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R Bosch

Publications and source records attributed to R Bosch.

At least 37 records · Page 2Linked to original sources
PubMed1996

Shortening induced deactivation in the guinea-pig urinary bladder.

Shortening induced deactivation, the depressant effect of active muscle shortening on the subsequently measured isometric force, has been shown in smooth muscle strips and rings. The guinea-pig bladder permits the investigation of this phenomenon in a whole organ preparation. Previous work in our laboratory showed that shortening of the in vitro guinea-pig detrusor muscle had a depressant effect on the isovolumetric pressure that could be generated immediately afterwards. To test the hypothesis that this was caused by deactivation, the effects of active and passive detrusor shortening on the subsequently measured isovolumetric pressure were compared. The isovolumetric pressures measured after 5 min periods of recovery were taken as control values. It was found that the isovolumetric pressure after passive shortening was 7% smaller than the isovolumetric pressure without preceding shortening. This difference was ascribed to viscoelastic relaxation during shortening. Active shortening had an additional 8% depressant effect on isovolumetric pressure compared with passive shortening. The effects of active and passive shortening differed significantly. It was concluded that shortening induced deactivation in the guinea-pig urinary bladder smooth muscle in toto can be considered proven. The fact that deactivation is shown both by striated and smooth muscle preparations is in line with the assumption that it is caused by reduced actin-myosin interaction. The hypothesis that (in striated muscle) the latter is effected by a decrease in troponin-calcium binding, however, needs reconsideration.

Animals↗
PubMed1996

True histiocytic lymphoma of the stomach associated with low-grade B-cell mucosa-associated lymphoid tissue (MALT)-type lymphoma.

True histiocytic lymphoma is considered a rare entity, and its diagnosis requires the concordance of morphological, immunophenotypic, and molecular findings. The association of malignant lymphoma with tumors in the monocyte-macrophage system has rarely been described. We present a case of mucosa-associated lymphoid tissue (MALT)-type low-grade B-cell lymphoma of the stomach, contiguous to a large tumoral mass that fulfills the morphological criteria (large cells with abundant pale cytoplasm and lobulated or kidney-shaped nuclei) and immunophenotypical features (human leukocyte antigen-DR locus, CD68, S-100, lysozyme immunoreactivity, and negative B- and T-cell markers) required for the diagnosis of histiocytic lymphoma. The patient remains in complete remission 18 months after surgery. The association of low grade-malignant lymphoma with tumors of monocyte-macrophage system cells is an exceedingly rare phenomenon. Whether these tumors are directly related or occur due to pure chance requires the identification of new cases and further study.

Antibodies↗
PubMed1996

Clinical and genetic aspects of two Spanish families with autosomal dominant retinitis pigmentosa (ADRP)

A study was made of two families with autosomal dominant retinitis pigmentosa (ADRP) from Valencia (Spain). One family (ADRP15) was found to have mutation in codon 114 of the rhodopsin gene that led to a substitution of a glycine for an aspartic acid. The second family (ADRP7) substituted an aspartic acid for valine in codon 173 of the peripherin-RDS gene. Rhodopsin is involved in 25% of ADRP cases and many mutations of this gene have been described as causing different forms of the disease, with variable severity and age at onset. ADRP has been classified as RP with a milder symptom evolution, a typical RP fundus pattern, and macular involvement occurring after the second decade of life. Peripherin-RDS gene mutations lead to RP or other retinopathies. Furthermore, two mutations in codon 172 have been described as causing macular dystrophy. In ADRP7, a mutation in neighboring codon 173 produced RP with an atypical fundus pattern and macular involvement within the first decade of life. These observations confirm the established clinical and genetic heterogeneity involved in this form of RP.

Adolescent↗
PubMed1996

Neurogenic modulation of urethral resistance in the guinea pig.

PURPOSE: The resistance offered to urinary flow by the urethra is one of the factors determining the course of micturition. It was the aim of the present work to study the dependence of urethral resistance on the degree of relaxation of the urethra. MATERIALS AND METHODS: Experiments were done in the guinea pig. Ten animals were used. In 5 animals saline was forced through the (unrelaxed) urethra at imposed flow rates in the range of 1.1 to 43.0 ml. per minute while the urethral pressure was measured. Second degree polynomials were fitted to the pressure/flow data. In the other 5 animals micturition contractions were evoked and pressure/flow plots were derived from the measured signals. A straight line was fitted to the lowest pressure values at each flow rate in these plots. These pressure values represent the most relaxed state of the urethra in these voidings. RESULTS: The pressures measured in the unrelaxed urethra were much higher than the pressures measured during voiding in the same flow rate range, but the intercepts of the mathematical equations fitted to the pressure/flow data on the pressure axis were not significantly different in the 2 groups. CONCLUSIONS: The unrelaxed urethra has a much "steeper" pressure/flow characteristic than the relaxed urethra. However, the urethral closing pressure, that is, the intercept of the pressure/flow characteristic on the pressure axis, does not depend on the state of relaxation of the urethra.

Animals↗
PubMed1995

ST segment elevation at the surface of a healed transmural myocardial infarction in pigs. Conditions for passive transmission from the ischemic peri-infarction zone.

BACKGROUND: Ischemia of the myocardium surviving an infarction induces ST segment elevation in infarct-related ECG leads. In cases with no viable tissues, ischemia adjacent to the infarction could induce a similar ECG pattern if there is ST segment potential transmission through the necrotic scar. We analyzed whether acute ischemia adjacent to a healed infarction with no viable tissue may induce ST segment elevation on the surface of the necrotic scar. METHODS AND RESULTS: Epicardial ST segment changes elicited during 30 minutes of acute reocclusion of the left anterior descending (LAD) coronary artery 2 cm above the first diagonal branch were analyzed by 32-channel mapping in 18 chloralose-anesthetized open-chest pigs with 1-month-old anterior infarctions induced by permanent ligature below the first diagonal branch (group 1). The effect of a previous infarction on the magnitude of ischemic ST segment changes was assessed by similar mapping in 21 control pigs submitted to a LAD ligature 2 cm above the first diagonal branch (group 2, n = 11) or just below this branch (group 3, n = 10). Myocardial perfusion after coronary ligature was estimated in 7 pigs with chronic infarction and in 3 control pigs by mapping of myocardial technetium-99m-methoxyisobutyl isonitrile (99mTc-MIBI) activity in transmural samples underlying each epicardial electrode. The width of cell layers surviving the infarction was measured and their viability after 60 minutes of coronary reocclusion was assessed by intracellular glycogen staining. Reocclusion of the LAD induced parallel ST segment elevation at the periinfarction zone and at the necrotic scar, although in the latter region the changes were less marked (maximal ST segment, 8.4 +/- 3.0 mV versus 2.7 +/- 1.8 mV, ANOVA, P < .001). ST segment elevation inside the scar was greater at the margins (3.9 +/- 1.8 mV) than at sites 20 mm toward the center (2.8 +/- 1.7 mV, P = .003). The necrotic area was virtually devoid of surviving cells except for a 0.22 +/- 0.04-mm-wide subendocardial band that continued to show a positive intracellular glycogen reaction after the second LAD ligature. Acute ischemia adjacent to the infarction (group 1) induced lower ST segment elevation than acute ischemia at a comparable cardiac region in noninfarcted pigs (group 2) (ANOVA, P = .02), despite the fact that these areas developed similar underperfusion after coronary occlusion (percent MIBI activity of that in normal myocardium, 7 +/- 8 versus 7 +/- 6, P = NS). ST segment changes in group 2 pigs were comparable to those induced in group 3 pigs with a 2-cm-lower coronary occlusion. CONCLUSIONS: Acute ischemia adjacent to a chronic infarction induces ST segment elevation at the surface of the scar despite the virtual absence of viable tissue within the infarction. Data suggest a passive ST segment potential transmission through the infarction. Moreover, ischemia adjacent to a chronic infarction induces lower ST segment elevation than ischemia not adjacent to a necrosis. The mechanisms accounting for these regional differences are probably independent of collateral myocardial perfusion and ischemia extension.

Animals↗
PubMed1995

Estimation of the lag time between detrusor pressure- and flow rate-signals.

In a urodynamic measurement setup there is a considerable spatial separation between the uroflowmeter and the location where the detrusor pressure is measured. Therefore, a "time shift" (or lag time correction) has to be applied to one of these signals in order to align related samples in studies where pressure and flow rate are considered simultaneously (e.g., assessment of bladder contractility or bladder outlet resistance). Currently, a heuristic value for this time shift of 0.8 s is applied. In this article, we present a method to estimate the lag time directly from the measurements. Using this method we have found, amongst others, that the mean lag time in our clinic is 0.6 s for males, 0.4 s for females voiding in sitting position, and 1.1 s for females voiding in standing position using a special receptacle in video urodynamics. Furthermore, we found that sphincter/urethral activity during voiding (which causes a drop in flow rate and an accompanying increase in detrusor pressure) is associated (on average) with shorter lag times than straining (when a positive pressure rise accompanies an increase in flow rate). Additionally strong evidence is provided that lag time correction is not a major source of error in urodynamics.

Female↗
PubMed1995

Neurogenic modulation of micturition: the relation between stimulation intensity and the maximum shortening velocity of the guinea pig detrusor muscle.

The course of micturition depends on bladder contractility and urethral resistance. The former is determined by geometrical, muscular and neurogenic factors. The muscular aspects of bladder contractility can be characterized by the parameters Pisv, the isovolumetric detrusor pressure, and vmax, the maximum (unloaded) shortening velocity of the detrusor muscle. The neurogenic control system of the urinary tract modulates bladder contractility, which might effectively change the values of Pisv and vmax. These parameters also depend on the instantaneous bladder volume. In previous work the dependence of Pisv on the intensity of stimulation and bladder volume was measured in guinea pig bladders in vivo and in vitro. In the present work vmax was derived in 5 guinea pig bladder in vitro, using electrical stimulation and the stop-flow technique. This technique implies that pressure values measured at a certain shortening velocity of the bladder circumference and in an isovolumetric contraction at the same volume are used to derive vmax mathematically from the Hill equation. vmax was independent of the bladder volume in the range of 0.6 to 6.1 ml., but it was significantly different for the two intensities of stimulation used. Therefore, it is concluded that the maximum shortening velocity of the guinea pig detrusor muscle depends on the intensity of stimulation. During submaximal stimulation the detrusor not only generates lower pressures, it also contracts more slowly. A possible explanation for this phenomenon is that the bladder is not uniformly stimulated. The isovolumetric pressure measured in the stop-flow test was compared with the isovolumetric pressure measured at the same bladder volume some minutes later. It was observed that shortening had a depressant effect of approximately 33% on the isovolumetric pressure. This implies that the clinically employed stop-flow test might underestimate detrusor contraction strength.

Animals↗
PubMed1994

Contractility of the guinea pig bladder measured in situ and in vitro.

To study the relative importance of neurogenic factors in detrusor contractility and to relate a total bladder in vitro contractility model to a previously described bladder wall strip model, active intravesical pressure values were compared in situ and in vitro in eight male guinea pigs. In situ, the active pressure was measured in spontaneous isometric and non-isometric micturition contractions. In vitro, the active pressure was measured in isometric contractions of the same bladders, developed in response to optimal electrical stimulation. The volume dependence of the active pressure generated by the bladder was measured in vitro in order to relate bladder capacity to the volume where the generated force is maximal and to determine the optimal volume at which to study detrusor contractility. The results indicated that in normal micturition the detrusor muscle was not fully stimulated: active pressure in isometric contractions in vivo was about 60% of the pressure values attained in vitro at the same bladder volume. Most micturitions occurred at a volume where the active pressure generated in vitro was about 80% of the maximal pressure. The active pressure-bladder volume relationship complied with the sliding filament-cross bridge theory. In whole bladder preparations active stress was about twice as high as in strips.

Animals↗
PubMed1994

Contractility parameters of the guinea pig bladder in situ: similarity to human bladder contractility.

The parameters P(isv) (active isovolumetric detrusor pressure) and Vmax (maximum shortening velocity), which characterize the contractility of the detrusor muscle, were determined in guinea pigs. To this end it was necessary to develop a method of measuring flow rates in these small animals. The values found were used to calculate the contractility parameter Wmax. Thirteen animals were used. The results found for P(isv) and Vmax were 43.0 +/- 3.7 cm. H2O and 20.2 +/- 3.7 mm. per second, respectively. The latter corresponded to about 0.38 muscle lengths per second, which is similar to values reported for bladder strips from other species. Previous work showed that in vitro P(isv) decreased with increasing bladder volume over a wide range of volumes. In vivo P(isv) seemed to be independent of bladder volume. This suggests that neurogenic stimulation intensifies as volume increases. Vmax also was independent of volume. Wmax appeared to be suitable for detecting differences in the contractility of the bladders of different animals. Values were not significantly different in isovolumetric and nonisovolumetric contractions. Normalized to the size of the bladder, the Wmax values indicated that the power generated by the guinea pig bladder is similar to the power generated by the human bladder.

Animals↗
PubMed1994

Low incidence of ventricular arrhythmias induced by ischaemia at the borders of a chronic infarct in a model with local postinfarction denervation.

OBJECTIVE: The aim was to assess the arrhythmogenic potential of acute ischaemia superimposed at the borders of a chronic myocardial infarct and to analyse the effects of myocardial necrosis on local autonomic innervation in pigs. METHODS: Ventricular arrhythmias were measured in alpha chloralose (100 mg.kg-1) anaesthetised open chest pigs during 60 min occlusion of the left anterior descending coronary artery 2 cm above the first diagonal branch (group I, n = 11) or just below this branch (group II, n = 12). These arrhythmias were compared with those induced in pigs with a one month old anteroseptal infarction (coronary ligature as in group II) submitted to a second occlusion 2 cm above the first (group III, n = 12). The area at risk after high or low ligature was measured in 12 control pigs using fluorescein. Sympathetic and parasympathetic innervation of the anteroseptal myocardium was studied in three pigs with a chronic anteroseptal infarction and in six pigs without infarction using adrenergic histofluorescence and acetylcholinesterase reaction. RESULTS: Compared with ischaemia alone, ischaemia at the borders of a chronic infarct induced a lower incidence of ventricular fibrillation (1/12 pigs v 11/11 in group I, p < 0.001, or 6/12 in group II, p < 0.05) and a tendency towards a lower occurrence of ventricular tachycardia (2/12 pigs v 8/11 in group I, p = 0.01, and 4/12 in group II) and fewer ventricular premature beats (mean number: 105 in group I v 30 in group III, p < 0.05). The mass of the ischaemic regions after low or high occlusion was 13.3(SD 3.0) g and 23.2(5.8) g, respectively. Adrenergic and cholinergic denervation was observed inside the necrotic area, along the subendocardium surviving the necrosis, and in a band of normal bordering myocardium [width: 3.2(2.0) mm for adrenergic and 2.1(1.2) mm for cholinergic denervation]. CONCLUSIONS: Acute ischaemia at the borders of a chronic anteroseptal infarct has a low arrhythmogenic potential in pigs. In this model the peri-infarction zone shows a band of sympathetic and parasympathetic denervation secondary to the necrosis.

Animals↗
PubMed1994

[Treatment of hypertrophic obstructive cardiomyopathy with dual chamber pacing. Use of isoproterenol in determining the optimal AV interval].

Dual chamber pacing may be used as an alternative in the treatment of selected patients who are refractory to conventional medical treatment of hypertrophic obstructive cardiomyopathy. When programming the pacemaker it is essential to know the value of the atrio-ventricular interval which is able to cause the greatest reduction in the left ventricle outflow tract pressure gradient. We have used isoproterenol to calculate the parameter mentioned above. This allowed us to know the optimum value, not only in non-active conditions, but also reproducing the changes in the pressure gradient in different physiological situations.

Atrioventricular Node↗
PubMed1993

Calcitonin gene-related peptide: possibly neurotransmitter contributes to penile erection in monkeys.

The distribution of calcitonin gene-related peptide (CGRP) immunoreactivity in the cavernous tissue and the erectile response to intracavernous injection of CGRP was investigated in 7 monkeys. Intracavernous CGRP increased cavernous arterial flow and induced cavernous smooth muscle relaxation and venous outflow occlusion. Intracavernous injection of CGRP antibody did not significantly change the erectile response to cavernous nerve stimulation. Histologic staining for CGRP immunoreactivity showed nerve fiber-like staining within the cavernous arterial wall and the cavernous smooth muscles. These data suggest that CGRP may contribute to penile erection in monkeys.

Animals↗
PubMed1993

Comparison of detrusor contractility of guinea pig bladders in situ and strips from these in vitro.

To study the relative importance of neurogenic factors in detrusor contractility, active bladder wall stress values were compared in situ and in vitro. Eight male guinea pigs were used. The active stress in the bladder wall in spontaneous micturition contractions was calculated from the results of urodynamic examinations and compared with the active stress developed in response to optimum electrical stimulation in full-thickness bladder wall strips taken from the same bladders. The results indicated that, in normal micturition, the detrusor muscle is not fully stimulated, and the rate of pressure development is not determined by mechanical factors. To identify topological variations of detrusor contractility, the strips were taken from three different locations. It was found that strips from the posterior wall contracted more forcefully than those from the anterior wall.

Animals↗
PubMed1993

Expression of the nifBfdxNnifOQ region of Azotobacter vinelandii and its role in nitrogenase activity.

The nifBQ transcriptional unit of Azotobacter vinelandii has been previously shown to be required for activity of the three nitrogenase systems, Mo nitrogenase, V nitrogenase, and Fe nitrogenase, present in this organism. We studied regulation of expression and the role of the nifBQ region by means of translational beta-galactosidase fusions to each of the five open reading frames: nifB, orf2 (fdxN), orf3 (nifO), nifQ, and orf5. Expression of the first three open reading frames was observed under all three diazotrophic conditions; expression of orf5 was never observed. Genes nifB and fdxN were expressed at similar levels. With Mo, expression of nifO and nifQ was approximately 20- and approximately 400-fold lower than that of fdxN, respectively. Without Mo, expression of nifB dropped three- to fourfold and that of nifQ dropped to the detection limit. However, expression of nifO increased threefold. The products of nifB, fdxN, nifO, and nifQ have been visualized in A. vinelandii as beta-galactosidase fusion proteins with the expected molecular masses. The NifB- fusion lacked activity for any of the three nitrogenase systems and showed an iron-molybdenum cofactor-deficient phenotype in the presence of Mo. The FdxN- mutation resulted in reduced nitrogenase activities, especially when V was present. Dinitrogenase activity in extracts was similarly affected, suggesting a role of FdxN in iron-molybdenum cofactor synthesis. The NifO(-)-producing mutation did not affect any of the nitrogenases under standard diazotrophic conditions. The NifQ(-)-producing mutation resulted in an increased (approximately 1,000-fold) Mo requirement for Mo nitrogenase activity, a phenotype already observed with Klebsiella pneumoniae. No effect of the NifQ(-)-producing mutation on V or Fe nitrogenase was found; this is consistent with its very low expression under those conditions. Mutations in orf5 had no effect on nitrogenase activity.

Acetylene↗