Subclavian vein and femoral vein catheterization for hemodialysis - one year comparison.
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Biomedical subjects
Publications and source records attributed to M Fernandes.
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1. Plasma volume, packed cell volume (PCV), blood pressure, extracellular fluid volume (ECFV) and evans blue disappearance rate were measured in conscious spontaneously hypertensive rats and in weight-matched Wistar normotensive rats. 2. Over the weight range studied (250-350 g), plasma and blood volumes were significantly lower in the spontaneously hypertensive rat. Extracellular fluid volumes were similar in the two groups. PCV and Evans blue disappearance rates were significantly higher in the spontaneously hypertensive rat. 3. Negative correlations were obtained between plasma volume and mean arterial pressure and between the plasma/interstitial fluid volume ratio and mean arterial pressure. 4. The normal extracellular fluid volume and the lack of correlation with mean arterial pressure excludes volume expansion as a pressor mechanism during the established phase of hypertension in the spontaneously hypertensive rat.
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In patients with essential hypertension, a variation in the plasma proteins was revealed by high-resolution sodium dodecyl sulphate polyacrylamide gel electrophoresis. This variation in plasma protein was not found in patients with hypertension secondary to renovascular or renal parenchymal disease.
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A case of multilocular cyst of the kidney with calcification is presented and pertinent literature is reviewed. With our present knowledge, a multilocular cyst cannot be clearly differentiated from a malignant renal tumor by preoperative evaluation. Conservative surgery with operative evaluation of the lesion is suggested.
We describe a patient with amyloidosis of renal pelvis and 2 patients with urinary bladder amyloidosis. Clinical presentation in all of the cases mimicked cancer of the respective sites. Clinical diagnosis of amyloidosis is not possible, making biopsy mandatory. Immunology of amyloid formation and treatment of amyloidosis are discussed.
1. Pentolinium tartrate (a ganglionic blocker) was injected in conscious rats during the early and late phases of two-kidney renal hypertension produced by aortic ligation. 2. In the early phase ( 5 days after aortic ligation), ganglionic blockade resulted in a decrease in blood pressure equal to that obtained in normotensive rats. Later, at days 12 and 40, for equally severe hypertension, ganglion blockade resulted in a greater decrease in blood pressure. 3. A 30 min infusion of [Sar1, Ala8]angiotensin II during the pentolinium-induced nadir in blood pressure resulted in a further decrease in blood pressure at day 5. Later, at days 12 and 40, this effect was smaller. 4. A 300 min infusion of [Sar1, Ala8]angiotensin II normalized the blood pressure in hypertensive rats at day 40. This delay response may be secondary to a central effect of the antagonist, reducing neurogenic tone or peripheral antagonism of locally generated angiotensin II in the blood vessel walls. 5. At day 40, removal of the small left kidney resulted in a greater decrease in blood pressure. This suggests the presence of a renal factor other than renin in the chronic phase of this hypertension.
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The interaction between d-amphetamine and ethanol with respect to locomotor activity, stereotyped behavior, and sleeping time was investigated in rats. Ethanol 0.8 g/kg i.p. enhanced and prolonged locomotor activity produced by d-amphetamine 1 mg/kg s.c. The increased motility after 5 mg/kg d-amphetamine was not influenced by alcohol 0.8 g/kg i.p. or 3.2 g/kg orally, but slightly protracted. Stereotyped head and paw movements, as well as stereotyped licking, were distinctly strengthened and protracted by 3.2 g/kg ethanol orally. The modified d-amphetamine motility and stereotypies can be explained by alcohol-induced proloneation of the life of d-amphetomine. The effect is produced by alcohol's inhibition d-amphetamine p-hydroxylation in rat liver. After 3.2 g/kg ethanol i.p., the sleeping time of male rats amounted to 153 min. Simultaneous administration of 5 mg/kg d-amphetamine s.c. reduced the sleeping time to 84 min. This is obviously based on a central antagonism.
Malignant fibrous histiocytomas are very rare, particularly those related to urogenital organs. We report herein the third known case of this entity involving the spermatic cord. Summary of the previously reported 2 cases is given with recent follow-up. Prognosis is poor.
1. Sar1-Ala8-Angiotensin II (an angiotensin antagonist) was infused in rats during the development and maintenance of renal hypertension produced by aortic ligation between renal arteries. 2. In the early phase (5 and 12 days after ligation), infusion of the antagonist markedly decreased blood pressure although it did not reach normal pressures. Later (day 40) only a modest decrease in blood pressure was noted. 3. Removal of the small left kidney always decreased the blood pressure to normal pressures. 4. It is concluded that the renin-angiotensin system is the major pressor component in the initiation of this hypertension. Later, other factors of renal origin assume a pressor function.
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d-Amphetamine increases the motor activity at a dose range of 0.5-4 mg/kg. delta(9)-Tetrahydrocannabinol (THC) diminishes this effect dose-dependently. Also, the hyperthermia caused by 5 mg/kg d-amphetamine is antagonized by THC, whereas the d-amphetamine induced stereotype movements (above 4 mg/kg) are prolonged by the cannabinoid. THC and d-amphetamine both reduce the food and water intake and the normal development body weight of rats. In combination the two substances have an additive effect. Rats treated with 5 mg/kg d-amphetamine show a significant enhancement of the dopamine (DA) concentration (26%) in the brain stem 2 h p.i. Pretreatment with 10 mg/kg THC, which also causes an increase of DA by 15%, raises the DA content by 50%. Norepinephrine (NE) in the brain stem and hypothalamus is reduced by d-amphetamine but THC has no effect on the concentration of this monoamine. After subchronical treatment with THC tolerance is demonstrable to all THC effects tested. But there is no cross tolerance between delta(9)-THC and d-amphetamine since the pharmacological as well as the biochemical effects of d-amphetamine occur despite the subchronical treatment with THC.
Tolerance to various effects of morphine in the rat can be quantified by means of a shift of semi-logarithmic dose-response curves. Tolerance to analgesia (hot plate, acetic acid writhing), catalepsy, and the tilted plane develops in a closely similar manner. Also, the stimulating effects of about 1 mg/kg morphine-HC1 tested in an open-field procedure are somewhat less pronounced in chronically treated rats than in naive ones. There is no correlation between tolerance development and the acute ED50 of different tests.
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