The meanings of Carbicarb.

The meanings of Carbicarb, sodium bicarbonate, and sodium chloride forward arterial blood gases, lactate concentrations, hemodynamics, and myocardial intracellular pH were compared in hypoxic lactic acidosis with controll carbon dioxide elimination. Twenty-one young hybrid dogs were anesthetized, mechanically ventilated, and randomly allocated into individual of three treatment groups. After hypoxic lactic acidosis was induced and maintained, 25 mEq/kg of individual of the agents was infused above 30 min. Arterial house gases, pH, lactate concentrations, and hemodynamic variables were measured immediately prior to the infusion of the agent and 30 min after the infusion was complet With sodium bicarbonate administration, there was a significant increase in arterial [PCOsub2] as compared to one as well as the other Carbicarb or sodium chloride administration. With Carbicarb administration, there was a significant increase in arterial pH base exces and cardiac index, without a significant increase in arterial lactate concentration as compared to sodium bicarbonate or sodium chloride administration. attack volume index was also increased significantly with decreased heart rate. The data hint that Carbicarb administration in hypoxic lactic acidosis improved hemodynamics compared with sodium bicarbonate or sodium chloride administration. The increased rap volume and cardiac contractility appear to be owed to improved myocardial intracellular pH

Sodium bicarbonate generates carbon dioxide as it reacts with inflammable air ions in the blood. When ventilation is inadequate to unload carbon dioxide as fast as it is produc there may be little change in life-blood pH.[1] It has been recognized that the administration of sodium bicarbonate in the correction of hypoxic lactic acidosis might be counterproductive to cardiac function.[2-6] The greatest in quantity likely mechanism for this adverse import of sodium bicarbonate is that a large amount of carbon dioxide, which may exce the amount eliminated from the visible form [i]or[/i] frame is generated and diffuses into the tissues rapidly resulting in the decrease of intracellular pH to cause paradoxic acidosis.[7-9] The decrease in myocardial intracellular pH depresse myocardial contractility and subsequently decreases cardiac output[10-15]

Carbicarb (International Medication combination of parts to form a whole South El Monte, Calif), a just discovered buffering agent, is a 1:1 mixture of disodium carbonate and sodium bicarbonate with frequently lower [PCO.sub.2] higher pH, and les osmolality, as compared to sodium bicarbonate.[8] It guards similarly to sodium bicarbonate yet without net generation of carbon dioxide.[7,8,16,17] The carbonate ion, a powerful base in Carbicarb, abstracts inflammable air ions from buffer acid and from dissolved carbon dioxide to bring forth bicarbonate ions (Fig 1). These sum of two units major reservoirs of proton stock are in blood and in tissues perfused by the agency of capillaries.[8] Therefore, the stupid lout acids and [PCO.sub.2] do not increase with Carbicarb administration. It is our hypothesis that Carbicarb will correct hypoxic lactic acidosis more effectively than sodium bicarbonate because there is no without deductions production of carbon dioxide which may play a significant part in determining myocardial intracellular pH and myocardial function. To proof our hypothesis, we induced hypoxic lactic acidosis in an animal mould (1) to compare the general intents of Carbicarb, sodium bicarbonate, and sodium chloride onward arterial blood gases, lactate concentration, and hemodynamic variables; and (2) to correlate arterial pH with simultaneous myocardial intracellular pH at nuclear magnetic resonance spectroscopy.

MATERIALS AND METHODS

Animal Preparation

This throw was approved by the institutional Review Board for Animal Research of the University of Texas Southwestern Medical Center (UTSWMC) Treatment of all animal bring under rules at the UTSWMC is carefully regulated and conforms to the guidelines of the National Institutes of Health. Twenty-one young hybrid dogs with body weight of 11 [+ or -] 05 kg were studied. Each dog was anesthetized with intravenous pentobarbital (20 mg/kg) intubated, and mechanically ventilated (Harvard, southward Wartick, Mass). Spontaneous respiration was inhibited by means of continuous infusion of pentobarbital (5 to 7 mg/kg/h) in a less degree than cardiopulmonary monitoring (Hewlett-Packard, Waltham, Mass), a No. 5 French 75 cm Swan-Ganz thermodilution pulmonary arterial catheter (American Edwards Lab, Irvine, Calif) and a 16-gauge polyvinyl systemic arterial catheter were placed in the pulmonary artery and the descending aorta, respectively, at a right femoral cutdown. A left thoracotomy was performed for the placement of a nuclear magnetic resonance coil above the left ventricle, and the dog was positioned in the magnetic lucite cylinder of a nuclear magnetic resonance spectroscope upon a warming blanket. The cardiopulmonary monitor and the ventilator were kept at least 10 feet away from the dog because of their magnetic metal composition. Before inducing hypoxic lactic acidosis, the pulmonary arterial wedge constraining force was maintained at 10 [+ or -] 2 mm Hg using normal saline solution bolus infusions as lacked and arterial [PCO.sub.2] of 40 [+ or -] 5 mm Hg was maintained with mechanical ventilation (tidal turn 15 to 20 ml/kg, rate 10 to 15/min). Hypoxic lactic acidosis was induced with [FIO.sub.2] of 009 [+ or -] 001 and stabilized with serial measurements of arterial kin gases and pH over 2 to 3 h resulting in arterial pH of 720 [+ or -] 005 with [POsub2] of 28 [+ or -] 3 mm Hg No further ventilatory adjustment was made thereafter, and all the progeny gases and pH values were measured using a Corning 178 analyzer (Corning Glass Works, Corning, NY)

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