A modified setup for cardiac output determination in case of an inaccessible pulmonary artery catheter.
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Biomedical subjects
Publications and source records attributed to D L Bourke.
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We reviewed anaesthetic records of 35 infants with a history of prematurity, who presented for elective herniorrhaphy. We applied a scoring system to help evaluate risk of postoperative complications. Six patients experienced postoperative complications. All six patients had a score of five or more and gave history of either apnoea or a history of moderate bronchopulmonary dysplasia. A preoperative history of apnoea and/or moderate bronchopulmonary dysplasia appear to be valuable markers for postoperative complications. A conceptual age of 40 weeks is an acceptable lower limit of age providing there is no history of apnoea or pulmonary disease.
Six healthy, consenting volunteer males received ketamine iv in five logarithmically scaled doses totaling 3 mg/kg on three occasions each. The sessions differed only in the initial injection of an unknown drug: placebo, morphine sulfate 0.2 mg/kg, or morphine sulfate 0.4 mg/kg. Initial and terminal steady-state ventilatory responses to CO2 (VERCO2) and isohypercapnic ventilation (end-tidal CO2 49.8 +/- 2.4 mmHg) during drug administration assessed CO2-mediated ventilatory drive. Oxygen concentration of 40% ablated hypoxic drive contribution. Morphine caused a decrease of isohypercapnic ventilation (VE) of 8.2 +/- 1.2 l/min after 0.2 mg/kg. Doubling the dose to 0.4 mg/kg gave a further depression of 6.6 +/- 1.8 l/min. No subject lost consciouness after morphine. Over a dose range of 0.39 to 3.0 mg/kg ketamine caused log-linear dose-related depression of 1.6 +/- 0.3 l/min for each doubling of dose, although the first significant depression of 4.9 +/- 1.1 l/min did not occur until the third dose (1.1 mg/kg) in the absence of morphine. All subjects were unconscious after 1.8 mg/kg ketamine. Slopes of the VERCO2 did not differ from control, regardless of the pretreatment, placebo, or morphine in the two doses. Ketamine alone, 3.0 mg/kg, caused a displacement of VERCO2 of +2.0 +/- 1.2 mmHg in CO2, while combination of ketamine and morphine in either dose caused a +10 mmHg displacement of VERCO2. Thus, ketamine appears qualitatively similar but less potent than premedicant doses of morphine in depressing respiration despite near equipotency in producing loss of consciousness.
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The extensor digitorum longus muscles of 4-6-week-old normal mice (129 ReJ) and dystrophic mice (129 ReJ dy/dy) were orthotopically transplanted. Grafted muscles were examined 1, 3, 7, 14, 20, 50, and 100 days post-transplantation. The myofibers of both types of grafts underwent a similar time course of necrosis and regeneration. Other than during the initial necrotic response, no evidence of necrotic myofibers was found in either type of grafted muscle. At 100 days post-transplantation, the grafted normal and dystrophic muscles were essentially similar, except that the dystrophic graft was of smaller size. Based on a comparison of the number of myofibers found at the 100-day grafts' widest girths [631 +/- 59 SEM, for normal grafts (Bourke and Ontell, 1984); 631 +/- 74 SEM, for dystrophic grafts], it is suggested that the regenerative capability of traumatized 4-6-week-old dystrophic muscle is similar to that of traumatized normal muscle. At 100 days post-transplantation, the grafted dystrophic muscle appeared "healthier" than untraumatized muscle from age-matched dystrophic mice, having less variation in myofiber diameter, better fascicular organization, and less connective tissue. The transplantation system demonstrates the possibility of modifying the expression of genetic programming of myopathic disorders using environmental manipulation.
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Succinylcholine was administered to 10 healthy unanesthetized volunteers to assess its effect on respiratory and nonrespiratory muscle strength and the ventilatory response to CO2. Iso hypercapnia with PETCO2 8-10 mmHg above control was maintained throughout the study, succinylcholine infusion rates were increased from 20 micrograms X kg-1 X min-1 until grip strength (GS) was 20% of control. CO2-stimulated ventilation was 16.1 +/- 1.8 l/min (mean +/- SD), approximately three times control, and remained at that level throughout the study because of nonsignificant decreases in tidal volume and increases in respiratory frequency. Respiratory strength, as measured by maximum inspiratory pressure (IP), maximum expiratory pressure (EP), and forced vital capacity (FVC), was spared relative to GS. When GS = 50% of control, IP = 86 +/- 8% of control, EP = 78 +/- 15%, and FVC = 86 +/- 9%. Wide variation occurred from subject to subject in the succinylcholine versus GS dose-response curve position. However, in all subjects the slope of the dose-response curve was very steep.
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Orthotopic transplants of whole extensor digitorum longus muscles were performed on six 4-6-week-old 129 ReJ mice. One hundred days posttransplantation, the animals were killed and the regenerated muscles were processed for electron microscopy. The grafts contained polygonal-shaped myofibers with persistent central nuclei, organized into discrete muscle fascicles. No central area of fatty infiltration or fibrosis was observed. The mean number of myofibers in a regenerating transplanted muscle, as determined from an ultrathin section taken from the graft's widest girth, was 631 (SEM = +/- 59), a reduction of approximately 32% from that found in age-matched control muscle (Ontell et al., 1983). By following the myofibers in spaced, serial ultrathin sections along their length, it was found that the branched, regenerating myofibers found in immature grafts of normal muscle (Ontell et al., 1982) persisted in stabilized, long-term transplanted muscle. The frequency of branching was determined by following each fiber found at the widest girths of four of the grafts in spaced, serial ultrathin sections (15-micron intervals) for approximately 2% of the total length of the grafts. Over this distance, 6.6% of the fibers were involved in the branching phenomenon. The persistence of branched fibers in long-term grafts and the frequency with which the branching phenomenon was found to occur may have physiological consequences and should be investigated.
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Each of six healthy volunteers was studied on three different occasions to determine the interactions of placebo-physostigmine, diazepam-physostigmine, and morphine-physostigmine with respect to respiration and psychomotor function. Respiratory measurements were made using the steady state and isohypercapnic techniques. Psychomotor function was assessed by the Trieger Dot Test (TDT) and compared with the Continuous Performance Test (CPT). Administration of physostigmine alone (3 mg, iv) did not affect ventilation. Diazepam (0.29 mg/kg, iv) did not cause a significant depression of ventilation in all subjects, although psychomotor function was impaired as measured by the CPT. The latter was unaffected by physostigmine. Administration of morphine (0.21 mg/kg, iv) caused a significant decrease in ventilation that was not antagonized by physostigmine. Morphine did not impair psychomotor function. The authors conclude that physostigmine is an ineffective antagonist of narcotic-induced respiratory depression and that the CPT correlates well with the TDT.