Abstract
Summary
The effects of electrolyte and water abnormalities on total peripheral resistance (TPR) were studied in anesthetized dogs. Cardiac input was maintained constant by means of a pump. A 5 min intranvenous (IV) infusion of isotonic KCl (N = 11) or MgCl2 (N = 11) solution at 1.91 cc/min increased plasma [K+] by 0.64 mEq/1 and increased [Mg2+] by 1.83 mEq/1. These abnormalities did not significantly alter TPR. A 5 min infusion of hypertonic saline solution at 7.64 cc/min increased plasma osmolality (Osm) 20 mOsm/1 (N = 10). TRP decreased an average of 5% (P < 0.05). Simultaneously increasing plasma [K+], [Mg2+], and Osm (N = 10) 0.4 mEq/1, 1.95 mEq/1, and 22 mOsm/1 respectively, produced a decrease in TPR of 11% (P < 0.05). Identical experiments were carried out in spinally anesthetized (procainized) dogs. Singly increasing plasma [K+] (N = 10), [Mg2+] (N = 10) or simultaneously increasing plasma [K+] and [Mg2+] (N = 8), produced significant decreases in TPR. Hypersomolality (N = 11) and the combination of hyperkalemia, hypermagnesemia and hyperosmolality (N = 10) produced significantly greater decreases in TPR than seen in spinally intact animals. Appropriate control solutions were infused for intact (N = 18) and spinally anesthetized (N = 20) dog experiments. These data strongly suggest that part of the fall in arterial blood pressure seen in intact dogs during various acutely produced electrolyte and water abnormalities is due, at least in part, to a fall in TPR. They also indicate that ABP responses in intact dogs during various single electrolyte abnormalities may be masked because of operable neurologic barostatic mechanisms.
This research was supported in part by NIH Grant HL-10899 and the Michigan Heart Association. This research represents partial completion of requirements for the Master of Science degree by G. W. Jelks, who was an NIH predoctoral trainee (HL 05873).
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