sodium-bicarbonate and Cerebral-Infarction

To evaluate the utility of transthoracic contrast echocardiography (cTTE) using vitamin B6 and sodium bicarbonate as contrast agents for diagnosing right-to-left shunt (RLS) caused by patent foramen ovale (PFO) compared to that of transesophageal echocardiography (TEE). We investigated 125 patients admitted to our neurology department with unexplained cerebral infarction and migraine. All patients underwent cTTE using vitamin B6 and sodium bicarbonate as contrast agents, after which they underwent transthoracic echocardiography. The Doppler signal was recorded during the Valsalva maneuver, and TEE examinations were performed. The feasibility, diagnostic sensitivity, and safety of cTTE and TEE for PFO recognition were compared. Evidence of PFO was found in 49 (39.20%) patients with cTTE, more than were detected with TEE (39, 31.20%) (χ

Topics: Adolescent; Adult; Aged; Cerebral Infarction; Contrast Media; Coronary Circulation; Echocardiography, Doppler, Color; Echocardiography, Transesophageal; Feasibility Studies; Female; Foramen Ovale; Foramen Ovale, Patent; Hemodynamics; Humans; Male; Microbubbles; Middle Aged; Migraine Disorders; Predictive Value of Tests; Reproducibility of Results; Sodium Bicarbonate; Valsalva Maneuver; Vitamin B 6; Young Adult

It has been demonstrated in many studies that intracellular brain acidosis during cerebral ischemia is a significant factor in perpetuating the cycle of cellular dysfunction leading to neuronal injury. The purpose of this study was to determine whether preischemic administration of alkalotic agents could reduce neuronal injury after focal cerebral ischemia.. Fifteen fasted rabbits under 1.0% halothane anesthesia were randomized into three groups: Group 1 rabbits were ischemic controls (n = 5) that underwent 4 hours of focal cerebral ischemia. Groups 2 and 3 rabbits underwent a paradigm similar to that of Group 1, except that they were pretreated with either sodium bicarbonate or Carbicarb at similar buffering capacities. Intracellular brain pH (pH(i)), regional cortical blood flow (rCBF), and intrinsic reduced nicotinamide adenine dinucleotide (NADH) fluorescence were measured with in vivo fluorescence imaging. At the end of each experiment, infarct volume expressed as a percentage of hemispheric volume was measured by triphenyltetrazolium chloride staining.. Preischemic alkalinization did not alter brain pH(i), rCBF, or NADH fluorescence. After 4 hours of ischemia, brain pH(i), rCBF, NADH fluorescence, and infarct volume measured 6.40 +/- 0.09 (mean +/- standard error), 11 +/- 2 ml/100 g/min, 165 +/- 8% of baseline control, and 37 +/- 3% in ischemic controls, respectively. In Group 2 animals treated with sodium bicarbonate, brain pH(i), rCBF, NADH fluorescence, and infarct volume improved significantly (P < 0.05, analysis of variance) to 6.74 +/- 0.08, 24 +/- 6 ml/100 g/min, 137 +/- 6% of baseline control, and 22 +/- 4%, respectively. Group 3 Carbicarb animals demonstrated improvements in brain pH(i), rCBF, and NADH fluorescence, with a significant reduction in infarct volume.. These findings suggest that pretreatment with alkalinizing agents may be a useful intervention to provide intraoperative cerebral protection from ischemic injury.

Topics: Alkalies; Animals; Brain; Brain Ischemia; Carbonates; Cerebral Cortex; Cerebral Infarction; Cerebrovascular Circulation; Drug Combinations; Hydrogen; Hydrogen-Ion Concentration; NAD; Neuroprotective Agents; Oxidation-Reduction; Rabbits; Sodium Bicarbonate

A patient with a history of cerebrovascular disease, hypertension, and previous gastrectomy developed metabolic alkalosis and myoclonus. His medications included the anti-hypertensive agents nicardipine hydrochloride, delapril, prazosin; dihydroergotoxin and ticlopidine for cerebral infarction; estazolam for insomnia; azuren-L-glutamine compound and S-M powder. In addition, he had taken 12 grams per day of Ohta's Isan antacid, which contained 625 mg sodium bicarbonate per 1.3 g of antacid powder over a 6-month period. This antacid is commonly used in Japan. This is the first report of a case of metabolic alkalosis and myoclonus secondary to ingestion of a commercially available antacid in Japan.

Topics: Aged; Alkalosis; Antacids; Cardiovascular Agents; Cerebral Infarction; Dyspepsia; Gastrectomy; Humans; Hypertension; Hypnotics and Sedatives; Hypokalemia; Male; Myoclonus; Sleep Initiation and Maintenance Disorders; Sodium Bicarbonate

We investigated the immediate effect of tris (hydroxymethyl) aminomethane (THAM) and NaHCO3 on focal cerebral ischemia produced by occlusion of the left middle cerebral artery (MCA) in cats. The animals were divided into three groups. In the control group, physiological saline was infused continuously. The THAM and NaHCO3 groups received continuous administration of 0.3 mol THAM and 7% NaHCO3, respectively, to normalize arterial pH. Local CBF measured in the marginal and suprasylvian gyri decreased less than 30 ml/100 g/min after the MCA occlusion and there were no significant differences among the three groups. Extracellular pH of the marginal gyrus (peri-infarct zone) decreased from 7.21 to 6.86 in the control group. However, extracellular pH did not show significant changes in the THAM and NaHCO3 groups. Intracellular pH of the infarct area decreased from 7.23 to 6.13 in the control group within 6 hours after occlusion. THAM had a tendency to normalize intracellular pH compared with that in the control and NaHCO3 groups. THAM significantly (p < 0.05) decreased water content of the gray matter in the marginal gyrus at 6 hours after occlusion and the infarct size compared with those in the control and NaHCO3 groups. Therefore, normalization of systemic and perifocal acidosis with THAM is effective for reducing cortical edema and infarct size in the early stage of focal cerebral ischemia probably due to the improvement of intracellular acidosis.

Topics: Acid-Base Equilibrium; Animals; Brain Edema; Brain Ischemia; Cats; Cerebral Cortex; Cerebral Infarction; Extracellular Space; Intracellular Fluid; Sodium Bicarbonate; Tromethamine

Metabolic acidosis in cerebral ischemia is considered deleterious to cell function and neurological outcome. Amelioration of systemic and focal cerebral acidosis by an alkalizing agent may reduce ischemic brain damage. The effects of 0.3 mol tris (hydroxymethyl)aminomethane (THAM) and 7% NaHCO3 on focal cerebral ischemia produced by occlusion of the middle cerebral artery (MCA) in cats were examined. In thirty six adult cats, adjustment was made so that PaO2 and PaCO2 would be maintained within the normal range with mechanical ventilation and oxygen inhalation. Focal cerebral ischemia was produced by coagulation of the left MCA using the transorbital approach. The animals were divided into 3 groups as follows. 1) The control group received continuous intravenous administration of physiological saline (2 ml/kg/hour). 2) The THAM group received continuous intravenous administration of 0.3 mol THAM (2 ml/kg/hour). 3) The NaHCO3 group received continuous intravenous administration of 7% NaHCO3 (0.7 ml/kg/hour)+physiological saline (1.3 ml/kg/hour). PaO2, PaCO2 and mean arterial blood pressure were maintained within the normal range in each group. In the THAM and NaHCO3 groups, arterial pH was maintained within the normal range, whereas in the control group, arterial pH gradually decreased from 7.42 +/- 0.04 to 7.30 +/- 0.09 at 6 hours after MCA occlusion. Intracellular pH, measured by magnetic resonance spectroscopy over the ischemic brain, decreased from 7.23 +/- 0.06 to 6.13 +/- 0.61 by MCA occlusion. In the THAM group, intracellular pH increased compared with that in the control and 7% NaHCO3 group. These values, however, were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acidosis; Animals; Bicarbonates; Blood Pressure; Body Water; Brain; Brain Edema; Brain Ischemia; Cats; Cerebral Infarction; Sodium; Sodium Bicarbonate; Tromethamine