Abstract
Evidence suggests that septic shock patients with chronic arterial hypertension may benefit from resuscitation targeted to achieve higher blood pressure values than other patients, possibly as a result of altered renal autoregulation. The effects of different vasopressor agents on renal autoregulation may be important in this context. We investigated the effects of arginine vasopressin (AVP) and norepinephrine (NE) on renal autoregulation in ovine septic shock. Sepsis was induced by fecal peritonitis. When shock developed (decrease in mean arterial pressure to <65 mmHg and no fluid responsiveness), animals were randomized to receive NE or AVP in a crossover design. Before the switch to the second vasopressor, the first vasopressor was discontinued for 30 min to ensure complete washout of the first vasopressor. Renal autoregulation was evaluated by recording the change in renal blood flow (RBF) in response to manual, stepwise reductions in renal inflow pressure. In this model, the lower limit of renal autoregulation was not significantly altered 6 h after sepsis induction (59 ± 9 vs. 64 ± 7 mmHg at baseline, P = 0.096). After development of shock, the autoregulatory threshold was lower with AVP than with NE (59 ± 5 vs. 65 ± 7 mmHg, P = 0.010). However, RBF was higher with NE both at the start of autoregulatory measurements (206 ± 58 vs. 170 ± 52 ml/min; P = 0.049) and at the autoregulatory threshold (191 ± 53 vs. 150 ± 47 ml/min; P = 0.008). As vasopressors may have different effects on renal autoregulation, blood pressure management in patients with septic shock should be individualized and take into account drug-specific effects.NEW & NOTEWORTHY Septic shock patients with chronic arterial hypertension may benefit from higher blood pressure targets due to underlying deficits in renal autoregulatory efficiency. The current study is the first to show that the choice of vasopressor agent can differentially affect renal autoregulation. These findings may contribute to more personalized blood pressure management in patients with septic shock.
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More From: Journal of applied physiology (Bethesda, Md. : 1985)
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