The American journal of physiology
-
Comparative Study
Fluid compartments in hemorrhaged rats after hyperosmotic crystalloid and hyperoncotic colloid resuscitation.
Postresuscitation organ failure may be associated with detrimental changes in body fluid compartments. We measured how shock and resuscitation acutely alters the interstitial, cellular, and plasma compartments in different organs. Nephrectomized, anesthetized rats were bled to 50 mmHg mean arterial pressure for 1 h, followed by 60 min of resuscitation to restore blood pressure using 0.9% normal saline (NS,n = 10), 7.5% hypertonic saline (HS,n = 8), 10% hyperoncotic albumin (HA, n = 8), or 7.5% hypertonic saline and 10% hyperoncotic albumin (HSA, n = 7). ⋯ ISFV was significantly reduced by HA groups in the skin. In all tissues, mean cell water in groups receiving HS was smaller; this was significant for heart, lung, muscle, and skin. In conclusion, 1) HS solutions mobilize fluid from cells while expanding both PV and ISFV, and 2) TW and cellular water increase with both isotonic crystalloids and hyperoncotic colloids in many tissues.
-
The influence of gravity, if any, on pharyngeal bolus transport is unknown. The aim of the present study was to evaluate the effect of gravity and body position on the radiological and manometric events during the normal oropharyngeal swallow. In eight healthy male volunteers, we performed simultaneous videoradiography and manometry, using a manometry catheter incorporating a perfused sleeve measuring upper esophageal sphincter pressure and three solid-state transducers recording pharyngeal pressures. ⋯ Total swallowing duration, oral and pharyngeal transit time, pharyngeal peristaltic amplitude and duration, the length of the bolus in the pharynx, and excursions of the hyoid and larynx were unaffected by body position. We conclude that intrabolus pressure is an important determinant of upper esophageal sphincter opening in the healthy oropharynx and that gravity does not influence pharyngeal bolus transport. The healthy upper esophageal sphincter has residual opening capacity that can be demonstrated by altering body posture.
-
The purpose of this study was to acquire a new correction factor for use in tracer estimations of plasma fatty acid oxidation that would fully account for label fixation during the infusion of fatty acid tracers. Thus volunteers were infused with 13C-labeled fatty acids and [1-14C]acetate in the basal state, during hyperinsulinemia-hyperglycemia (clamp), and during 1 h of cycling exercise. ⋯ Isotopically determined plasma fatty acid oxidation rates (mumol.kg-1.min-1) were 1.7 +/- 0.2, 0.8 +/- 0.2, and 6.4 +/- 0.5 (no correction); 2.1 +/- 0.2, 1.0 +/- 0.2, and 6.7 +/- 0.5 (bicarbonate correction); and 3.1 +/- 0.2, 1.5 +/- 0.2, and 8.2 +/- 0.4 (acetate correction). We conclude that use of the acetate correction factor in place of the bicarbonate correction factor should improve the accuracy of isotopic measurements of plasma fatty acid oxidation, because it accounts for label fixation that might occur at any step between the entrance of labeled acetyl-CoA into the tricarboxylic acid cycle until the recovery of label in breath CO2.
-
In this study, we first tested the hypothesis that the previously demonstrated circulatory failure and thrombocytopenia induced by intracaval administration of thromboxane A2 (TxA2) analogues in nonpregnant (NP) rabbits [G. Losonczy, I. Mucha, J. ⋯ Similar results were obtained with the second TxA2 analogue I-BOP. Pregnancy-induced enhancement of blood pressure elevation may be the consequence of peripheral vasoconstriction, which was not seen in NP rabbits. Thus the actions of TxA2 analogues U-46619 and I-BOP are markedly influenced by the route of administration.(ABSTRACT TRUNCATED AT 250 WORDS)
-
Aquaporin-2 (AQP2) is the predominant vasopressin-regulated water channel of the renal collecting duct. We tested whether vasopressin induces translocation of AQP2 from intracellular vesicles into the apical plasma membrane. AQP2 was quantitated in plasma membrane and intracellular vesicle fractions prepared from the inner medulla of one kidney from each rat before or 20 min after intravenous 1-desamino-8-D-arginine vasopressin (DDAVP) treatment, using immunoblotting and densitometry. ⋯ Immunofluorescence confirmed a marked DDAVP-induced redistribution of AQP2 from intracellular to plasma membrane domains. Furthermore, quantitative immunoelectron microscopy demonstrated a 3.4-fold increase in apical plasma membrane to intracellular vesicle labeling ratio. These results provide a direct in vivo demonstration of vasopressin-induced translocation of AQP2 into the apical plasma membrane.