bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acid—Base Changes after Cardiorespiratory Arrest in the Dog
Authors: Greenwood P. V. , Rossall R. E. , Kappagoda C. T. 
Published: August 2015

1. To assess the non-respiratory acid—base disturbance which results from cardiorespiratory arrest experiments were performed on anaesthetized dogs, and circulatory arrest was established either by inducing ventricular fibrillation or by complete occlusion of the great veins.
2. In the first series of experiments (group A) the period of cardiorespiratory arrest was limited to 2·0–3·5 min. It was shown that the non-respiratory component of the ensuing acid—base disturbance as expressed by the non-respiratory pH was small: in nine episodes of circulatory arrest after occlusion of the great veins there was a mean reduction in the non-respiratory pH of 0·04 pH unit (range 0·025–0·055), and in seven episodes of ventricular fibrillation the mean reduction was 0·024 pH unit (range 0–0·055).
3. In the second series of experiments (group B) the period of cardiorespiratory arrest was varied from 3·0 to 11·0 min. It was found that the degree of non-respiratory acidaemia was correlated with the duration of arrest but the magnitude of these changes was not large.
Lack of Effect of Somatostatin on Iodothyronine Release from the Perfused Canine Thyroid
Authors: Laurberg P. 
Published: August 2015

1. This study has evaluated the effect of somatostatin (0.1 or 3 μg/ml) on the release of thyroxine, 3,5,3′-tri-iodothyronine and 3,3′,5′-tri-iodothyronine from perfused thyroid lobes.
2. Somatostatin did not affect either the total release of iodothyronines or the ratio between various iodothyronines in thyroid effluent from unstimulated and thyrotrophic hormone stimulated thyroid lobes.
3. The results lend no support to the idea that somatostatin present in the parafollicular cells of the thyroid should have regulatory function on thyroidal secretion of iodothyronines.
Cyclic Nucleotide Excretion in Human Malignancies
Authors: Hunt N. H. , Smith B. , Pembrey R. 
Published: August 2015

1. Urinary cyclic nucleotide excretion was studied in 51 patients with malignant tumours and in 24 control subjects.
2. Adenosine 3′:5′-cyclic monophosphate excretion was normal in patients with tumours.
3. Urinary excretion of guanosine 3′:5′-cyclic monophosphate was significantly greater than normal in patients with lymphoid tumours (both sexes) and in male patients with myeloid tumours or malignant melanoma.
4. Guanosine 3′:5′-cyclic monophosphate excretion was normal in patients with breast carcinoma or colonic adenocarcinoma.
The Metabolism of a Physiological Dose of Radioactive Cholecalciferol (vitamin D3) to its Hydroxylated Metabolites in Man
Authors: Stanbury S. W. , Mawer E. Barbara 
Published: August 2015

1. The metabolism of an intravenous pulse-dose of 65 nmol (25 μg) of double-isotope-labelled cholecalciferol has been studied in 28 individuals. The subjects comprised 19 with serum concentrations of 25–hydroxycalciferol (25–(OH)D) ≤ 25 nmol/l, of whom 12 had clinical osteomalacia, and nine with serum 25–(OH)D &gt; 25 nmol/l (30–125 nmol/l).
2. The concentrations in serum of radioactive cholecalciferol, 25–hydroxycholecalciferol (25–(OH)D3) and the three dihydroxylated metabolites: 1,25–, 24,25– and 25,26–dihydroxycholecalciferol (1,25–(OH)2D3, 24,25-(OH)2D3 and 25,26–(OH)2D3) were measured for up to 10 days after the injection.
3. The temporal relationships between the formation of individual radioactive metabolites and factors apparently influencing their production are described and their molar concentrations in serum calculated.
4. Formation of radioactive 1,25-(OH)2D3 was detectable only in vitamin D—deficient subjects. Between individuals, its maximum serum concentration was correlated significantly and inversely with serum calcium but with no other measured variable. In the individual, concentrations of radioactive serum 1,25-(OH)2D3 varied directly with radioactive serum 25-(OH)D3.
5. The failure to detect formation of radioactive 1,25–(OH)2D3 in vitamin D—replete subjects suggests that current estimates of the daily turnover of the hormone in the normal individual may be severalfold too high.
6. Radioactive 25,26–(OH)2D3 was produced rapidly by all subjects and in greater amounts by vitamin D—deficient individuals. Between subjects and in the individual its concentration in serum correlated only with the radioactive serum 25–(OH)D3. Production of this metabolite appeared to be unregulated and dependent solely on the concentration of its precursor.
7. In vitamin D—replete subjects, production of 24,25–(OH)2D3 was also apparently determined by precursor concentration. In vitamin D—depleted subjects, production of radioactive 24,25–(OH)2D3 was variably delayed for up to or more than 10 days.
8. There appeared to be a constraint on the quantitative hepatic production of 25–(OH)D which is not explained by simple feed—back inhibition.
9. If sterols other than 1,25–(OH)2D3 are required to initiate the mineralization of osteomalacic bone, after correction of vitamin D deficiency in man, 25–(OH)D3 and 25,26–(OH)2D3 are produced sufficiently rapidly to meet this hypothetical requirement, but not 24,25–(OH)2D3.
The Effects of the Antagonists of the Renin—Angiotensin System on Cardiovascular Response to Lower-Body Subatmospheric Pressure in the Anaesthetized Cat
Authors: Adigun S. A. , Clough D. P. , Conway J. , Hatton R. 
Published: August 2015

1. Lower-body subatmospheric (negative) pressure led to a prompt reduction in central venous pressure and arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. These reflex responses have been used to investigate the role angiotensin plays in blood pressure control.
2. The initial plasma renin activity (2.9 ng of angiotensin I h−1 ml−1) did not change during the brief lowering of pressure. Before pressure was lowered neither the angiotensin-converting enzyme inhibitor nor a competitive antagonist, [Sar1,Ala8]-angiotensin II, lowered arterial pressure.
3. Nevertheless, after inhibition of the renin-angiotensin system by these agents, the reduction in blood pressure induced by lower-body negative pressure became greater and the blood pressure recovery was impaired.
4. The findings suggest that angiotensin, at a blood concentration which has no direct effect on blood pressure, interacts with the sympathetic nervous system to maintain arterial blood pressure.
Cholesterol and Bile Acid Metabolism in Obesity
Authors: Leijd Barbro 
Published: August 2015

1. The present study was undertaken to determine the influence of obesity on bile acid kinetics and cholesterol balance in man.
2. Fourteen obese and normolipidaemic patients (160 ± 6% of ideal body weight, mean ± sem) were studied under standardized dietary conditions. Bile acid kinetics were determined with the aid of 14C-labelled cholic acid and chenodeoxycholic acid. Cholesterol balance was calculated as the sum of bile acid synthesis plus daily faecal excretion of neutral C27 steroids minus dietary intake of cholesterol. The results obtained were compared with previously published data on control subjects (n = 13).
3. The cholesterol balance was higher in the obese patients (2.61 ± 0.27 mmol/day) than in the control subjects (1.78 ± 0.22 mmol/day), owing to a higher excretion of neutral steroids. When expressed per kg of body weight the cholesterol balance was quite normal in the obese patients.
The Removal of Infused Leucine after Injury, Starvation and other Conditions in Man
Authors: Elia M. , Farrell Rose , Ilic Vera , Smith R. , Williamson D. H. 
Published: August 2015

1. To investigate the effects of starvation, elective surgery, accidental injury and other clinical conditions on the metabolism of branched-chain amino acids in man, we have measured the basal concentration of leucine and the removal and metabolic effects of infused l-leucine.
2. The blood concentration of leucine was significantly increased by surgery, starvation and accidental injury, and decreased in cirrhosis. It tended to increase in diabetes and was unaffected by muscular dystrophy.
3. The half-life of infused leucine was nearly doubled by 4 days of complete starvation, unaltered by surgery and decreased by severe accidental injury. Infusion with Intralipid, which increased free fatty acid and ketone-body concentrations, had no effect on the removal of a leucine load. The clearance rate of infused leucine was reduced in diabetes and muscular dystrophy and increased in cirrhosis.
4. The effects of infused leucine on blood glucose and ketone bodies differed according to the groups studied.
5. Since the traumatized patients were given sufficient energy and nitrogen and disposed of a leucine load at a different rate from the starved patients, the causes of the increase in blood concentration of leucine in these two conditions are different.
Plasma High-Density Lipoprotein Metabolism in Subjects with Primary Hypertriglyceridaemia: Altered Metabolism of Apoproteins AI and AII
Authors: Rao S. N. , Magill P. J. , Miller N. E. , Lewis B. 
Published: August 2015

1. The metabolism of the major proteins of plasma high-density lipoprotein (HDL), apoproteins AI and AII, have been studied in 10 normotriglyceridaemic subjects and in 11 hypertriglyceridaemic subjects (plasma triglyceride 4.5–25 mmol/l) by kinetic analysis of the plasma specific radioactivity versus time curves of the apoproteins after intravenous injection of autologous 125I-labelled high-density lipoprotein.
2. The specific radioactivity versus time curves of both apoproteins (followed for 14 days) were bi-exponential in all subjects.
3. The plasma apoprotein AI and AII concentrations were significantly lower in the hypertriglyceridaemic subjects than in the normotriglyceridaemic subjects. Kinetic analysis showed that this was associated with a lower rate of synthesis of apoprotein AI (P &lt; 0.01) and a higher fractional catabolic rate of apoprotein AII (P &lt; 0.01) in the hypertriglyceridaemic group.
4. There were no significant differences between the two groups in the synthetic rate of apoprotein AII, the fractional catabolic rate of apoprotein AI or the intravascular/extravascular distributions of the apoproteins.
5. Thus hypertriglyceridaemia appears to be frequently associated with divergent abnormalities of the metabolism of the major high-density lipoprotein apoproteins.
Rectal Mucosal Histamine Release in Ulcerative Colitis
Authors: Rampton D. S. , Murdoch R. D. , Sladen G. E. 
Published: August 2015

1. Rectal dialysis in vivo was used to assess rectal mucosal release of histamine in patients with ulcerative colitis and in control subjects.
2. Rectal mucosal histamine release was significantly increased in ulcerative colitis, whether the patients were in remission or relapse. The highest values were found in active colitis, but in several such patients histamine release was within the control range. Measurement of rectal mucosal electrical potential difference suggested that increased mucosal histamine release in this group of patients was not due to enhanced epithelial permeability.
3. Rectal dialysis appears to be a useful method for assessing mucosal histamine production and the results obtained are consistent with the hypothesis that immediate hypersensitivity reactions could be of importance in some patients with ulcerative colitis.
Evidence in Vivo for a Circulating Natriuretic Substance in Rats after Expanding the Blood Volume
Authors: Knock Catherine A. , De Wardener H. E. 
Published: August 2015

1. Five rats were volume expanded by infusing a volume of blood equivalent to one-third of the estimated blood volume. In six control experiments the same transfusion was given without expanding the blood volume, as an equal volume of blood was simultaneously removed. Sodium excretion increased significantly more after the blood volume was expanded than in the control experiments.
2. Pairs of rats placed on opposite scale pans of a trip balance were cross-circulated by means of arteriovenous bypasses. The blood volume of the rats could be kept constant by keeping the balance in equilibrium.
3. One of each pair of rats received a blood transfusion which either did or did not expand its blood volume. Sodium excretion was measured in the transfused rat and in the recipient rat, the blood volume of which was kept constant.
4. Sodium excretion in the six recipient rats cross-circulated with rats with an expanded blood volume was not significantly different from that in six recipient rats, cross-circulated with rats given a transfusion which did not expand the blood volume.
5. The cross-circulation experiments were repeated, with the difference that the urine of the transfused rat was reinfused. Under these conditions, sodium excretion in 11 recipient rats cross-circulated with blood volume expanded rats was significantly greater than in eight recipient rats cross-circulated with rats given a transfusion which did not expand the blood volume.
6. In cross-circulation experiments in which a blood transfusion was not given urine reinfusion of one rat did not affect sodium excretion of the other rat.
7. It is concluded that the rise in urinary sodium excretion which occurs in an isovolaemic recipient rat cross-circulated with a urine reinfused rat with an expanded blood volume is due to a change in the concentration of a circulating substance.
Further Evidence in Vivo for a Circulating Natriuretic Substance after Expanding the Blood Volume in Rats
Authors: Knock Catherine A. 
Published: August 2015

1. The blood volume of 18 rats was expanded with blood with which they were equilibrated. In another 18 rats undergoing the same experimental protocol, the blood volume was not expanded.
2. In some rats the urine was reinfused.
3. A 1 ml portion of plasma obtained either 1 h after the blood volume was expanded, or at an equivalent time from the control rats, was injected intravenously into an assay rat.
4. The injection of plasma produced a gradual and significant rise in sodium excretion in the assay rat when it was obtained from an animal with an expanded blood volume, the urine of which was being reinfused.
5. When the increase in blood volume was sustained by a preceding bilateral nephrectomy, instead of urine reinfusion, the injection of 1 ml of plasma into an assay rat did not cause a rise in urinary sodium excretion.
6. It is concluded that the natriuresis involved in the assay rat was caused by a natriuretic substance in the 1 ml of plasma obtained from the blood-volume-expanded urine-reinfused rat.
7. The experiments suggest that the natriuretic substance is excreted in the urine and may be produced in the kidney.
Evidence That the Acute Hypotensive Effect of Captopril in Dogs is Not Wholly Explained by a Reduction of Plasma Angiotensin II and its Direct Vasoconstrictor Effect
Authors: Tree M. , Morton J. J. 
Published: August 2015

1. Captopril infused into sodium-loaded dogs produced a fall in both blood pressure [117 ± 9.7 to 96.6 ± 11.4 (sd) mmHg] and plasma angiotensin II [11.0 ± 3.0 to 1.6 ± 1.3 (sd) pmol/l]. Plasma aldosterone fell while both blood angiotensin I and renin concentration rose.
2. Angiotensin II was infused at 2, 6, 18 and 54 ng min−1 kg−1 into sodium-depleted dogs. Plasma angiotensin II and arterial pressure both rose and were related in a dose-response curve.
3. On a separate occasion the same dogs were given an intravenous infusion of captopril (6 mg h−1 kg−1) and the angiotensin II infusion was repeated. Again plasma angiotensin II and arterial pressure rose but the dose-response curve was displaced downwards; a higher concentration of angiotensin II being required to produce the same blood pressure as in the dogs not given captopril.
4. These findings suggest that the acute hypotensive effect of captopril is not wholly explained by a decrease in plasma angiotensin II concentration and the consequent reduction of its acute vasoconstrictor effect.
Identification of Renin and Renin-like Enzymes in Rat Brain by a Renin-Specific Antibody
Authors: Dzau V. J. , Brenner Amy , Emmett Neremiah , Haber E. 
Published: August 2015

1. The major angiotensin I-generating activity of rat brain extracts has a pH optimum different from that of renal renin and is not inhibited by renin specific antibody.
2. Affinity chromatography utilizing renin specific antibody, pepstatin and α-casein yielded fractions that resembled renal renin more closely with respect to antibody inhibition and pH optimum as well as an absence of the ability to hydrolyse haemoglobin.
3. We conclude that rat brain contains a host of enzymes with angiotensin I-generating activity including acid and neutral proteases and an enzyme with the immunochemical identity of renal renin. The biosynthetic origins of this renin-like protein remain uncertain.
Sternomastoid Muscle Function and Fatigue in Man
Authors: Moxham J. , Wiles C. M. , Newham D. , Edwards R. H. T. 
Published: August 2015

1. A technique has been devised to measure the effect of stimulation frequency on the contraction force in an accessory muscle of respiration, the sternomastoid, in man. The frequency/force curve was found to be very similar to that of the quadriceps and adductor pollicis muscles.
2. Fatigue of the sternomastoid due to inspiratory loading or sustained maximum voluntary ventilation resulted in reduced force generation at low stimulation frequencies compared with maximum force. This type of fatigue frequently persisted for several hours.
3. If low frequency fatigue were to develop in patients with pulmonary disease it could have important consequences for the development of respiratory failure.
Converting Enzyme Inhibition during Chronic Angiotensin II Infusion in Rats: Evidence against a Non-Angiotensin Mechanism
Authors: Textor S. C. , Brunner H. R. , Gavras H. 
Published: August 2015

1. To investigate the non-angiotensin effects of converting enzyme inhibition, angiotensin II was infused intravenously at 30 ng/min for 9 days in conscious rats to produce moderate blood pressure elevation. One group was given captopril (SQ 14 225) by gavage (100 mg/kg twice daily) and the other glucose.
2. After 7 days of captopril administration, enzyme blockade was confirmed by a tenfold greater depressor sensitivity to exogenous bradykinin and a markedly decreased plasma angiotensin converting enzyme activity.
3. Mean arterial pressure, heart rate and plasma renin activity were not different between captopril and glucose-treated groups in the presence of angiotensin II. Metabolic studies also revealed no long-term differences in water and food intake, weight change or sodium and potassium metabolism.
4. These findings suggest that, in the presence of angiotensin II, there is no detectable haemodynamic or metabolic effect of converting enzyme inhibition in rats and, therefore, that bradykinin plays little or no role in its long-term antihypertensive action.
Increase in Prostaglandins during Converting Enzyme Inhibition
Authors: Swartz S. L. , Williams G. H. , Hollenberg N. K. , Crantz F. R. , Levine L. , Moore T. J. , Dluhy R. G. 
Published: August 2015

1. Because changes in the plasma concentration of angiotensin II and bradykinin appear inadequate to account completely for the hypotensive response to captopril, we measured changes in plasma prostaglandins in response to increasing doses of captopril in nine supine normal male subjects studied on both a high (200 mol/l) and low (10 mol/l) sodium intake.
2. On both the high and low sodium diets, captopril induced significant (P&lt;0.01) increments in the 13,14-dihydro-15-keto metabolite of the vasodilatory prostaglandin E2, which correlated significantly with the fall in blood pressure (P&lt;0.0001).
3. No significant changes were noted in the plasma levels of 6-keto-prostaglandins F1α or thromboxane B2, the stable products of prostacyclin and thromboxane A2 respectively.
Leucocyte Electrolytes and Sodium Efflux Rate Constants in the Hypertension of Pre-Eclampsia
Authors: Forrester T. E. , Alleyne G. A. O. 
Published: August 2015

1. Leucocyte electrolytes were measured in pre-eclampsia and comparison was made with leucocytes from normal primigravidae and from the original pre-eclamptic subjects 6 months after delivery when blood pressure had returned to normal.
2. In pre-eclamptic subjects, leucocyte sodium was elevated and potassium depressed, and the rate constant for sodium efflux was depressed.
3. These changes returned to normal after delivery.
4. An increase in cellular sodium as a result of altered sodium pump activity may be the cause of hypertension in pre-eclampsia.
Characterization of the Sympatho-Facilitative Area Postrema Pathway
Authors: Barnes Karen L. , Ferrario C. M. 
Published: August 2015

1. The mechanism by which the area postrema augments central sympathetic drive during electrical stimulation is presently unknown. This pathway may involve either direct facilitation of brain-stem vasomotor neurons or inhibition of the sympatho-inhibitory baroreceptor relay in the nucleus tractus solitarii.
2. The present study employed selective lesions within the solitary tract nucleus to assess the participation of the primary baroreceptor relay in the pressor response during electrical stimulation of the area postrema.
3. The magnitude of the pressor response was unchanged after destruction of the solitary tract and lateral solitary nucleus which centrally interrupted the baroreceptor reflex. However, microknife cuts through the medial solitary nucleus, which spared the carotid sinus reflex, significantly reduced the magnitude of the area postrema pressor response.
4. Previous anatomical studies support these results and confirm that, although the area postrema pressor pathway traverses the most medial portion of the solitary complex, it does not produce augmented sympathetic outflow by inhibition of the primary baroreflex relay.
Pseudohypertension in Sinoaortic-Denervated Rats
Authors: Norman R. A. , Coleman T. G. , Dent Ann C. 
Published: August 2015

1. Mean arterial pressure was determined continuously over a 24-h period by computerized data collection in eight control and nine sinoaortic-denervated rats housed in standard-sized metabolic cages. In addition, direct and indirect pressure measurements were made while the rats were resting in a Lucite restrainer.
2. Pressure measurements made during restraint indicated that the baroreceptor-denervated rats were hypertensive: mean aortic pressure averaged 145 ± 3.4 mmHg (mean ± sem) in denervated rats vs 119 ± 2.8 mmHg in control rats (P&lt;0.001), and tail-cuff pressure averaged 156 ± 5.4 mmHg compared with 121 ± 2.7 mmHg in the control group (P&lt;0.001).
3. In contrast, continuous pressure monitoring showed the sinoaortic-denervated rats were normotensive (mean arterial pressure averaged 119 ± 4.7 mmHg vs 119 ± 3.1 mmHg in control rats).
4. Apparently arterial pressure is elevated during restraint in sinoaortic-denervated rats and pressure measurements made under these conditions give a false indication of hypertension.