AJVR, Vol 67, No. 5, May 2006 801 A cidosis and hypocalcemia commonly develop in many critically ill dogs 1–3 and also in some dogs undergoing general anesthesia. 4–6 In these dogs, it is important to tightly control PaO 2 to ensure normal blood oxygenation. In studies 7,8 in dogs, our research group determined that metabolic acidosis directly stimulates PTH secretion, that the acidosis-induced increase in arterial Ca 2+ concentration reduces the mag- nitude of PTH stimulation during metabolic acidosis, and that metabolic acidosis enhances the stimulation of PTH secretion during the induction of hypocal- cemia. In those studies, arterial blood gases were mea- sured, and as a result, we became aware that both metabolic acidosis and changes in arterial Ca 2+ concen- tration affected PaO 2 values. Metabolic acidosis is known to increase PaO 2 val- ues in dogs. The prevailing opinion is that the increase in PaO 2 results from a reduction in the alveolar-to-arte- rial O 2 difference caused by a shift in the oxygen- hemoglobin dissociation curve (Bohr effect). 9,10 In an earlier study, 11 it was suggested that the metabolic aci- dosis-induced increase in PaO 2 might result from a more homogeneous distribution between ventilation and perfusion in the lungs. However, none of those studies evaluated the effect of the increase in arterial Ca 2+ concentration that occurs during metabolic acido- sis. The purpose of the study reported here was to eval- uate the effects of metabolic acidosis and changes in arterial blood Ca 2+ concentration on PaO 2 values in anesthetized dogs. Materials and Methods Healthy mixed-breed dogs (18 males and 13 females) that were 2 to 5 years old were used in the study. The mean ± SE weight of the dogs was 26 ± 2 kg, and each was in good body condition (body score, 3/4). All animals received humane care in compliance with the Principles of Laboratory Animal Care, formulated by the National Society for Medical Research and the Guide for the Care and Use of Laboratory Animals prepared by the National Academy of Sciences. 12 Experimental protocols were reviewed and approved by the Ethics Committee for Animal Research of the Universidad de Cordoba. After withholding of food for 12 hours, dogs were pre- medicated with ketamine a (7.5 mg/kg, IM), fentanyl b (75 Received July 12, 2005. Accepted November 8, 2005. From the Departmento de Medicina y Cirugía Animal, Universidad de Córdoba, Ctra Madrid-Cadiz, km 396, 14014 Córdoba, Spain (Lopez, Estepa, Aguilera-Tejero); the Department of Medicine, University of California-Los Angeles, West Los Angeles VA Medical Center, 11301 Wilshire Blvd, Los Angeles, CA 90073 (Felsenfeld); and the Departmento de Nefrología y Unidad de Investigación, Hospital Universitario Reina Sofia,14004 Córdoba, Spain (Rodriguez). Supported by Spanish Government Grants BFI2001-1901 and SAF2001-0350 from the Ministerio de Ciencia y Tecnologia, the Plan Andaluz de Investigación (Grupo CTS-179), and the Fundacion Reina Sofia-Cajasur, Spain. Presented in part as an abstract at the 22nd Symposium of the Veterinary and Comparative Respiratory Society, Montreal, October 2004. Address correspondence to Dr. Aguilera-Tejero. Effect of changes in ionized calcium concentration in arterial blood and metabolic acidosis on the arterial partial pressure of oxygen in dogs Ignacio Lopez, DVM, PhD; Arnold J. Felsenfeld, MD; Jose C. Estepa, DVM, PhD; Mariano Rodriguez, MD, PhD; Escolastico Aguilera-Tejero, DVM, PhD Objective—To evaluate the effects of metabolic aci- dosis and changes in ionized calcium (Ca 2+ ) concen- tration on PaO 2 in dogs. Animals—33 anesthetized dogs receiving assisted ventilation. Procedure—Normal acid-base status was maintained in 8 dogs (group I), and metabolic acidosis was induced in 25 dogs. For 60 minutes, normocalcemia was maintained in group I and 10 other dogs (group II), and 10 dogs were allowed to become hypercal- cemic (group III); hypocalcemia was then induced in groups I and II. Groups II and IV (5 dogs) were treat- ed identically except that, at 90 minutes, the latter underwent parathyroidectomy. At intervals, variables including PaO 2 , Ca 2+ concentration, arterial blood pH (pHa), and systolic blood pressure were assessed. Results—In group II, PaO 2 increased from baseline value (96 ± 2 mm Hg) within 10 minutes (pHa, 7.33 ± 0.001); at 60 minutes (pHa, 7.21 ± 0.02), PaO 2 was 108 ± 2 mm Hg. For the same pHa decrease, the PaO 2 increase was less in group III. In group I, hypocal- cemia caused PaO 2 to progressively increase (from 95 ± 2 mm Hg to 104 ± 3 mm Hg), which correlated (r = –0.66) significantly with a decrease in systolic blood pressure (from 156 ± 9 mm Hg to 118 ± 10 mm Hg). Parathyroidectomy did not alter PaO 2 values. Conclusions and Clinical Relevance—Induction of hypocalcemia and metabolic acidosis each increased PaO 2 in anesthetized dogs, whereas acidosis-induced hypercalcemia attenuated that increase. In anes- thetized dogs, development of metabolic acidosis or hypocalcemia is likely to affect ventilatory control. (Am J Vet Res 2006;67:801–808) ABBREVIATIONS PTH Parathyroid hormone Ca 2+ Ionized calcium pHa Arterial blood pH Unauthenticated | Downloaded 08/14/22 11:07 AM UTC