Erin J Whalen1, Alan Kim Johnson2, Stephen J Lewis3. 1. Department of Psychology, University of Iowa, Iowa City, IA, USA; Department of Pharmacology, University of Iowa, Iowa City, IA, USA; The Cardiovascular Center, University of Iowa, Iowa City, IA, USA. Electronic address: erin.whalen@novartis.com. 2. Department of Psychology, University of Iowa, Iowa City, IA, USA; Department of Pharmacology, University of Iowa, Iowa City, IA, USA; The Cardiovascular Center, University of Iowa, Iowa City, IA, USA. 3. Department of Pediatrics, Case Western Reserve University, Cleveland, OH, USA. Electronic address: sjl78@case.edu.
Abstract
PURPOSE: The objectives of this study were (i) to characterize the hemodynamic responses caused by controlled hemorrhage (HEM) in pentobarbital-anesthetized rats, and (ii) to determine the responses elicited by systemic bolus injections of isotonic saline (0.15M) or hypertonic saline (3M) given 5min after completion of HEM. RESULTS: Controlled HEM (4.3±0.2ml/rat at 1.5ml/min) resulted in a pronounced and sustained fall in mean arterial blood pressure (MAP) to about 40mmHg. The fall in MAP was associated with a reduction in hindquarter vascular resistance (HQR) but no changes in renal (RR) or mesenteric (MR) vascular resistances. Systemic injections of isotonic saline (96-212μmol/kg i.v., in 250-550μl) did not produce immediate responses but promoted the recovery of MAP to levels below pre-HEM values. Systemic injections of hypertonic saline (750-3000μmol/kg, i.v., in 250-550μl) produced immediate and pronounced falls in MAP, RR, MR and especially HQR of 30-120s in duration. However, hypertonic saline prompted a full recovery of MAP, HQR and RR to pre-HEM levels and an increase in MR to levels above pre-HEM values. CONCLUSIONS: This study demonstrates that (i) HEM induced a pronounced fall in MAP which likely involved a fall in cardiac output and HQR, (ii) isotonic saline did not fully normalize MAP, and (iii) hypertonic saline produced dramatic initial responses, and promoted normalization of MAP probably by restoring blood volume and cardiac output through sequestration of fluid from intracellular compartments.
PURPOSE: The objectives of this study were (i) to characterize the hemodynamic responses caused by controlled hemorrhage (HEM) in pentobarbital-anesthetized rats, and (ii) to determine the responses elicited by systemic bolus injections of isotonic saline (0.15M) or hypertonicsaline (3M) given 5min after completion of HEM. RESULTS: Controlled HEM (4.3±0.2ml/rat at 1.5ml/min) resulted in a pronounced and sustained fall in mean arterial blood pressure (MAP) to about 40mmHg. The fall in MAP was associated with a reduction in hindquarter vascular resistance (HQR) but no changes in renal (RR) or mesenteric (MR) vascular resistances. Systemic injections of isotonic saline (96-212μmol/kg i.v., in 250-550μl) did not produce immediate responses but promoted the recovery of MAP to levels below pre-HEM values. Systemic injections of hypertonicsaline (750-3000μmol/kg, i.v., in 250-550μl) produced immediate and pronounced falls in MAP, RR, MR and especially HQR of 30-120s in duration. However, hypertonicsaline prompted a full recovery of MAP, HQR and RR to pre-HEM levels and an increase in MR to levels above pre-HEM values. CONCLUSIONS: This study demonstrates that (i) HEM induced a pronounced fall in MAP which likely involved a fall in cardiac output and HQR, (ii) isotonic saline did not fully normalize MAP, and (iii) hypertonicsaline produced dramatic initial responses, and promoted normalization of MAP probably by restoring blood volume and cardiac output through sequestration of fluid from intracellular compartments.
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