Esterase and lipase activities released into the blood by intravenous injection of heparin.
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Female broilers were evaluated at 4, 5, and 6 wk of age (1.2, 1.8, and 2.3 kg BW, respectively) to assess changes in cardiac output and related hemodynamics associated with BW gain, and to evaluate cardiopulmonary hemodynamic adjustments occurring secondary to i.v. injections of epinephrine (0.1 mg/ kg BW). Cardiac output increased with BW (253, 348, and 434 mL/min at 4, 5, and 6 wk, respectively) due to increases in stroke volume (0.70, 1.03, and 1.33 mL/beat) that more than compensated for reductions in heart rate (362, 337, and 328 bpm). Normalization for BW eliminated the differences in cardiac output and stroke volume. Increases in cardiac output were not associated with age- or BW-related increases in mean systemic arterial pressure (101.5, 108.6, and 108.0 mm Hg) due to corresponding reductions in total peripheral resistance (0.41, 0.32, and 0.26 relative resistance units). Epinephrine initially triggered immediate (within 90 s) threefold increases in total peripheral resistance and pulmonary vascular resistance, which, in turn, increased the systemic arterial pressure and pulmonary arterial pressure in spite of concurrent reductions in cardiac output that were associated with diminished venous return and dependent reductions in stroke volume and heart rate. Within 150 s after epinephrine injection, the systemic and pulmonary vascular resistances returned to preinjection control levels. By 300 s postinjection, stroke volume and heart rate increased, causing cardiac output to rise above preinjection control levels, which, in turn, elicited variable pulmonary arterial pressure responses apparently reflecting individual variability in the capacity for flow-dependent pulmonary vasodilation. These studies demonstrate that chronic (age- and BW-related) and acute (epinephrine-induced) changes in cardiac output in broilers reflect complex interactions among hemodynamic variables that include stroke volume, heart rate, and systemic and pulmonary vascular resistances.
The ability of hCG and LH to induce testosterone (T) secretion by Leydig cells is well documented. However, the influence of the pulsatile nature of LH secretion, with varying frequency and amplitude, on T production in vivo is less clear. In our earlier studies on the relationship between pulsatile LH release and T secretion in adult male rats, no simple causality was observed. The recent availability of rat recombinant (rec) LH prompted us to study the effects of one and of three i.v. pulses of different doses of rat recLH on T secretion in adult male rats rendered hypogonadotropic by treatment with the GnRH antagonist cetrorelix. One or three supraphysiological pulses of 1.0 microg of rat recLH produced similar maximal T responses. In contrast, high physiological LH pulses (0.1 microg) produced discrete T-response peaks, whereas multiple low pulses of LH (0.03 microg) were needed before a T response was achieved. The T stimulation was greatly diminished after an LH pulse of 0.1 microg if rats had been treated on the previous day with pulses of 0.03 vs. 0.1 microg rat recLH, apparently because of prolonged LH deprivation and lack of Leydig cell priming due to the GnRH antagonist treatment. The novel preparation of rat recLH provides a physiologically relevant tool for studying the complex relationship between pulsatile LH release and T secretion in male rats.
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The purpose of this randomized, double-blind study was to determine if isoproterenol 5 micrograms iv produces a consistent, noticeable tachycardia in healthy, laboring women. Maternal heart rate, fetal heart rate, and uterine contractions were continuously recorded and maternal blood pressure was measured every minute for 10 min before and after each patient received either normal saline (NS group; n = 10) or isoproterenol 5 micrograms (ISO group; n = 10) iv. The data-collecting investigator and a nurse palpating the patient's radial artery determined which solution they thought had been administered. The authors analyzed the maternal heart rate tracings using baseline-to-peak (a greater than or equal to 25 beat/min maternal heart rate increase occurring within 120 s of drug injection and lasting greater than or equal to 15 s) and peak-to-peak (a greater than or equal to 10 beat/min increase in the maximum maternal heart rate during the 2-min postinjection over the maximum maternal heart rate during the 2 min preinjection) criteria for detection of an intravascular marker. Mean maternal heart rate in the ISO group was significantly higher than in the NS group 20, 30, 40, 50, and 60 s following the injection (P less than 0.01). The peak-to-peak criterion and the data-collecting investigator correctly classified all patients. Five ISO group patients were not identified by the baseline-to-peak criterion. The nurse palpating the mother's radial artery misidentified two patients. Systolic blood pressure was significantly higher in ISO group than in NS group patients 1 min (P less than 0.05) and 2 min (P less than 0.01) following drug injection. Diastolic and mean blood pressures did not change. No fetal distress occurred. Isoproterenol 5 micrograms is an effective marker of intravascular injection in laboring women; however, the safety and efficacy of epidural isoproterenol must be demonstrated in animals before isoproterenol can be incorporated in an epidural anesthesia test dose.
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In this study, we investigated different functional characteristics of the rat liver macrophage population after a single i.v. injection of liposome-encapsulated muramyl dipeptide (MDP) or its lipophilic derivative muramyl tripeptide-phosphatidylethanolamine (MTP-PE). The in situ induced tumoricidal activity of the liver macrophage population was determined in vitro against C26 colon adenocarcinoma cells. For investigating which cells are responsible for the observed cytotoxic effects, subfractions of the liver macrophage population, differing in cell size, were isolated at different intervals after injection of the liposomal muramyl peptides. From these subfractions, the number of cells, degree of cytotoxicity, and the response to an additional activation with free MDP in vitro were determined. Maximal induction of tumoricidal activity of the liver macrophage population was reached between 12 and 24 hours after injection of liposomal MDP, while no significant differences between the subfractions were observed. Heterogeneity of tumor cytolytic capacity was observed in subfractions of macrophages isolated at 2 and 48 hours after injection. At these time points, highest cytolytic activity was observed for the small to intermediate-size macrophages. No significant cytotoxicity was detectable in any subfraction 72 hours after injection of liposomal MDP. An identical pattern of macrophage tumoricidal activity was observed after injection of liposomal MTP-PE, although slightly lower cytotoxicity levels were found. When isolated during the first 12 hours after injection of liposomal MDP, the macrophage population was unable to respond to a subsequent in vitro exposure to MDP, with respect to tumor cytotoxicity. Twenty-four and 48 hours after injection, the smallest cells could be slightly reactivated, whereas the larger cells still remained unresponsive.(ABSTRACT TRUNCATED AT 250 WORDS)
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