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[Patho-physiological aspects in csf proteins (author's transl)].

Electrophoresis and immunoelectrophoresis of cerebrospinal fluid of 201 patients with inflammatory CNS diseases revealed that over a total protein value from 0 to greater than 1, 2 g/1 there was merely a decrease in pre-albumins and a difference in the gamma-globulins as a pointer to immune reactions. Comparison with the absolute values indicated an increase of all fractions in inflammatory and non inflammatory diseases caused by impairment of the blood-CSF barrier. Again there was evidence of immune reaction in the gamma-globulin range. Impairment in the blood-CSF barrier was demonstrated by an increased concentration of IgG, IgA and IgM. An immune reaction was revealed by higher IgG values.

Blood-Brain Barrier

Reactivity of isolated canine bronchus and pulmonary blood vessels to autonomic, autacoid agents and antigen.

Adult dogs were sensitized to horse plasma. Reactivity of isolated bronchus and pulmonary blood vessels to antigen and some selected autonomic and autacoid agents were studied. Pulmonary veins contracted to bradykinin, 5-HT, PGF2alpha, PGE2, histamine, carbachol and antigen (Schultz-Dale reaction). Pulmonary arterial strips contracted to 5-HT and histamine, but only weakly to horse plasma. Bronchial strips contracted to carbachol, 5-HT, histamine and horse plasma, relaxed to isoprenaline, PGE1 and PGE2. Subsequent antigen challenge produced 'desensitization'. Allowing the tissues to 'rest' for 1 and 2 h resulted in partial 'recovery' of the anaphylactic response. This investigation suggests that the contractions of sensitized pulmonary vein and bronchus to specific antigen may contribute to the patho-physiology of pulmonary hypersensitivity in dogs.

Anaphylaxis

[Mitral stenosis on conventional radiographs. II. The relationship between pulmonary venous and arterial hypertension, their haemodynamic parameters and calcified mitral valves (author's transl)].

In the second paper, the relationship between pulmonary venous and arterial hypertension and calcification in the mitral valve is analysed statistically and its patho-physiological significance discussed. In one hundred cases of mitral stenosis the left atrium, as seen on the lateral projection, was always enlarged, but its size was independant of atrial pressure or the pressure gradient across the mitral valve. Apart from pulmonary fibrosis and haemosiderosis, the abnormal findings increased with increasing mean atrial pressure. Pulmonary-arterial mean pressure of more than 30 mmHg was found particularly in the presence of mitral valve calcification (94%). Calcification of the valve is the most important and reliable indicator for evaluating the severity of the stenosis.

Adult

Decreased venous distensibility in essential hypertension: lack of systemic hemodynamic correlates.

Venous distensibility in essential hypertension has been reported to be unchanged or decreased; its pathophysiologic role is uncertain. In 27 male hypertensive patients and 21 normotensive control subjects, forearm venous distensibility and capillary filtration rate at 30 cm of H2O distending pressure were measured by strain gauge plethysmography. Plasma renin activity (PRA), plasma volume (PV) by the Evans blue dye dilution technique, mean arterial pressure (MAP) by cuff, and cardiac output (CO) by the CO2 rebreathing method were also measured. Compared to values in normotensive control subjects, forearm venous distensibility in hypertensive subjects was decreased (P less than 0.05); the forearm venous pressure-volume curves (deflation phase) were shifted in the direction of the pressure axis (P less than 0.02); and the capillary filtration rate was increased (P less than 0.05). Venous distensibility changes in hypertensive subjects were unrelated to PRA, MAP, PV, CO, stroke volume, and total peripheral resistance. These findings confirm previous reports of decreased venous distensibility in hypertension and provide direct evidence for increased capillary filtration rate. In view of the lack of significant correlation between venous distensibility and the measured hemodynamic parameters, a patho-physiologic role for venous distensibility in hypertension could not be established.

Blood Pressure

A comparative study of the electrode systems of three pH and blood gas apparatus.

We present a comparative evaluation of the electrode systems of three modern blood gas analysers: IL-413, ABL-1 and AVL-937C. The response curves, accuracy and precision of the pH-, pCO2- and pO2-electrodes were established with tonometered blood and buffer solutions. pH values (range 6.8-7.8) measured on the AVL deviate (-0.03 pH for blood and +0.03 pH for buffer) from those of BMS2 Mk2; whereas on the IL and ABL analysers the pH values deviate by not more than 0.01 pH. The standard deviation was better than 0.005 pH. pCO2 values of blood and buffer (range 14-106 mm Hg) deviate from the calculated tonometer values by quantities ranging from 3 to 10 mm Hg. The average precision (CV)1) of the pCO2 measurement on each analyser was better than 1.8%. pO2 values of blood (range 0-130 mm Hg) did not differ by more than 3 mm Hg from the calculated values. Above 130 mm Hg a linear negative increasing difference was seen. For buffer solutions a linear relationship between pO2 difference and pO2 value was found over the whole range from zero up to 642 mm Hg: a positive difference below and a negative difference above the pO2 of the previous calibration; if the calibration pO2 is higher, the sample pO2 is shifted to a higher value. The average precision of the pO2 measurements was better than 3%. In the (patho)-physiological range the three instruments may provide suitable results for the clinician. Suggestions are made for standardization and improvement of the electrode systems.

Blood Chemical Analysis

[Luteal insufficiency and benign breast diseases. Study in the light of data from the combined LH-RH + TRH test together with the study of ovarian steroids].

Luteal deficiency has been attributed a patho-physiologic role in benign fibro-cystic breast disease, whereas Prolactin would not be involved in this disease. To tes these hypotheses, patients with fibro-cystic breast disease have been investigated through the combined LH-RH + TRH test, coupled with ovarian steroids estimations. 63 menstruating patients with ovulatory cycles, as evidenced by the temperature curve and proven fibro-cystic breast disease, as demonstrated by senography and thermogrphy and/or operation, have been selected for this study. The findings do not favour the role of luteal dificiency but rather the role of PRL hyperactivity in the pathol-physiology of fibro-cySTIC BREAST DISEASE.

Breast Diseases

[Splenohepatoplasty in the treatment of hepatic cirrhosis].

The authors review the patho-physiologic arguments that have determined Bénichoux to recommend spleno-hepatoplasty in the treatment of hepatic cirrhosis, and present a group of 7 personal observations in which they have tested this type of intervention. The technique employed is described, as well as the follow-up of the cases that had a favourable evolution. In one of the observations differences between the samples obtained by bioptic puncture before the intervention and those obtained at one and two years after surgery, have demonstrated a marked reduction in the intensity of inflammatory reactions, as well as evident reparation processes in the hepatocytes. The authors consider the intervention as a new type of therapy, allowing for re-vascularization of the ischaemic hepatic tissue, as well as for a slow porto-caval derivation with remarkable results for the cirrhotic patients.

Adolescent

L-Thyroxine effects upon ATPase activities of several subcellular fractions of liver of the rat and the guinea pig.

The effect of thyroxine administration upon ATPase activity of several subcellular fractions of livers from rats and guinea pigs has been studied. To determine a patho-physiological dose of levo thyroxine [T4] for guinea pigs, a dose-response curve was examined of T4 effect upon oxidative phosphorylatin of guinea pig liver mitochondria. Maximum stimulation of mitochondrial respiration without uncoupling of oxidative phosphorylation was found with 15 microgram of T4 per 100 g body weight per day. This dose of T4 stimulated Mg++ activated ATPase of plasma membranes of guinea pigs and slightly stimulated Mg++ activated ATPase of guinea pig liver nuclear membranes. Rat liver nuclear membrane ATPase was not responsive to thyroxine at doses from 5 to 150 microgram per 100 g body weight. T4 significantly stimulated Ca++ or Mg++ ATPase of mitochondria and microsomes from both rat and guinea pig liver. Microsomes from both species were maximally activated by Mg++ and no significant additional stimulation with Ca++ was found. Mitochondrial ATPase from both species showed significantly greater Ca++ plus Mg++ ATPase activity than did Mg++ alone. Ca++ activated ATPase was approximately equal to dinitrophenol stimulated mitochondrial ATPase. Maximum activation of microsomal ATPase in both species was found with 1 mM calcium. We conclude that at physiological-intracellular concentrations of Ca++ and Mg++, thyroxine probably stimulates Mg++ activated microsomal ATPase and Ca++ activated mitochondrial ATPase. A potential role of Ca++ as a moderator of thyroxine stimulated activity in mitochondria and the relation of calcium to other metabolic reactions that are thyroxine sensitive is discussed.

Adenosine Triphosphatases

Experimental workflows for the accurate identification of mitochondrial redox events.

The study of redox biology has been growing constantly since the last decades. Over these years, redox processes have been linked to an extraordinarily wide range of physiological and pathological events, becoming recognized as central mechanisms underlying many of them. In this context, it becomes essential to understand the advantages and limitations of the tools under use, to recognize the specific controls required for each measurement and to accurately distinguish between distinct redox mechanisms. So far, multiple and excellent reviews have dealt with either the tools, the protocols or the mechanisms involved in reactive oxygen species (ROS) production and quenching, a.k.a. redox events. However, a review outlining the workflows to appropriately detect them is still lacking. We define workflow as the combination of tools, methods and mechanistic knowledge that allow the definition of a specific redox event. In this review, we aim to provide an optimal workflow for the research on mitochondrial redox events. To this end, we first summarize the molecular tools available to measure and quench ROS. We then explain the mechanisms of ROS production and scavenging in several of the cellular compartments, with special focus on mitochondria, as well as their implication in physiology and disease. Finally, we use the knowledge in all sections to build a recommended experimental workflow, illustrated by several cases of study. This review will enable the reader to understand how specific mitochondrial redox events can be accurately measured, considering all technical, methodological and mechanistical variables and limitations required for their reliable detection and interpretation.

(Patho)physiology