The American journal of physiology
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Studies were conducted in the African lungfish (Protopterus annectens) to investigate the role of lung inflation on control of the duration of the lung breath. The studies were done in decerebrate spinalectomized animals. Two types of tests were performed: 1) a no-inflation test (airway occluded) in which the lungs were not inflated during an air breath, and 2) an inflation test in which the lungs were inflated at the onset of the lung breath to different levels of intrapulmonary pressure (2.5, 5.0, 7.5, and 10.0 cmH2O). ⋯ Vagotomy, however, largely abolished the effect of lung inflation on breath duration. Because there is such similarity between these results and effect of lung inflation on control of inspiratory time in mammals, it is postulated that neural circuits for control of respiratory timing were already developed and similar in the lungfish. Because the muscles used in the lungfish to ventilate the lung are totally different (buccal force pump) from those in mammals, the neural circuits for timing control and those for shaping the pattern of motor output appear to be separate.(ABSTRACT TRUNCATED AT 250 WORDS)
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Previous studies in our laboratory have demonstrated that burn injury (45% total body surface area, 3rd-degree scald burn) diminishes contractile and relaxation function in the isolated perfused guinea pig heart. The mechanisms responsible for the burn-mediated dysfunction are not well understood. Therefore the purpose of this study was to examine the inotropic response to isoproterenol, a beta-adrenergic agonist, and burn-induced alterations in beta-adrenergic receptors (beta-AR) in adult guinea pig hearts. ⋯ Agonist competition curves were performed in the presence or absence of 0.1 mM 5'-guanylyl imidodiphosphate. There was no difference in Bmax in membranes from sham-burned and burned hearts; however, the affinity of beta-AR was significantly decreased after burn injury compared with sham burn [dissociation constant = 32.5 +/- 1.9 (mean +/- SE), n = 10, vs. 26.7 +/- 1.7 pM, n = 10, P = 0.039]. Furthermore, the fraction of receptors in a high-affinity state (those functionally coupled to Gs protein) was significantly decreased after burn injury compared with sham burn (41.2 +/- 4.7%, n = 9, vs. 54 +/- 2%, n = 9, P = 0.023).(ABSTRACT TRUNCATED AT 250 WORDS)
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Although calcium antagonists produce salutary effects after shock and ischemia, it is unknown whether such agents restore the depressed cardiac output (CO) and renal function in a nonheparinized model of trauma-hemorrhage and resuscitation. To study this, rats underwent a midline laparotomy (i.e., trauma induced) and were bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of the maximum bleedout was returned in the form of Ringer lactate (RL). They were then resuscitated with four times the volume of shed blood with RL over 60 min. ⋯ Although GFR decreased in both groups, the values in diltiazem-treated animals were significantly higher than those in the sham-operated animals. Furthermore, diltiazem markedly decreased tissue water content. Thus diltiazem appears to be a promising adjunct in the treatment of hemorrhagic shock even in the absence of blood resuscitation.
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To assess the contributions of arginine vasopressin (AVP) V1- and V2-receptors to the ovine fetal responses to AVP, we studied V2-receptor stimulation in the presence of V1-receptor blockade, and selective V2-receptor stimulation in chronically catheterized fetal lambs. AVP administration (20 ng/kg) to the saline infused fetuses (n = 8; 132 +/- 2 days) significantly increased mean arterial pressure (MAP; 45 +/- 2 to 53 +/- 4 mmHg) and urine osmolality (Uosm; 134 +/- 13 to 379 +/- 42 mosmol/kgH2O) and decreased heart rate (HR; 168 +/- 3 to 147 +/- 5 beats/min) and urine flow (V; 0.48 +/- 0.10 to 0.19 +/- 0.03 ml/min). V1-receptor antagonist infusion, [d(CH2)5,Tyr(Me)]AVP (n = 7; 134 +/- 1 days) had no effect on fetal MAP, Uosm, HR, or V. ⋯ In a second series of animals (n = 6; 131 +/- 1 days), selective V2-receptor agonist infusion [desmopressin (DDAVP)] had no effect on fetal MAP or HR while initial changes in V and Uosm were identical to the effects of AVP alone. Our results demonstrate clear discrimination of V1- and V2-receptor-mediated events in the fetal MAP and renal responses to AVP. Moreover, the HR response to AVP is not mediated by the population of V1-receptors blocked by [d(CH2)5,Tyr(Me)]AVP or V2-receptors stimulated by DDAVP, suggesting the presence of additional AVP receptor subclass(es) during fetal life.
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To clarify the effect of intermittent positive-pressure ventilation (IPPV) on systemic circulation, mean systemic filling pressure (Psf) and circulating blood volume were measured together with other hemodynamic parameters of capacitance vessel. Change in circulating blood volume was determined by dilution with 51Cr-labeled erythrocytes. Vascular compliance (Cvas) was measured from the change in Psf caused by a bolus injection of blood. ⋯ The resistance to venous return did not change significantly, but there was a significant increase in total peripheral resistance. Neither Cvas nor circulating blood volume was changed significantly by IPPV. These results indicate that during IPPV the increased Pcv attenuates the pressure gradient for venous return and decreases CO and that the compensatory increase in Psf is caused by a blood shift from unstressed to stressed blood volume.