The effect of hypercapnia on the arrhythmogenic dose of epinephrine (ADE) was investigated in 14 horses. Anesthesia was induced with guaifenesin and thiamylal sodium and was maintained at an end-tidal halothane concentration between 0.86 and 0.92%. Base-apex ECG, cardiac output, and facial artery blood pressure were measured and recorded. The ADE was determined at normocapnia (arterial partial pressure of carbon dioxide [Pa(CO2)] = 35 to 45 mm of Hg), at hypercapnia (Pa(CO2) = 70 to 80 mm of Hg), and after return to normocapnia. Epinephrine was infused at arithmetically spaced increasing rates (initial rate = 0.25 micrograms/kg of body weight/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate, to the nearest 0.25 micrograms/kg/min, at which 4 premature ventricular complexes occurred in a 15-second period. The ADE (mean +/- SD) during hypercapnia (1.04 +/- 0.23 micrograms/kg/min) was significantly (P < 0.05) less than the ADE at normocapnia (1.35 +/- 0.38 micrograms/kg/min), whereas the ADE after return to normocapnia (1.17 +/- 0.22 micrograms/kg/min) was not significantly different from those during normocapnia or hypercapnia. Baseline systolic and diastolic arterial pressures and cardiac output decreased after return to normocapnia. Significant differences were not found in arterial partial pressure of O2 (Pa(O2)) or in base excess during the experiment. Two horses developed ventricular fibrillation and died during normocapnic determinations of ADE. Hypercapnia was associated with an increased risk of developing ventricular arrhythmias in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.

Adrenaline is widely used drug to combat several conditions such as allergy and anaphylaxis. The current work was to investigate the renal and hepatic complications following adrenaline injection, in addition, the impact of Cleome (SAMWA) methanolic extract on adrenaline- induced renal and hepatic alterations. Twenty-four male Wister rats were divided equally into four groups; Normal control group received oral distilled water for 30 consecutive days and administered subcutaneous saline on the 31st and 32nd days. The Cleome extract (200 mg/kg) group received Cleome methanolic extract (200 mg/kg, P.O) for 30 consecutive days and administered subcutaneous saline on the 31st and 32nd days. The adrenaline group received distilled water orally for 30 consecutive days and administered subcutaneous adrenaline (2 mg/kg, s.c.) divided into two doses (1 mg/kg, s.c) each on the 31st and 32nd days. Cleome extract (200 mg/kg)/ adrenaline received Cleome methanolic extract (200 mg/kg, P. O) for 30 consecutive days and administered subcutaneous adrenaline (2 mg/kg, s.c.) divided into two doses (1 mg/kg, s.c) each on the 31st and 32nd days. Liver and kidney function biomarkers in addition to histopathological analyses were evaluated. Adrenaline caused alteration in liver and kidney function biomarkers without affecting the histological structure of the liver and the kidney. SAMWA methanolic extract pretreatment significantly decreased serum urea, uric acid, aspartate aminotransferase (AST), alanine transaminase (ALT) and Alkaline Phosphatase (ALP). SAMWA ameliorated serum albumin reduction and total protein induced by adrenaline injection. SAMWA methanolic extract could protect liver and kidney of rats exposed to adrenaline.