical exercise can enhance neuroplasticity and thus reduce the risk of several neurodegenerative diseases (e.g., dementia). However, the underlying neurobiological mechanisms of exercise induced neuroplasticity are still largely unknown. One potential mediator of exercise effects is the neurotrophin BDNF, which enhances neuroplasticity via different pathways (e.g., synaptogenesis, neurogenesis, long-term potentiation). Current research has shown that (i) increased peripheral lactate levels (following high intensity exercise) are associated with increased peripheral BDNF levels, (ii) lactate infusion at rest can increase peripheral and central BDNF levels and (iii) lactate plays a very complex role in the brain’s metabolism. In this review, we summarize the role and relationship of lactate and BDNF in exercise induced neuroplasticity.

Effect of Aggressive Fluid Therapy on Outcomes after Endoscopic Retrograde Cholangiopancreatography: A Randomized Controlled Clinical Trial

BACKGROUND Pancreatitis is a serious complication of endoscopic retrograde cholangiopancreatography (ERCP), which may lead to death. The purpose of this study was to evaluate the preventive effect of aggressive fluid therapy on the incidence of post-ERCP pancreatitis. METHODS In double-blind controlled condition, 240 patients were selected and divided into two groups. The treatment of the intervention group (n = 120) included a dose of 20 mL/kg of ringer lactate infusion within 90 minutes before ERCP and 3 mL/kg/h during ERCP followed by 3 mL/kg/h up to 8 hours. The treatment of the control group (n = 120) included a dose of 1.5 mL/kg of ringer lactate infusion during ERCP up to 8 hours later. Firstly, the patients were evaluated in terms of excessive fluid and serum amylase and pain level, and then they were re-evaluated 2, 8, and 24 hours after ERCP. RESULTS The mean age of the patients was 51.57 ± 13.5 years. Most of the patients were female (54.5%). Pancreatitis was developed in 26 patients including 5.83% of the patients in the intervention group and 15.83% of the patients in the control group (p = 0.013). Pancreatic pain was seen in 7.5% of the patients in the intervention group and in 27.5% of the control group (p < 0.005). Hyperamylasemia was seen in 20.83% of the patients in the intervention group and in 35% of the control group (p = 0.014). The mean days of hospital admission was 1.308 ± 0.807 in the intervention group and 1.425 ± 0.876 in the control group (p = 0.275). CONCLUSION Aggressive fluid therapy with ringer lactate solution before ERCP can effectively prevent postERCP pancreatitis, pancreatic pain, and hyperamylasemia.