The effect of asphyxia on the plasma glucose-concentration in new-born calves.
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Biomedical subjects
Publications and source records attributed to M Silver.
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1. The response of the adrenal medulla to the intra-arterial injection of angiotensin, bradykinin and acetylcholine and to splanchnic nerve stimulation has been investigated in day-old and 3- to 18-month-old calves and in adult cats.2. Bradykinin and angiotensin had no appreciable effect on catecholamine release in the day-old calf nor did these peptides potentiate the response of the gland to acetylcholine.3. In older calves the response of the gland to bradykinin and angiotensin was marginally above the control output, whereas acetylcholine and splanchnic nerve stimulation caused a 10-100 fold increase in the rate of secretion. The response to acetylcholine but not to the peptides was related to the dose administered.4. The adrenal medulla of the cat was stimulated by angiotensin and bradykinin but the maximum amounts released by the peptides were much smaller than the discharge elicited either by splanchnic nerve stimulation or by acetylcholine. No dose-response relationship could be found for either adrenaline or noradrenaline released by angiotensin, or for noradrenaline released by bradykinin. The slight increase in adrenaline output which followed the injection of bradykinin was dependent on the dose but the slope of the curve (b = 0.161) was much less than that for acetylcholine (b = 0.636).
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Ferrobacillus ferrooxidans, grown on either elemental sulfur or ferrous sulfate, was able to use either substrate as an energy source for the assimilation of CO(2). In both cases, 0.01 mumole of carbon was incorporated per mumole of oxygen utilized. Glucose inhibited substrate oxidation and CO(2) fixation. Sulfur and iron oxidation were inhibited 5 to 15% and 40 to 50%, respectively, in the presence of 10% glucose. Under the same conditions, CO(2) assimilation was inhibited 50% with elemental sulfur as the energy source, and was almost totally inhibited when ferrous iron was used.
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1. The output of adrenaline and noradrenaline from the adrenal medulla during asphyxia, stimulation of the splanchnic nerves or the intra-arterial injection of acetylcholine, has been investigated in foetal and new-born calves up to 3 weeks of age.2. Between 180 days' gestation and term ( approximately 281 days) the response of the foetal adrenal gland of the calf to asphyxia appeared to be independent of its nerve supply and the discharge consisted largely of noradrenaline. A similar type of discharge was obtained after the intra-arterial injection of acetylcholine, but stimulation of the splanchnic nerves resulted in only a small discharge of both adrenaline and noradrenaline.3. Rapid changes occurred in the response of the adrenal medulla to all forms of stimulation during the first 24 hr after birth. For the first 4-6 hr the adrenal medulla was hypersensitive; thereafter the response rapidly declined and a variable period of depressed excitability followed. The changes affected the output of noradrenaline rather than that of adrenaline and were more pronounced during asphyxia or after the intraarterial injection of acetylcholine. Within 24 hr of birth the amount of noradrenaline released in response to either form of stimulation was less than 25% of that found immediately after birth.4. During the hypersensitive phase immediately after birth splanchnic nerve activity appeared to potentiate the direct effect of asphyxia on the noradrenaline cells since the maximum output of noradrenaline was attained more rapidly and at a higher P(O2) if the splanchnic nerves were intact.5. The non-nervous direct response of the adrenal medulla to asphyxia decreased rapidly after birth and disappeared within 24 hr. It did not reappear at any age and was a feature of foetal life.6. The recovery of the response to acetylcholine occurred between 3 and 8 days after birth with a return of the high level of noradrenaline secretion; no similar increase in the output of adrenaline occurred at this stage.7. The response to asphyxia was not restored to the level found in the new-born calf until 2-3 weeks after birth. At this time the effect on the adrenal medulla appeared to be mediated almost entirely by the splanchnic nerves.8. The effects of chloralose and pentobarbitone anaesthesia on the changes in the nervous response to asphyxia after birth were compared. Essentially the same pattern of changes was found with both anaesthetics although the absolute level of discharge under chloralose was greater and a considerably larger amount of adrenaline was secreted at 3 weeks of age.9. At certain ages stimulation of the splanchnic nerves enhanced the response of the adrenal medulla to subsequent injections of acetylcholine. The noradrenaline output was only significantly increased by this procedure during the period of depressed excitability whereas the adrenaline discharge was always increased throughout the first 3 weeks of life.10. The changes in adrenaline and noradrenaline content of the adrenal glands during the 3-week period after birth were investigated. The noradrenaline concentration was low immediately after birth during the hypersensitive phase and increased during the period of reduced sensitivity. The output of this amine was thus inversely related to its content in the adrenal gland. A similar relation did not occur with adrenaline, the concentration of which remained relatively constant during the first 3 weeks of life.
Margalith, P. (Syracuse University, Syracuse, N.Y.), Marvin Silver, and D. G. Lundgren. Sulfur oxidation by the iron bacterium Ferrobacillus ferrooxidans. J. Bacteriol. 92:1706-1709. 1966.-Sulfur and iron oxidation has been studied manometrically by use of Ferrobacillus ferrooxidans grown on either elemental sulfur or ferrous iron as the primary energy source. The iron-oxidizing enzyme was shown to be constitutive, since iron was oxidized as rapidly by sulfur-grown cells as by iron-grown cells. Sulfur-grown cells had a better capacity for oxidizing sulfur than did iron-grown cells; however, no lag in oxidation was seen in either case. The sulfur-oxidizing system was not inducible, and it is suggested that the different oxidative capacities are due to the heterogeneous mixture of cell types in the culture population.
Chest injuries are the cause of death in 25% of trauma fatalities, and a major contributing factor in an additional 50%. Pneumothorax, the second most common chest injury, may often be initially overlooked. Administration of anesthesia and mechanical ventilation may produce enlargement of a pneumothorax and clinical deterioration. We reviewed 90 trauma patients who had been admitted with a diagnosis of pneumothorax or who had developed pneumothoraces after hospital admission. In 35 cases (38.8%), initial supine chest x-ray study failed to detect a pneumothorax, and the diagnosis was made on CT scan of the chest or abdomen performed within 2 hours of admission. In 15 of these cases (42.8%), identification of the pneumothorax on CT scan resulted in alterations in management, including chest tube placement in 10 patients and intensified monitoring in 5 patients. Failure to identify pneumothoraces in trauma patients may lead to deterioration and significant complications in patients requiring anesthesia or mechanical ventilation. CT scan may facilitate identification in these cases.
New containers allow storage of platelet concentrates (PC) at 22 degrees C for up to 7 days, during which glycolytic and oxidative metabolism is vigorous. Recent evidence suggests that 85 percent of adenosine triphosphate regeneration is based on oxidative metabolism and that substrates other than glucose may be used. Because platelets can oxidize free fatty acids (FFA) as a possible source of energy during storage, the authors studied their availability, distribution, and turnover. Plasma FFA concentration was unchanged after 1 day of PC storage but significantly increased on Days 3, 5, and 7. Platelet-free plasma (PFP) stored under the same conditions as PC demonstrated a progressive increase in FFA, suggesting that some of the FFA accumulating in PC were derived from plasma rather than platelets. Indeed, during PC storage, plasma triglycerides decreased significantly, suggesting that they are a possible source of the increased levels of FFA found on Day 3 and thereafter. Thus, PC have a plasma FFA pool available continuously for oxidation during storage. Studies with radiolabeled palmitate suggested that FFA oxidation by platelets occurs during storage. The current findings show that plasma FFA could be a significant substrate for oxidative metabolism during storage of PC and that the oxidized FFA are replenished at least in part from plasma. These results may allow platelet storage to be improved, particularly in synthetic media.
Aspects of the cell kinetics of the developing intestinal epithelium of fetal sheep were investigated by autoradiography. The sites of (3H)-thymidine uptake were localized in the small intestinal epithelium of fetal sheep from 60 to 145 days' gestation. Labeled cells were always confined to the intervillus progenitive zone, either between the bases of adjacent villi in the younger fetuses or in crypts. There were no labeled cells within the villus epithelium. Labeled and unlabeled cells within the progenitive zones were counted in proximal and distal regions of the small intestine. The proportion of cells labeled (PCL) was unaffected by the route of administration of (3H)-thymidine into the fetus. There was no clear age-related trend in PCL of the distal region (mean distal PCL, 0.23 +/- 0.03). On the other hand, in proximal regions, PCL was at its highest value at 60 days (0.33), falling to a minimum of 0.14 at 130 days, before rising to 0.25 (+/- 0.04) at 136 days. These results demonstrate that the proliferation of enterocytes in utero is qualitatively similar to that in the adult, being confined to a distinct progenitive zone. Such a finding is an important first step in understanding changes in enterocyte structure and function, since this may, as seen in the adult, be largely determined by the rates of division and renewal.
BACKGROUND: Vascular endothelial growth factor (VEGF), an endothelial cell mitogen that promotes angiogenesis, was initially identified as a vascular permeability factor (VPF). Abundant evidence suggests that angiogenesis is preceded and/or accompanied by enhanced microvascular permeability. The mechanism by which VEGF/VPF increases vascular permeability (VP), however, has remained enigmatic. Accordingly, we used an in vivo assay of VP (Miles assay) to study the putative mediators of VEGF/VPF-induced permeability. METHODS AND RESULTS: VEGF/VPF and positive controls (platelet-activating factor [PAF], histamine, and bradykinin) all increased vascular permeability. Prior administration of the tyrosine kinase inhibitors genistein or herbimycin A prevented VEGF/VPF-induced permeability. Placenta growth factor, which binds to Flt-1/VEGF-R1 but not Flk-1/KDR/VEGF-R2 receptor tyrosine kinase, failed to increase permeability. Other growth factors such as basic fibroblast growth factor (FGF), acidic FGF, platelet-derived growth factor-BB, transforming growth factor-beta, scatter factor, and granulocyte macrophage-colony stimulating factor (8 to 128 ng) failed to increase permeability. VEGF/VPF-induced permeability was significantly attenuated by the nitric oxide (NO) synthase inhibitors N(omega)-nitro-L-arginine (10 mg/kg) or N(omega)-nitro-L-arginine methyl ester (20 mg/kg) and the cyclooxygenase inhibitor indomethacin (5 mg/kg). The inactive enantiomer N(omega)-nitro-D-arginine methyl ester (20 mg/kg) did not inhibit VEGF/VPF-induced permeability. In vitro studies confirmed that VEGF/VPF stimulates synthesis of NO and prostaglandin metabolites in microvascular endothelial cells. Finally, NO donors and the prostacyclin analogue taprostene administered together but not alone reproduced the increase in permeability observed with VEGF/VPF. CONCLUSIONS: These results implicate NO and prostacyclin produced by the interaction of VEGF/VPF with its Flk-1/KDR/VEGF-R2 receptor as mediators of VEGF/VPF-induced vascular permeability. Moreover, this property appears unique to VEGF/VPF among angiogenic cytokines.
BACKGROUND: The effect of aging on angiogenesis in ischemic vascular disease has not been studied. Accordingly, we investigated the hypothesis that angiogenesis is impaired as a function of age. METHODS AND RESULTS: Forty days after the resection of 1 femoral artery, collateral vessel development was significantly impaired in old (aged 4 to 5 years; n=7) versus young (aged 6 to 8 months; n=6) New Zealand White (NZW) rabbits on the basis of reduced hindlimb perfusion (ischemic: normal blood pressure ratio=0.58+/-0.05 versus 0.77+/-0.06; P<0.005), reduced number of angiographically visible vessels (angiographic score=0.48+/-0.05 versus 0.70+/-0.05; P<0.01), and lower capillary density in the ischemic limb (130.3+/-5.8/mm2 versus 171.4+/-9.5/mm2; P<0.001). Angiogenesis was also impaired in old (aged 2 years) versus young (aged 12 weeks) mice as shown by reduced hindlimb perfusion (measured by laser Doppler imaging) and lower capillary density (353.0+/-14.3/mm2 versus 713.3+/-63.4/mm2; P<0.01). Impaired angiogenesis in old animals was the result of impaired endothelial function (lower basal NO release and decreased vasodilation in response to acetylcholine) and a lower expression of vascular endothelial growth factor (VEGF) in ischemic tissues (by Northern blot, Western blot, and immunohistochemistry). When recombinant VEGF protein was administered to young and old rabbits, both groups exhibited a significant and similar increase in blood pressure ratio, angiographic score, and capillary density. CONCLUSIONS: Angiogenesis responsible for collateral development in limb ischemia is impaired with aging; responsible mechanisms include age-related endothelial dysfunction and reduced VEGF expression. Advanced age, however, does not preclude augmentation of collateral vessel development in response to exogenous angiogenic cytokines.
Temperament is a theoretical concept used to understand individual's behavioral styles. In this study, temperament was measured in 13-month-old infants (N = 51) and their mothers, who were also observed together in a teaching situation. The purpose of the study was to determine the relationships between maternal and infant temperaments and interactive behaviors in the teaching situation. Mothers were given 10 minutes to teach infants four tasks designed to assess qualitative aspects of the interaction. In general, the interaction between mother and infant had a synchronous quality that was influenced by, but largely independent of, the temperamental characteristics of mother and infant. Responsive maternal teaching behaviors were significantly related to positive infant affect during teaching. Weak relationships were found between the temperament variables and interactive behaviors in the teaching situation. When mothers and infants were matched on temperament characteristics, no effects of matching temperaments on interactive behaviors in the teaching situation were found. These findings suggest that mothers are able to adjust their behaviors to compensate for their infant's temperament. Based on these data, nurses can focus on the dynamics of the interactions themselves and avoid making judgments based on temperament alone when evaluating mother-infant relationships.
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