Effect of clonidine on gastrointestinal transit time.

BACKGROUND/AIMS: Orocecal time can be measured by lactulose H2 breath test. Duodenal entry time can be evaluated by measuring D-xylose; the duodeno-cecal time can be derived by subtracting duodenal entry time from orocecal time. In this study we established the normal value of these parameters for our laboratory in males and also evaluated the effect of clonidine on these parameters. METHODOLOGY: In 9 healthy male volunteers orocecal time was measured by the lactulose H2 breath test. Duodenal entry time was established by measuring blood D-xylose. Duodenocecal time was derived by subtracting duodenal entry time from orocecal time. RESULTS: The mean orocecal time was 54.44 + 3.77 minutes; the mean duodenal entry time was 17.22 + 3.15 minutes and the mean duodenocecal time was 37.22 + 3.16 minutes. CONCLUSIONS: Oral clonidine prolonged orocecal, duodenal entry and duodenocecal times in only 33% of the subjects.

Treatment of liver injuries at level I and level II centers in a multi-institutional metropolitan trauma system. The Midwest Trauma Society Liver Trauma Study Group.

OBJECTIVE: The development of trauma systems and trauma centers has had a major impact on the fate of the critically injured patient. However, some have suggested that care may be compromised if too many trauma centers are designated for a given area. As of 1987, the state of Missouri had designated six adult trauma centers, two Level I and four Level II, for the metropolitan Kansas City, Mo, area, serving a population of approximately 1 million people. To determine whether care was comparable between the Level I and II centers, we conducted a concurrent evaluation of the fate of patients with a sentinel injury, hepatic trauma, over a 6-year period (1987-1992) who were treated at these six trauma centers. METHODS: All patients during the 6-year study period who suffered liver trauma and who survived long enough to be evaluated by computerized tomography or celiotomy were entered into the study. Patients with central nervous system trauma were excluded from analysis. Information concerning mechanism of injury, RTS, Injury Severity Score (ISS), presence of shock, liver injury scoring, mode of treatment, mortality, and length of stay were recorded on abstract forms for analysis. Care was evaluated by mortality, time to the operating room (OR), and intensive care unit (ICU) and hospital length of stay. RESULTS: Over the 6-year period 300 patients with non-central nervous system liver trauma were seen. Level I centers cared for 195 patients and Level II centers cared for 105. There was no difference in mean ISS or ISS > 25 between Level I and II centers. Fifty-five (28%) patients arrived in shock at Level I centers and 24 (23%) at Level II centers. Forty-eight patients (16%) died. Thirty-two (16%) died at Level I centers, and 16 (15%) died at Level II centers. Twenty of 55 patients (36%) in shock died at Level I centers, and 11 of 24 (46%) died at Level II centers (p = 0.428). Forty-three patients (22%) had liver scaling scores of IV-VI at Level I centers, and 10 (10%) had similar scores at Level II centers (p < 0.01). With liver scores IV-VI, 22 of 43 (51%) died at Level I centers and 10 of 14 (71%) died at Level II centers (p = 0.184). There was no difference in mean time or in delays beyond 1 hour to the OR for those patients in shock between Level I and II centers. There was a longer ICU stay at Level II centers (5.0 +/- 8.3 vs. 2.8 +/- 8.4 days, p = 0.04). This difference was confined to penetrating injuries. There was no difference in hospital length of stay. CONCLUSIONS: In a metropolitan trauma system, when Level I and II centers were compared for their ability to care for victims of hepatic trauma, there was no discernible difference in care rendered with respect to severity of injury, mortality, delays to the OR, or hospital length of stay. It was observed that more severe liver injuries were seen at Level I centers, but this did not seem to significantly affect care at Level II centers. There was a longer ICU stay observed at Level II centers owing to penetrating injuries, possibly because there were fewer penetrating injuries treated at these facilities. Although the bulk of patients were seen at Level I centers, care throughout the system was equivalent.

Ethylene is not involved in the blue light-induced growth inhibition of red light-grown peas.

Although the growth of intact plants is inhibited by irradiation with blue light, the growth rate of isolated stem segments is largely unaffected by blue light. We hypothesized that this loss of responsiveness was a result of ethylene production as part of the wounding response. However, we found no interaction between ethylene- and blue light-induced growth inhibition in dark- or red light-grown seedlings of pea (Pisum sativum L.). Inhibition of growth begins in dark-grown seedlings exposed to blue light within 3 min of the onset of blue light, as was known for red light-grown seedlings. By contrast, ethylene-induced inhibition of growth occurs only after a lag of 20 to 30 min or more (dark-grown seedlings) or 60 min (red light-grown seedlings). Also, the inhibition response of red light-grown seedlings is the same whether ethylene is present from the onset of continuous blue-light treatment or not. Finally the spatial distribution of inhibition following blue light was different from that following ethylene treatment.

Adaptation to dim-red light leads to a nongradient pattern of stem elongation in cucumis seedlings.

Relative growth rate determinations on 5-millimeter regions of cucumber (Cucumis sativus L.) hypocotyls show that dim-red light-grown seedlings have an even distribution of growth along the stem axis. This contrasts with the apical to basal graded decline in growth rate seen in dark-grown seedlings, including dark-grown cucumber seedlings used as controls in this study. Dark-grown seedlings convert to the nongradient pattern when transferred to dim-red light. The small amount of light required suggests that the change in developmental pattern may happen in the natural light environment.

Cell Wall Free Space of Cucumis Hypocotyls Contains NAD and a Blue Light-Regulated Peroxidase Activity.

Solutions were obtained from the cell wall free space of red light-grown cucumber (Cucumis sativus L.) hypocotyl sections by a low-speed centrifugation technique. The centrifugate contained NAD and peroxidase but no detectable cytoplasmic contamination, as indicated by the absence of the activity of glucose-6-phosphate dehydrogenase from the cell wall solution. Peroxidase activity centrifuged from the cell wall of red light-grown cucumber hypocotyl section could be resolved into at least three cathodic isoforms and two anodic isoforms by isoelectric focusing. Treatment of red light-grown cucumber seedlings with a 10-minute pulse of high-intensity blue light increased the level of cell wall peroxidase by about 60% and caused a qualitative change in the anodic isoforms of this enzyme. The increase in peroxidase activity was detectable within 25 minutes after the start of the blue light pulse, was maximal at 35 minutes, and declined to control levels by 45 minutes of irradiation. The inhibitory effect of blue light on hypocotyl elongation was more rapid than the effect of blue light on total wall peroxidase activity, leading to the conclusion that growth and peroxidase activity are not causally related.

Phytochrome induces changes in the immunodetectable level of a wall peroxidase that precede growth changes in maize seedlings.

The regulatory pigment phytochrome induces rapid and opposite growth changes in different regions of etiolated maize seedlings: it stimulates the elongation rate of coleoptiles and inhibits that of mesocotyls. As measured by a quantitative immunoassay, phytochrome also promotes rapid and opposite changes in the extractable content of a Mr 98,000 anionic isoperoxidase in the cell walls of these same organs: it induces a decrease of this peroxidase in coleoptiles and an increase in mesocotyls. The peroxidase changes precede the growth changes. As measured by video stereomicroscopy or a position transducer, red light (R), which photoactivates phytochrome, stimulates coleoptile elongation with a lag of about 15-20 min and suppresses mesocotyl growth with a lag of 45-50 min. R also induces a 50% reduction in the extractable level of the anionic peroxidase in coleoptile walls in less than 10 min and a 40% increase in the level of this peroxidase in mesocotyl walls within 30 min. Ascorbic acid, an inhibitor of peroxidase activity, blocks the effects of R on mesocotyl section growth. These results are relevant to hypotheses that postulate that certain wall peroxidases can participate in light-induced changes in growth rate by their effects on wall extensibility.

Inhibition of stem elongation in cucumis seedlings by blue light requires calcium.

The effects of blue light and calcium on elongation of hypocotyl segments of Cucumber (Cucumis sativa L. cv Burpee's Pickler) were studied. Cucumber seedlings grown in dim red light showed a rapid decline in the rate of hypocotyl elongation when irradiated with high intensity (100 micromoles per square meter per second) blue light. In intact, 4-day-old seedlings the inhibition began within 2 minutes after the onset of blue-light irradiation and reached a maximum of approximately 55% within 4 minutes. Hypocotyl segments cut from 4-day-old seedlings also showed an inhibition of elongation in response to blue light when segments were floated on aqueous buffer and exposed to blue light for 3 hours. In the presence of 2 micromolar indole-3-acetic acid, blue light caused a 50% inhibition of elongation. Buffering free calcium in the incubation medium with 0.1 millimolar ethylene glycol bis(-aminoethyl ether)- N,N,N',N'-tetraacetic acid eliminated the blue-light inhibition of segment elongation. Several experiments confirmed a specific requirement for calcium for the blue-light-induced inhibition of segment elongation. Treating segments with 0.2 micromolar fusicoccin abolished the inhibition of elongation by blue light as did buffering the medium at pH 4. Adding 1 millimolar ascorbate to incubation medium also eliminated the inhibition of segment elongation caused by blue light. Several compounds implicated in cell-wall redox reactions alter the magnitude of the blue-light-induced inhibition. The activity of peroxidase isolated from the cell-wall free space of cucumber hypocotyls was inhibited by ascorbate and low pH. The results are consistent with the hypothesis that blue light inhibits elongation by inducing an increase in cell-wall peroxidase activity and implicate calcium ions in the response to blue light.

Photobiology of phytochrome-mediated growth responses in sections of stem tissue from etiolated oats and corn.

The far-red reversibility of the phytochrome-controlled stimulation of elongation of coleoptile sections by low fluence red light has been characterized in subapical coleoptile sections from dark-grown Avena sativa L., cv Lodi seedlings. The fluence dependence of the far-red reversal was the same whether or not the very low fluence response is also expressed. The capacity of far-red light to reverse the red light-induced response began to decline if the far-red light was given more than 90 minutes after the red irradiation. Escape was complete if the far red irradiation was given more than 240 minutes after the red irradiation. Sections consisting of both mesocotyl and coleoptile tissue from dark-grown Avena seedlings were found to have physiological regulation of the very low fluence response by indole 3-acetic acid and low external pH similar to that seen for sections consisting entirely of coleoptile tissue. The fluence-dependence of the red light-induced inhibition of mesocotyl elongation was studied in mesocotyl sections from dark grown Zea mays L. hybrid T-929 seedlings. Ten micromolar indole 3-acetic acid stimulates the control elongation of the sections, while at the same time increasing the sensitivity of the tissue for the light-induced inhibition of growth by a factor of 100.

Physiological mechanism of the auxin-induced increase in light sensitivity of phytochrome-mediated growth responses in Avena coleoptile sections.

The physiology of the auxin-induced 10,000-fold increase in light sensitivity of a phytochrome-mediated growth response (Shinkle and Briggs, 1984 Proc Natl Acad Sci USA 81: 3742-3746) has been characterized in subapical coleoptile sections from dark-grown oat (Avena sativa L. cv Lodi) seedlings. Six micromolar indole-3-acetic acid (IAA) must be present for 1 hour before to 2 hour after irradiation in order to confer maximal sensitivity to light. The direct effect of IAA on growth can be separated from its effect on light sensitivity. Several classes of synthetic auxins will substitute for IAA in inducing an increase in sensitivity to light, as will both the phytotoxin fusicoccin and treatment of sections with pH 4.5 buffer. The increase in sensitivity to light induced by 6 micromolar IAA is completely inhibited by buffering the sections at pH 5.9 with 30 millimolar 2-(N-morpholino)ethanesulfonic acid. These findings suggest that the capacity to respond to very low fluences of light is regulated by extracellular pH.Between 10 and 15 millimolar K(+) will inhibit the induction of the increased sensitivity to light, independent of the mechanism of induction. The effect of K(+) appears to be specific to the process by which the sections respond to very low levels of light.

Indole-3-acetic acid sensitization of phytochrome-controlled growth of coleoptile sections.

Addition of 6 muM indole-3-acetic acid (IAA) to incubation buffer increases the sensitivity of coleoptile sections cut from dark-grown Avena sativa L. cv. Lodi to red light by a factor of 10,000, relative to the response in the absence of added IAA, without changing the maximum amount of light-induced growth. From 0.03 to 4 muM IAA sections show at least a 100-fold increase in sensitivity to red light relative to the response in the absence of added IAA. In this IAA concentration range, the light-induced increase in elongation shows two phases of response to red-light fluence, which are separated by a plateau. The biphasic fluence-response curve is also characteristic of the red-light-induced stimulation of coleoptile growth in intact dark-grown seedlings. The effect of IAA on the sensitivity of the phytochrome-mediated growth response appears to be on some step in the transduction of the phytochrome signal, rather than on the growth response itself.

Auxin concentration/growth relationship for Avena coleoptile sections from seedlings grown in complete darkness.

A biphasic auxin dose-response curve has been obtained for indole-acetic acid (IAA)-stimulated growth of subapical sections of coleoptiles from totally dark-grown oats (Avena sativa L. cv Lodi). The curve for growth at 6 h is composed of a log-linear phase and a modified bell-shaped phase separated by a plateau. The curve is log-linear from 0.003 to 0.4 micromolar IAA when sections are incubated in pH 5.9 buffer. The plateau of IAA concentration-neutral growth is seen from 0.4 to 4.0 micromolar IAA. Further increase in growth occurs from 4.0 to 10 micromolar IAA. Changing the pH of the buffer from 5.9 to 5.5 or 6.2 changes the shape of the curve, shifting the plateau to lower IAA concentration, or abolishing it, respectively. The synthetic auxin 2,4-dichlorophenoxyacetic acid also shows a biphasic dose-response curve, but the synthetic auxin 1-naphthalene acetic acid does not. The plateau is not affected by the auxin-transport inhibitor 2,3,5-triiodobenzoic acid. The plateau is eliminated by taking sections from coleoptiles grown under continuous dim red light. We advance a model to account for these results based on two modes of auxin uptake into the cell: carrier-mediated uptake and uptake via chemiosmotic diffusion.