A complication of catheterization of the left internal jugular vein.
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Biomedical subjects
Publications and source records attributed to C R Benedict.
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Plasma concentrations of adrenaline and noradrenaline were measured sequentially over the immediate post-operative period following clipping of an intracranial aneurysm in 11 patients. Those patients who developed local cerebral vasospasm showed a sustained rise in plasma catecholamines, particularly noradrenaline, whilst those patients who developed generalised cerebral vasospasm showed early peaks of very high concentrations of adrenaline and noradrenaline which preceded radiological evidence of generalized vasospam.
The delta(13)C values for seagrasses collected along the Texas Gulf Coast range from -10.9 to -11.4 per thousand. These values are similar to the delta(13)C values of terrestrial C(4) plants, but seagrasses lack bundle sheath cells which are important in determining the delta(13)C values of C(4) plants. This work attempts to explain the reason the delta(13)C values of seagrasses resemble the delta(13)C values of C(4) plants.Investigations on the photosynthetic characteristics of seagrasses show that dissolved CO(2) is the species of inorganic carbon absorbed or accumulated by Thalassia testudinum. The rate of photosynthetic CO(2) fixation varies from 9.6 to 129.0 micromoles CO(2) per milligram chlorophyll per hour in the presence of 0.042 to 1.9 millimolar dissolved CO(2) due to the high resistances of Thalassia leaves to CO(2) diffusion. Phosphoglyceric acid is the first stable product of photosynthetic CO(2) fixation in Thalassia which is a Calvin cycle plant. The light/dark ratios of (14)CO(2) release from submerged Thalassia leaf sections at 1, 21, and 100% O(2) indicate a small apparent photorespiration. Dark respiration continues in the light and is stimulated by 21 and 100% O(2). The low apparent photorespiration may be due to membrane and H(2)O resistances to CO(2) diffusion with subsequent refixation of the photorespired CO(2). The internal pool of CO(2) is not in equilibrium with the external pool of CO(2) which results in a closed system in the seagrasses.The delta(13)C value of CO(2) in sea H(2)O in isotopic equilibrium with HCO(3) (-) is -10.3 per thousand and the delta(13)C value of hexoses isolated from the leaves of Thalassia is -11.5 per thousand. In the closed system of the seagrasses there is a -1.2 per thousand fractionation of CO(2) by ribulose-1,5-bisphosphate carboxylase and the Calvin cycle. This contrasts to a fractionation of about -17 to -27 per thousand of the stable carbon isotopes of CO(2) by the Calvin cycle in the open system of terrestrial C(3) plants where the internal pool of CO(2) is in equilibrium with atmospheric CO(2).Among C(3) plants the seagrasses are very unusual in fixing CO(2) by the Calvin cycle in a closed system. This closed system metabolism is analogous to the fixation of CO(2) by the Calvin cycle in the bundle sheath cells of C(4) plants where all of the (12)CO(2) and (13)CO(2) is fixed by ribulose-1,5-bisphosphate carboxylase. Therefore, the reasons the delta(13)C values of seagrasses and C(4) plants are similar are: (a) the delta(13)C value of dissolved CO(2) in seawater resembles the delta(13)C value of the C(4) acids and the delta(13)C value of CO(2) in the bundle sheath cells, and (b) there is no fractionation of the stable carbon isotopes of CO(2) in the closed systems of the seagrasses or the bundle sheath cells of C(4) plants.
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The enzymic fractionation of the stable carbon isotopes of CO(2) (Deltaco(2)) was determined using a purified preparation of ribulose-1,5-bisphosphate (RuBP) carboxylase isolated from cotton (a C(3) plant) leaves. The bicarbonate concentration in the reaction mixture saturated the enzyme and furnished an infinite pool of (12)CO(2) and (13)CO(2) for enzyme fractionation. The RuBP was 96 to 98% pure. The phosphoglycerate synthesized in the reaction mixtures was purified free of RuBP, phosphoglycolate, and other phosphate esters by column chromatography on Dowex 1-Cl(-) resin. The average Deltaco(2) value of -27.1% was determined from five separate experiments. A discussion of the isotope fractionation associated with photosynthetic CO(2) fixation in plants shows that the enzymic fractionation of stable carbon isotopes of CO(2) by RuBP carboxylase is of major importance in determining the delta(13)C values of C(3) plants.
1. The effects of atenolol on diurnal blood pressure control, heart rate and plasma catecholamines were studied in nine hypertensives, six of whom also received diuretics. The patients completed a double-blind trial in which the effects of once and twice daily administration of atenolol were compared with placebo. 2. Atenolol (100 mg) given once a day produced significant reduction in diurnal blood pressures recorded at home but the effect was slightly less than either 50 mg given twice a day or 200 mg once a day. 3. Effects on heart rate and blood pressure were seen within 36 hours of the first dose, and were near maximal at 72 hours. After cessation of the drug, mean resting heart rate increased gradually and reached pre-treatment levels five days later, suggesting strong tissue binding of atenolol. Blood pressure increased more slowly over 8--10 days. 4. Plasma noradrenaline levels were increased at rest with atenolol. This argues strongly against the antihypertensive effect of atenolol being due to a reduction of sympathetic nerve activity. 5. Once daily administration of atenolol in this group of patients with mild hypertension produced satisfactory diurnal blood pressure control and beta blockade without "rebound" hypertension on cessation of therapy.
1 Plasma noradrenaline concentration in rats was measured during prolonged cold-stress and repeated swim-stress. 2 Cold exposure for 6 h caused a rise in plasma noradrenaline which reached a peak at 4 h. 3 Administration of desmethylimipramine and normetanephrine to block neuronal and extra-neuronal uptake of noradrenaline raised plasma noradrenaline concentration without changing the pattern of the response to cold exposure. 4 Repeated cold exposure on subsequent days produced no change in the pattern of plasma noradrenaline concentration. 5 Five successive 1-min swims at 30-min intervals caused a rise in plasma noradrenaline concentration which was maximal after the third swim. 6 It is suggested that prolonged and repeated activation of sympathetic nerve terminals leads to a decline in noradrenaline release.
In patients with myocardial infarction, with or without cardiogenic shock, plasma noradrenaline and adrenaline concentrations are increased. However, plasma noradrenaline concentrations are considerably higher in patients with cardiogenic shock when compared with those with uncomplicated myocardial infarction. Plasma noradrenaline and adrenaline concentrations showed a sustained increase until death in patients with cardiogenic shock whereas those concentrations were back to normal levels by the end of the third day in patients with uncomplicated myocardial infarction. Plasma dopamine-beta-hydroxylase activities in both the groups were within normal range and did not show any significant variation throughout the period of study.
Maximal increments in adrenaline and dexamethasone (DXM) plasma concentrations were observed c15 (T50 40 min) and 30 (T50 210-240 min) minutes after an i.v. DXM dose (6 mg/m2 BSA) in man. There appears, however, to be no direct interaction between these agents in the development of induced neutrophilia, which occurs c240 min postinjection.
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Changes in plasma concentrations of adrenaline and noradrenaline were measured when sodium nitroprusside (SNP) was used for the induction of hypotension in healthy adults undergoing middle ear surgery (group 1) and patients undergoing neurosurgery for subarachnoid haemorrhage (group 2). The mean catecholamine concentrations before the infusion of SNP were four to five times greater in group 2 than in group 1. Group 1 showed significant increases in plasma catecholamines during hypotension induced with SNP, the increase correlating significantly with the degree of hypotension and the rate of infusion of SNP. Group 1 showed an increase in heart rate of about 10%, which could not be related to the catecholamine concentrations. In group 2, changes in plasma catecholamines following infusion of SNP were inconsistent. This may have been because the sympatho--adrenal medullary system was already maximally active and was unable to respond further to induced hypotension.
1 A method is described for repeated sampling of plasma noradrenaline (NA) in freely moving rats. Na concentration does not change during the day or after adrenalectomy. 2 Exogenous NA has a half-life of 1.5 min; drugs which block neuronal and extra-neuronal uptake lengthen this to 6.3 min. 3 Swim-stress leads to a steep rise followed by a rapid decline in plasma NA concentration. 4 This method of plasma NA sampling can serve as a measure of both steady and rapid changes in release rate over long periods of time.
Metabolic and endocrine studies on a 7-year-old boy who presented with hypoglycaemic convulsions are reported in detail, proving the diagnosis of isolated ACTH deficiency--a rare cause of hypoglycaemia in childhood. Adrenaline secretion during insulin-induced hypoglycaemia was reduced. Low blood alanine levels occurred during starvation-induced hypoglycaemia, together with raised total blood ketone bodies; blood glucose did not increase adequately after oral alanine at this time. Hypoglycaemia in isolated ACTH deficiency appears to be due to a combination of impaired alanine mobilisation and a decreased rate of gluconeogenesis.
Plasma adrenaline and noradrenaline concentrations were measured in 21 patients after subarachnoid haemorrhage and in 13 control patients. Plasma noradrenaline concentrations were significantly raised in patients recovering from subarachnoid haemorrhage, confirming clinical evidence of overactivity of the sympathetic nervous system. Plasma noradrenaline concentrations in patients with a poor result were significantly higher at the time of admission than in patients with a good result, and the differences became more significant two to three days later. Therefore, the measurement of plasma noradrenaline concentrations may be a valuable test to assist clinical assessment in distinguishing between the two groups preoperatively.
In six patients within 12 hours of surgical correction of aortic coarctation there was a 750% increase in plasma noradrenaline concentrations accompanied by an increase in systolic and diastolic blood pressures. The magnitude of the postoperative increase in noradrenaline concentrations was related to the preoperative level of the pressure gradient across the coarctation. Six months after operation plasma noradrenaline concentrations were still significantly elevated. In nine patients who underwent other types of major surgery there was a small increase in plasma noradrenaline concentrations and a return to levels within the normal range within 24 hours. Various explanations for the rise in plasma noradrenaline concentrations are considered. In particular the possibility is raised that after surgical correction of aortic coarctation the increased levels indicate a marked increase in sympathetic nervous system activity; this may be mediated by baroreceptor mechanisms and may persist for up to six months after surgery.
Plasma adrenaline and noradrenaline concentrations and dopamine-beta-hydroxylase activities were measured in patients with septicaemic, traumatic or haemorrhagic shock. Irrespective of the type of shock plasma adrenaline and noradrenaline concentrations were increased above the normal range. This is in keeping with the clinical features of increased sympathetic nervous system and adrenal medullary activity present in these patients. Plasma dopamine-beta-hydroxylase activities were within the normal limits in all forms of shock indicating the poor relationship of this measurement to sympathetic nervous system activity. In patients who died plasma noradrenaline concentrations remained persistently elevated above normal while in those who survived there was a rapid decline towards the normal range.
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1. The initial blood pressure response to saralasin (Sar1-Ala8-angiotensin II) infusion was examined in 15 normal subjects, eight patients with untreated essential hypertension and 65 patients established on chronic haemogialysis (including six anephric patients), and related to measurements of plasma renin activity (PRA), angiotensin II, plasma catecholamines (noradrenaline and adrenaline), blood volume and extracellular fluid volume ([35S]sulphate space or exchangeable sodium). 2. A transient rise in arterial pressure, maximum after 5-6 min, occurred in all normal subjects, patient with essential hypertension and anephric patients, and in 41 of the 59 dialysis patients with kidneys. 3. In the normal subjects, saralasin infusion resulted in a significant rise in plasma noradrenaline (mean increase 360%, P less than 0-02) without change in plasma adrenaline concentration. The change in noradrenaline was significantly related to the change in mean blood pressure (P less than 0-05) and was similar to the response to 5 min of a 40 degree head-up tilt. 4. An increase in plasma noradrenaline also occurred in dialysis patients (P less than 0-005) but the change in mean blood pressure with saralasin in this group was inversely related to PRA (P less than 0-001) and angiotensin II (P less than 0-001), directly related to blood volume (P less than 0-001), but unrelated to the change in plasma noradrenaline. 5. The pressor response to saralasin may be mediated not only by angiotensin-like action on vascular receptors but also by an action on the central or peripheral autonomic nervous system.