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J Scholz

Publications and source records attributed to J Scholz.

At least 19 recordsLinked to original sources
PubMed1992

Relationship between plasma potassium and ventilation during successive periods of exercise in men.

During and after two successive incremental cycle ergometer tests (tests A and B), plasma potassium concentration ([K+]p), plasma pH (pHp), plasma partial pressure of carbon dioxide, blood lactate concentration ([Lac-]b) and ventilation (VE) were measured. While there was a good correlation between the increase in [K+]p and VE or pHp, respectively, in test A, in test B a close correlation was found only between the increase in VE and [K+]p (r greater than 0.9 for nearly all single cases; r was 0.84 and 0.89 for all (pooled) cases in tests A and B, respectively; the correlation coefficients between changes in pHp and VE in tests A and B were r = 0.74 and r = 0.28, respectively, and r = 0.89 and r = 0.10 between the changes in [Lac-]b and VE in tests A and B). The close relationship for individuals between VE and [K+]p in tests A and B supported the hypothesis that the extracellular increase in [K+] may contribute to the ventilatory drive during exercise. The comparison of the results of tests A and B further indicated that the relationship between pHp and VE was dependent on the experimental design, and that pHp and VE changes are unlikely to be cause and effect.

Adult↗
PubMed1992

Plasma potassium and ventilation during incremental exercise in humans: modulation by sodium bicarbonate and substrate availability.

It has recently been demonstrated that, compared to normal conditions, ventilation (VE) was increased during exercise after glycogen depletion, in spite of a marked increase in plasma pH (pHP). It was further demonstrated that VE in patients with McArdle's syndrome was reduced when substrate availability was improved. In the present experiments, six endurance trained men performed two successive cyclo-ergometric incremental exercise tests (tests A, B) after normal nutrition (N) and after a fatty meal in conjunction with a sodium bicarbonate (NaHCO3) solution (FSB) or without NaHCO3 (F), and the relationship between VE, plasma potassium concentration ([K+]P), and pHP was checked. Plasma free fatty acid concentration ([FFA]P) was markedly increased in the F and FSB trials (P < 0.001). In FSB pHP was significantly increased, compared to N and F (P < 0.001). In all the B tests, pHP increased during moderate and intense exercise and in FSB, remained alkalotic even during maximal exercise intensity. In contrast, VE and [K+]P changes were almost equal in all the trials and in tests A and B. It was found that exercise-induced changes of VE and [K+]P in the present experiments were not markedly affected by [FFA]P or pHP values and that these changes also occurred independently of changes in pHP or plasma bicarbonate concentration. The often used glycogen depletion strategy may have slightly increased VE but apparently did not overcompensate for a possible decrease in VE due to increased pHP.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1992

Existence and alpha 1-adrenergic stimulation of inositol polyphosphates in mammalian heart.

The concentration-response curves and the time course of the effects of phenylephrine (0.01-100 microM) on force of contraction and on inositol polyphosphates in isolated electrically stimulated perfused rat hearts (Langendorff technique) were studied. A nonradiometric high performance liquid chromatography metal dye detection technique was used to determine absolute concentration masses/changes of inositol polyphosphates in heart. Products measured after separation with high performance liquid chromatography were inositol 1,4,5-trisphosphate (1,4,5-IP3), inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP4) and its isomer 1,3,4,6-IP4, inositol 1,3,4,5,6-pentakisphosphate (1,3,4,5,6-IP5), and inositol hexakisphosphate (IP6). 1,4,5-IP3 (significant at 10 microM) and both IP4 isomers (significant at 1 microM) increased after alpha-adrenoceptor stimulation, whereas 1,3,4,5,6-IP5 and IP6 remained unaffected. Phenylephrine had a concentration-dependent positive inotropic effect (significant at 1 microM). All effects were antagonized by the alpha 1-adrenoceptor antagonist prazosin (0.1 microM), indicating receptor-mediated effects. In a time course study 1,4,5-IP3 was the first compound to increase significantly, within 1 min after stimulation; this rise was followed by an increase in 1,3,4,5-IP4 beginning within 2 min. The increase in all other inositol polyphosphates was slower (5-10 min). The increase in the force of contraction started at 2 min. For comparison, the effects of the beta-adrenoceptor agonist isoprenaline were studied. Isoprenaline produced a positive inotropic effect similar to that of phenylephrine, but all inositol polyphosphates remained unaffected. In conclusion, for the first time the existence of 1,3,4,5,6-IP5 and IP6 was observed in the heart. However, the physiological role of these inositol polyphosphate isomers in the heart remains to be elucidated, because, from the time course, they appear to have no acute intracellular second messenger function. Increased inositol polyphosphate turnover may be involved in the mechanism(s) whereby alpha 1-adrenoceptor stimulation produces an increase in myocardial force of contraction. Because the increase in 1,4,5-IP3 precedes and that in 1,3,4,5-IP4 coincides with the increase in the force of contraction, 1,4,5-IP3 may initiate and 1,3,4,5-IP4 may maintain the positive inotropic effect of alpha 1-adrenoceptor agonists.

Animals↗
PubMed1991

[Treatment with clonidine in a case of the short bowel syndrome with therapy-refractory diarrhea].

A patient with refractory diarrhoea (up to 10 l/d) following colectomy and ileostomy was treated with clonidine, after loperamide, tinctura opii, cholestyramine and somatostatin had failed to reduce stool volume to less than 6 l/d. Under combined treatment with clonidine (1200 micrograms/d) and somatostatin (6 mg/d), which was well tolerated, stool weights were normalised within 24 hours. This case report on the successful anti-diarrhoeic effect of clonidine is completed by experimental data from rat jejunal and duodenal segments. In the presence of the adenylate cyclase-stimulating agent forskolin, clonidine normalised both mucosal cAMP content and cAMP-induced hypersecretion in rat intestine. This suggests that the anti-diarrhoeic effect of clonidine in-vitro results from an alpha 2-receptor mediated inhibition of the stimulated adenylate cyclase. Case report and experimental data therefore support the theory that therapeutical application of clonidine in diarrhoea may be successful.

Adenylyl Cyclase Inhibitors↗
PubMed1991

[Malignant hyperthermia and inositol phosphate metabolism in the heart and skeletal musculature].

There are recent reports that inositol phosphate metabolism is involved in the development of malignant hyperthermia (MH). Consequently, we investigated the basal concentration of inositol phosphate products in skeletal and heart muscles of malignant hyperthermia-susceptible (MHS) and healthy control (MHN) swine. Different inositol phosphates were measured by high pressure liquid chromatography, including inositol trisphosphate, tetrakisphosphate, pentakisphosphate and hexakisphosphate. All inositol phosphate products measured had a higher concentration in MHS than MHN in skeletal (304-1330%) as well as heart muscles (134-440%). An activation of the inositol phosphate metabolism has been shown to mobilise intracellular calcium from the sarcoplasmic reticulum. It is therefore concluded that, firstly, besides involvement of the skeletal muscles a primary myocardial abnormality in MHS is possible; and secondly, the idea that the inositol phosphate metabolism could be involved in the development of MH is additionally supported.

Animals↗
PubMed1991

[Ryanodine-induced contractures for the diagnosis of malignant hyperthermia susceptibility].

The halothane-caffeine contracture test is presently the most well-established method for identification of malignant hyperthermia susceptibility (MHS) or non-susceptibility (MHN). However, 10-20% of the patients tested are classified as equivocal (MHE), i.e. their susceptibility remains uncertain. A genetic disorder of the calcium releasing ryanodine receptor has been postulated recently. Therefore, 12 patients were tested in addition to the protocol of the European Malignant Hyperthermia Group (EMHG) for dose- and time-dependent contracture after ryanodine application. In this study, contracture of 0.2g appeared significantly earlier in MHS patients (17.5 +/- 1.7 min; n = 5) during cumulative ryanodine exposition (0.4-0.8-1.6-10.0 mumol/l) than in MHN (38.2 +/- 5.4 min; n = 5). A significant difference between MHS (10.0 +/- 1.7 min; n = 6) and MHN (19.8 +/- 0.6 min; n = 3) was also seen after bolus application of ryanodine (10.0 mumol/l). One patient classified as MHE according to the EMHG protocol, manifested as MHN after the ryanodine contracture test. This study supports previous work suggesting the ryanodine contracture test as an improvement in the in-vitro diagnosis of MH susceptibility.

Adolescent↗
PubMed1991

Possible involvement of inositol-lipid metabolism in malignant hyperthermia.

Alpha-adrenoceptor stimulation may induce malignant hyperthermia (MH) in vivo. Consequently, we have investigated the effects of the alpha-adrenoceptor agonist phenylephrine and, for comparison, the effects of the beta-adrenoceptor agonist isoproterenol on inositol-lipid metabolism of malignant hyperthermia susceptible (MHS) and healthy control (MHN) swine. The experiments were performed on electrically stimulated (frequency 0.2 Hz) trabeculae isolated from the right ventricles of the hearts of MHS and MHN animals. After labelling with [3H]inositol for 6 h, different inositol phosphates were measured by high pressure liquid chromatography, including inositol 1-phosphate, inositol 1,4-bisphosphate, inositol 1,3,4-trisphosphate, inositol 1,4,5-trisphosphate (1,4,5-IP3) and inositol 1,3,4,5-tetrakisphosphate. After stimulation with isoproterenol, the inositol phosphate content did not increase or vary between muscle from MHS and MHN animals. In contrast, all inositol phosphates increased after stimulation with phenylephrine in both muscle types, the effects being greater in MHS than in MHN, especially as regards 1,4,5-IP3 content. As 1,4,5-IP3, a presumed second messenger, has been shown to mobilize intracellular calcium, it is concluded that an enhanced alpha-adrenergic response is involved in the development of MH.

Animals↗
PubMed1991

Effects of caffeine, halothane, succinylcholine, phenylephrine and isoproterenol on myocardial force of contraction of malignant hyperthermia susceptible swine.

The effects of caffeine, halothane, succinylcholine, phenylephrine and isoproterenol on force of contraction were studied in electrically driven (0.2 Hz) trabeculae isolated from the right ventricles of the hearts of malignant hyperthermia susceptible (MHS) and healthy control (nMHS) swine. Caffeine (0.1-10 mmol/l) had positive inotropic effects, amounting to 275 +/- 35% of control in nMHS and 268 +/- 34% in MHS (n = 16). Halothane (0.25-4 vol%) decreased the force of contraction maximally to 52 +/- 4% in nMHS and 51 +/- 5% of control in MHS (n = 16). Propranolol did not change these effects. Succinylcholine (0.1-10000 mumol/l) had a small positive inotropic effect in both groups, which was blocked by propranolol. Phenylephrine (0.1-300 mumol/l) increased the force of contraction maximally to 188 +/- 24% of control in nMHS and to 193 +/- 23% in MHS (n = 16). The inotropic effect was blocked by prazosin but not by succinylcholine (1 mmol/l). Isoproterenol (0.01-10 mumol/l) had a positive inotropic effect of maximally 275 +/- 21% of control in nMHS and 396 +/- 31% in MHS (n = 17) (P less than 0.05). Succinylcholine potentiated this effect, and propranolol shifted the concentration-response curves to the right. We conclude that caffeine, halothane, succinylcholine and phenylephrine have similar inotropic effects in the hearts of nMHS and MHS, whereas isoproterenol has a significantly greater effect in MHS than in nMHS.

Animals↗
PubMed1991

[Metal-cancellous bone femoral component and total endoprosthesis for surgical treatment of malignant tumors].

Adequate surgical treatment of malignent tumors of the femur requires radical bone resection with resulting major bone defects. Using the uncemented cancellous bone/metal femoral component or a total prosthesis limb-preserving surgery is possible. Reliable primary and secondary fixation ensures good functional results. The surgical procedure is described on the basis of several cases.

Bone Transplantation↗
PubMed1990

Effects of carbachol and (-)-N6-phenylisopropyladenosine on myocardial inositol phosphate content and force of contraction.

1. The effects of carbachol and the A1-adenosine receptor agonist (-)-N6-phenylisopropyladenosine (PIA) on force of contraction and inositol lipid metabolism were studied in electrically driven left auricles and papillary muscles isolated from guinea-pig hearts. Both carbachol and PIA (0.01-10 microM) had concentration-dependent negative inotropic effects in auricles. In papillary muscles PIA had no inotropic effect. Carbachol also had no inotropic effect at low concentrations (0.01-1 microM) but at 10-100 microM it exerted a slight positive inotropic effect. 2. In auricles and papillary muscles both carbachol and PIA concentration-dependently increased inositol trisphosphate (IP3; significant at 1 microM). Accordingly phosphatidylinositol bisphosphate (PIP2), the precursor of IP3, was reduced. All effects of carbachol and PIA were antagonized by atropine (10 microM) and 1,3-dipropyl-8-cyclopentylxanthine (DPCPX; 20 microM) respectively, indicating receptor-mediated effects. 3. In auricles the negative inotropic effects of carbachol and PIA preceded the increase in IP3. 4. In papillary muscles the increase in IP3 preceded the slight positive inotropic effect of carbachol, indicating that the M-cholinoceptor-mediated increase in IP3 and force of contraction may be related. However, PIA showed a comparable increase in IP3 but no inotropic effect, indicating a dissociation between those parameters. 5. In conclusion, in previous studies a close relation between increases in IP3 and force of contraction has been shown after alpha 1-adrenoceptor stimulation. The present study with carbachol supports this view. However, the present data for PIA could not show such a close relationship, questioning the role of IP3 as an endogenous regulator of force of contraction.

Animals↗
PubMed1990

Evidence for the existence of inositol tetrakisphosphate in mammalian heart. Effect of alpha 1-adrenoceptor stimulation.

The time course of the effects of phenylephrine (10 mumol/l) on force of contraction and on inositol phosphates in electrically driven left auricles from rat hearts labeled with [3H]inositol was studied. All experiments were performed in the presence of propranolol (1 mumol/l) and LiCl (10 mmol/l). Products measured after separation with high-performance liquid chromatography were inositol 1-phosphate (1-IP1), inositol 1,4-bisphosphate (1,4-IP2), inositol 1,3,4-trisphosphate (1,3,4,-IP3), inositol 1,4,5-trisphosphate (1,4,5-IP3), and inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP4). All inositol phosphates increased after stimulation with phenylephrine. 1,4,5-IP3 was the first compound to rise maximally within 30 seconds; this rise was followed by an increase in 1,3,4,5-IP4 and 1,4-IP2 beginning within 2 minutes. The increase in 1,3,4-IP3 and 1-IP1 was slower and did not reach steady state within 15 minutes. The positive inotropic effect of phenylephrine was maximal after 5 minutes. It is concluded that the increase in the presumed second messengers 1,4,5-IP3 and 1,3,4,5-IP4 coincides with the positive inotropic effect after alpha 1-adrenoceptor stimulation. Since the increase in 1,4,5-IP3 precedes the increase in force of contraction, 1,4,5-IP3 may initiate the positive inotropic effect of alpha 1-adrenoceptor agonists and 1,3,4,5-IP4 maintains the increase in force of contraction.

Animals↗
PubMed1990

[The effects of incremental PEEP on atrial natriuretic peptide, right atrial pressure and the size of the right atrium in anesthetized patients].

8 ASA class II-III patients (50-67 years) undergoing traumatic-surgical procedures were studied. Since the release of atrial natriuretic peptide (ANP) is stimulated by volume loading and increased right atrial pressure (RAP), the effects of incremental positive end-expiratory pressure (PEEP) on ANP-concentration, RAP and right atrial dimensions were investigated. Anaesthesia was induced with intravenous etomidate and vecuronium and maintained after endotracheal intubation with 66% N2O in O2 and ethrane (0.4-0.6 Vol.-%). A catheter was inserted into the A. radialis for blood sampling and determination of mean arterial pressure (MAP). For determining endsystolic (RAESA) and end-diastolic (RAEDA) areas of the right atrium a 5 MHz transoesophageal echocardiographic (TEE)-probe was positioned at the level of the foramen ovale. Under TEE-control a catheter was placed into the right atrium for measurement of RAP. The method for ANP determination was based on a direct radioimmunoassay that is specific for human ANP (ANP-J125). PEEP was incrementally raised from 0 to 16 mbar in 4 mbar steps each for 5 min and thereafter reduced to 0 mbar. During the investigation no significant differences were detectable for MAP, heart rate, end-expiratory CO2 partial pressure and the arterial O2 saturation. However, 16 mbar PEEP ventilation increased plasma ANP concentrations (from 44.3 +/- 9.7 to 58.1 +/- 8.7 pg/ml) and RAP (from 4.4 +/- 0.9 to 10.7 +/- 0.9 mmHg) whereas the right atrial dimensions RAESA (from 9.4 +/- 1.0 to 4.6 +/- 0.6 cm2) and RAEDA (from 5.9 +/- 1.2 to 3.2 +/- 0.4 cm2) decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Cultural expressions affecting patient care.

No course or book will be of value in nursing patients from other cultures unless the nurse uses the knowledge about these cultures provided therein along with his or her own skills of observation, to assess the cultural factors involved in the health care of each individual. Madeline M. Leininger has said that in making a cultural assessment, "We talk to the members of the family as well as the patient about their health values, beliefs, and practices. Some of the many things we explore are how they keep well, who helps them when they're sick, and what folk remedies they use". Leininger further notes (1980) that "like a flowing river, culture is the underlying force that guides people's preferences and their thinking and action patterns." Many cultures have large networks of people who help out in times of illness and stress. Dr. Leininger says, "They are expected to be caring persons; it's a culturally defined role". To understand the process of how the cultural milieu affects responses to an illness like cancer, the patient must be viewed as a member of a family. This family, in turn, is influenced by its membership in an ethnic or minority group, which defines for the family members the culturally prescribed beliefs and behaviors that are acceptable. These beliefs and behaviors form the foundation upon which these individuals view illness, as well as outline how they respond to the diagnosis and the disease itself. As nurses, we must be interested in learning about and understanding the influence that culture has on our patient care. It is hoped that the information in this article will increase your knowledge base and give you greater insight into your patients because the "need to know" will continue to grow as health care clients increasingly demand and expect both respect and the effective application of their cultural beliefs and values to their health care.

Cultural Characteristics↗
PubMed1989

[Inositol trisphosphate, a new "second messenger" for positive inotropic effects on the heart?].

Myocardial alpha 1-adrenoceptors mediate a positive inotropic effect and influence the inositol phosphate cycle. The receptor-stimulated, phospholipase C-mediated hydrolysis of phosphatidylinositol bisphosphate (PIP2) results in the generation of two novel second messengers, inositol trisphosphate (IP3) and diacylglycerol (DG). This effect is concentration-dependent and precedes the increase in force of contraction. Recently, it has been shown that the alpha 1-adrenoceptor-mediated increase in IP3 and force of contraction exists in the human heart as well. Possible mechanisms for an inositol phosphate-mediated positive inotropic effect are: (i) release of Ca2+ from the sarcoplasmic reticulum, elicited by IP3, (ii) increase in Ca2+ sensitivity of the contractile proteins, elicited by IP3, inositol tetrakisphosphate (IP4) and/or DG, (iii) increase in slow Ca2+ inward current, elicited directly by IP4 and/or indirectly by DG through a phosphorylation of the protein kinase C substrate in the sarcolemma. In ventricular cardiac preparations muscarinic agonists have a weak positive inotropic effect, but in cardiac atrial preparations they have a negative inotropic effect. In both preparations, these different effects coincide with a concentration-dependent increase in IP3. Thus, the possible positive inotropic effect in atrial preparations is probably masked by an activation of a K+ outward current. The relationship between the inositol phosphate cycle and the positive inotropic effect is in some points still speculative because not all of the mechanisms discussed are well settled yet. However, the stimulation of myocardial phosphoinositide breakdown resulting in an increased IP3 may be involved in the mechanism(s) whereby alpha1-adrenergic and muscarinic receptor stimulation exert an increase in myocardial force of contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Epidemiology of molluscum contagiosum using genetic analysis of the viral DNA.

The molecular epidemiology of molluscum contagiosum virus (MCV) infections was investigated by restriction endonuclease analysis of the genomes of 222 separate isolates collected from 147 patients living in Germany (33 patients), Hong Kong (6 patients), and Scotland (108 patients). MCV type 1 (MCV-1) caused 96.6% of the infections, and MCV type 2 (MCV-2) caused 3.4%. However, isolates from four of the 142 MCV-1-infected patients and two of the five MCV-2-infected patients showed minor differences in their DNA restriction patterns because of the loss of a single or very few recognition sites for the enzymes used. No genome variations were detected amongst isolates collected from different sites or on several occasions from individual patients or from closely related patients. Southern blot hybridization revealed a high level of relatedness between MCV-1 and 2. No differences were seen in the appearance or anatomical localization of lesions caused by either virus type. In particular, there was no preferred genital localization for MCV-2 infections.

Adolescent↗