sodium-bicarbonate and Cerebrovascular-Disorders

To review the data on pharmacology, pathophysiology and treatment of cocaine toxicity, with particular relevance to the heart and cardiovascular system.. Published epidemiology, laboratory and clinical studies on the pharmacology, electrophysiology and pathophysiology of cocaine toxicity and its treatment.. Cocaine toxicity-related morbidity and mortality are frequent due to the potent pharmacological effects of the drug as an indirect-acting sympathomimetic agent and its class I antiarrhythmic property paradoxically inducing pro-arrhythmia. The cardiac and cardiovascular toxic effects of cocaine include various degrees of myocardial ischemia, cardiac arrhythmias, cardiotoxicity, hypertensive effects, cerebrovascular effects and a hypercoagulable state. Treatment of cocaine toxicity must be based on the multiple factors leading to the toxicity. Sodium bicarbonate appears to have an important role in the acute setting with conduction abnormalities, seizures or acidosis. Unopposed alpha-stimulation provided by beta-blockade should be avoided. Central nervous system hyperexcitability should be treated with diazepam. The use of calcium antagonists appears logical.. Cocaine is an alkaloid with widespread illicit use. The rationale for treating acute cocaine intoxication has become clearer and more logical with increased knowledge of its mechanisms of action.

Topics: Arrhythmias, Cardiac; Cerebrovascular Disorders; Cocaine; Heart; Humans; Hypertension; Myocardial Ischemia; Sodium Bicarbonate

To estimate the quantitative reactivity of cerebral blood flow (CBF), the effects of sodium bicarbonate on the end-tidal CO2, arterial PaCO2, HCO3-, PH and CBF were examined. The CBF was measured by 133Xe inhalation method with ring type SPECT (HEADTOME). Activation study with sodium bicarbonate administration was performed after 30 minute of resting study, and the reactivity of each parameters was investigated. The arterial HCO3- and PH increased with similar reactivity, but PaCO2, end-tidal CO2 and CBF in the non-injured hemisphere changed with irregular reactivity. The excellent correlation between PaCO2 and end-tidal CO2 was vanished by the administration of sodium bicarbonate. The reactivity of CBF did not correlate with reactivity of PaCO2 and end-tidal CO2, but correlated with arterial HCO3- and PH. Thus the measurement of arterial HCO3- and PH may be indispensable to estimate the CBF reactivity with the administration of sodium bicarbonate.

Topics: Aged; Bicarbonates; Carbon Dioxide; Cerebrovascular Circulation; Cerebrovascular Disorders; Female; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Sodium; Sodium Bicarbonate; Tomography, Emission-Computed, Single-Photon; Xenon Radioisotopes

1. To test the hypothesis that NaCl increases blood pressure, while NaHCO3 does not, we measured the effect of an NaHCO3-containing mineral water on blood pressure in stroke-prone spontaneously hypertensive (SHR-SP) and Wistar-Kyoto (WKY) rats. We compared mineral water with equimolar amounts of NaCl and demineralized drinking water in six groups of 20 rats each over 24 weeks. 2. NaCl consistently increased blood pressure in both SHR-SP and WKY compared with demineralized water, while mineral water did not. 3. We studied the possible role of sodium-regulating hormones. Sodium, potassium-dependent adenosine triphosphatase activity was decreased by NaCl and by age, but not by mineral water. The concentration of atrial natriuretic peptide was greater in SHR-SP, but was not influenced by the two regimens. Components of the renin-angiotensin-aldosterone system and 18-hydroxydeoxycorticosterone tended to decrease with NaCl, but not with mineral water. 4. Plasma pH values in the six groups of rats were not different; however, SHR-SP had consistently lower PCO2 and HCO3- values and higher anion gap values than WKY rats. These values were not influence by the two regimens. 5. NaCl elevates blood pressure in SHR-SP while NaHCO3 does not. The changes in hormones regulating sodium homoeostasis suggest that NaCl induces volume expansion while NaHCO3 does not. The effect may be related to influences on renal sodium reabsorption by chloride and bicarbonate. The possible role of increased proton excretory activity in SHR-SP remains to be determined.

Topics: Animals; Bicarbonates; Blood Pressure; Body Weight; Cerebrovascular Disorders; Erythrocytes; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Sodium; Sodium Bicarbonate; Sodium Chloride; Time Factors; Water-Electrolyte Balance