Renal function following sea snake venom (Lapemis hardwicki) administration in dogs treated with sodium bicarbonate solution.
The effects of sea snake venom (SSV) on renal function were studied in two groups of anesthetized experimental dogs pretreated with intravenous infusion of 4.2 gm% NaHCO3 solution. Animals were envenomated by intramuscular injection of SSV at a dosage of 0.34 mg/kg. Systemic hemodynamics showed no significant changes except for a tendency of decrease in cardiac output (CO). The glomerular filtration rate (GFR), the rate of urine flow (V) and effective renal plasma flow (ERPF), and effective renal blood flow (ERBF) significantly decreased, while filtration fraction (FF) significantly increased at 180 min after envenomation. Envenomated animals showed a reduction in renal fraction (RF), while renal vascular resistance (RVR) increased stepwise throughout the experimental periods. Animals pretreated with sodium bicarbonate showed no significant changes of CO, TPR MAP, HR, and packed cell volume (PCV) while receiving sea snake venom. Animals pretreated with sodium bicarbonate showed no changes in GFR, ERPF, ERBF, RF, and RVR after envenomation. The rate of urine flow markedly increased in envenomated animals which received pretreatment with bicarbonate. After envenomation alone, there were no differences in the plasma concentration of sodium (PNa) and chloride (PCl) as compared to the control value, whereas the plasma concentration of potassium (PK) increased at 180 min after envenomation. Animals pre-treated with bicarbonate showed a stepwise increase in both UNaV, FE(NA), U(Cl)V, and FE(Cl) accompanying SSV injection. Neither PNa nor PCl were affected, while PK significantly decreased in animals given SSV with bicarbonate loading. UKV and FEK increased stepwise in envenomated animals treated with bicarbonate throughout the period of study. All groups of animals given SSV, with or without NaHCO3 infusion, showed a marked elevation of the concentration of urinary myoglobin (U(Mb)), plasma lactate dehydrogenase (LDH), and plasma creatine phosphokinase (CPK) throughout experimental periods. The urinary myoglobin excretion markedly increased in animals after SSV injection accompanied by NaHCO3 infusion. It can be concluded that large amounts of myoglobin present in the renal tubules in envenomated animals can precipitate, particularly under acidic conditions, resulting in increased intratubular pressure and subsequently decreased renal hemodynamics including GFR and ERBF. An infusion of NaHCO3 to render urine more alkaline could have a protective role against depression of renal function following sea snake venom administration.
Sakwiwatkul
K
K
Department of Physiology, Faculty of Veterinary Science, Chulalongkorn University, Queen Saovabha Memorial Institute, Thai Red Cross Society, Patumwan, Bangkok.
Chaiyabutr
N
N
Sitprija
V
V
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002713:Chlorine / Q000097:blood / Q000652:urine; D003402:Creatine Kinase / Q000097:blood; D004285:Dogs; D004546:Elapid Venoms / Q000633:toxicity*; D005919:Glomerular Filtration Rate / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D007273:Injections, Intramuscular; D007275:Injections, Intravenous; D007770:L-Lactate Dehydrogenase / Q000097:blood; D007928:Lethal Dose 50; D008297:Male; D051379:Mice; D011188:Potassium / Q000097:blood / Q000652:urine; D012079:Renal Circulation / Q000187:drug effects*; D012964:Sodium / Q000097:blood / Q000652:urine; D017693:Sodium Bicarbonate / Q000494:pharmacology*; D016482:Urinalysis
D004546:Elapid Venoms; D002713:Chlorine; D017693:Sodium Bicarbonate; D012964:Sodium; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D011188:Potassium