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Biomedical subjects

N Mayer

Publications and source records attributed to N Mayer.

At least 73 records · Page 4Linked to original sources
PubMed1983

[Effects of morphine on the control of the cardiovascular system by the carotid-sinus-reflex and by the carotid chemoreflex].

The effects of morphine (2 mg/kg i.v.) on the carotid baroreceptor control and the carotid chemoreceptor control of the circulation were examined in 12 chronically instrumented dogs. Bilateral carotid occlusion in conscious dogs with spontaneous ventilation increased heart rate (decrease in cardiac cycle length by 19 +/- 2%; mean +/- S.E.M.), mean arterial pressure (38 +/- 3%) and mean iliac resistance (33 +/- 11%). Morphine, however, failed to change these reactions significantly. Chemoreceptor stimulation, accomplished by intracarotid injections of nicotine (4-8 micrograms), in conscious dogs with spontaneous ventilation elicited complex effects on heart rate and mean iliac resistance--due to secondary stimulation of pulmonary inflation reflexes. Chemoreceptor stimulation in conscious dogs with ventilation controlled increased cardiac cycle length (246 +/- 17%) and elicited intense iliac vasoconstriction, i.e. mean iliac resistance rose by 288 +/- 25%. Morphine significantly (p less than 0.01) attenuated the increase in cardiac cycle length and in iliac resistance with chemoreceptor stimulation (42 +/- 10% and 64 +/- 9%, respectively). Thus, morphine interferes with the carotid chemoreceptor control of the circulation while the efficacy of the carotid-sinus-reflex seems to be well maintained.

Animals↗
PubMed1983

[Effect of morphine on circulatory control in acute progressive hemorrhage].

The effects of acute, progressive haemorrhage, 1 ml/s were examined in the same mongrel dogs on separate days, unanaesthetized and anaesthetized with morphine (2 mg/kg i.v.) and with administration of nasal oxygen to maintain arterial blood gases at physiological levels. In normal, unanaesthetized dogs mean arterial pressure was well maintained through 30 ml/kg of blood loss. Cardiac output fell with haemorrhage (70 +/- 2%; mean +/- S.E.M.) but heart rate and total peripheral resistance rose by 72 +/- 11% and by 124 +/- 11%, respectively. Morphine induced slight but significant changes in heart rate and mean arterial pressure but did not affect the ability to withstand hemorrhage. Thus, in contrast to barbiturates and volatile anaesthetics, morphine does not seem to comprise the efficacy of the rapidly acting pressure control system in response to progressive hemorrhage. The results of the present investigation are not consistent with the hypothesis that opioids are hypotensive factors in hypovolaemic shock.

Acute Disease↗
PubMed1982

[Cardiac and peripheral vascular effects of the volatile inhalational anaesthetic enflurane in chronically instrumented dogs (author's transl)].

While enflurane is generally held to induce arterial hypotension, its overall effects on left ventricular (LV) performance are less clear. Accordingly, mongrel dogs were chronically instrumented with miniature LV pressure transducers, with aortic and left atrial catheters and with electromagnetic flow probes and hydraulic cuff occluders on a common iliac artery. A pair of ultrasonic transducers was implanted on opposing endocardial surfaces to measure LV internal minor axis diameter. Experiments were performed 2 to 9 weeks after surgery when the animals were resting quietly without premedication. Enflurane (2 and 4 vol.-%) decreased mean arterial pressure by 27% and 36% and led to a progressive, dose-dependent decrease in myocardial contractility and induced striking peripheral vasodilatation, i.e. LV-dP/dtmax was reduced by 32% and 54% and iliac conductance rose by 101% and 163%. However, the decrease in contractility was not associated with an increase in LV preload, i.e. LV-end-diastolic diameter was decreased by 2 vol.-%, while it was not significantly different from control values with 4 vol.-%. Thus, in intact chronically instrumented dogs the direct negative inotropic effect of enflurane is modified by a synchronous decrease in myocardial loading conditions.

Aerosols↗
PubMed1982

Effects of antibodies against nerve growth factor on the postnatal development of substance P-containing sensory neurons.

Administration of anti-nerve growth factor (NGF)-antibodies to newborn rats produces a marked but reversible reduction of the substance P content in dorsal root ganglia. This is in contrast to the effect of anti-NGF-antibodies on sympathetic ganglia, where they cause a destruction of the adrenergic neurons as is evident in the irreversible reduction of tyrosine hydroxylase activity.

Animals↗
PubMed1980

Requirement of nerve growth factor for development of substance P-containing sensory neurones.

The protein nerve growth factor (NGF) is known to be essential for the maturation and maintenance of adrenergic neurones and for the development of sensory neurones during critical stages of embryonic life. The investigation of the physiological importance of NGF for the development of sensory neurones has been hampered so far by the lack of biochemical marker substances for these neurones. The demonstration that the undecapeptide substance P(SP) is present in sensory neurones suggests that it might be such a marker. SP is synthesized in dorsal root ganglia (DRG) and transported to the terminals of C-fibres located in the dorsal horn of the spinal cord and in the skin. Its release can be demonstrated from the central and peripheral endings of sensory nerve fibres which seem to have an important role in pain perception. We have investigated the effects of NGF and of purified anti-NGF antibodies on the content of SP in rat DRG and in their respective target organs, namely the spinal cord and the skin. The effects on sympathetic ganglia were included in order to control the effectiveness of both NGF and its antibody. We report here that NGF leads to an increase in SP in spinal ganglia, as previously shown by Kessler and Black. However, in contrast to these authors, we describe that the administration of anti-NGF antibodies produces a marked reduction of the SP content in sensory neurones and in their respective nerve terminals.

Animals↗
PubMed1980

Regional distribution and biochemical properties of 125I-Tyr8-substance P binding sites in synaptic vesicles.

1. Binding of 125I-Tyr8-substance P (SP) to synaptic vesicles shows an uneven distribution within the brain and the spinal cord. The regional distribution has a positive correlation with the SP-content, except in the hypothalamus. 2. Ca2+ and MG2+-ions (1 and 10 mM) decrease the number of binding sites without alteration of affinity. EDTA and EGTA enhance SP-binding which is interpreted as being due to removal of the inhibitory influence of endogenous Ca2+ and Mg2+ through chelation with these agents. No significant inhibition of SP binding was observed by Na+ or K+ in concentrations below 100 mM. 3. Pretreatment of synaptic vesicles with trypsin or with phospholipase A2, C and D leads to a total loss of SP binding showing a proteolipid or a joint protein-phospholipid nature of these binding sites. SH groups do not contribute to SP binding since no effect of N-ethylmaleimide and monoidoacetic acid on SP binding was found.

Animals↗
PubMed1980

Effect of capsaicin pretreatment on substance P binding to synaptic vesicles.

Newborn or adult rats were pretreated with 50 mg kg-1 capsaicin. At the age of 2 to 4 months, binding of 125I-labelled Tyr8-substance P to synaptic vesicles prepared from different regions of the nervous system was examined. In both groups, capsaicin pretreatment led to a significant decrease in the number of binding sites in dorsal roots and spinal cord without having an effect on affinity. This decrease parallels the depletion of the substance P content (Gamse et al., 1980) and can be explained by degeneration of primary sensory neurons in newborn treated rats and by depletion of vesicles in adult treated rats.

Aging↗
PubMed1980

Hybridoma cell lines secreting monoclonal antibodies to mouse H-2 and Ia antigens.

Hybridoma cell lines secreting antibodies to mouse H-2 or Ia antigens have been generated by fusing mouse immune lymphocytes with appropriate myeloma lines. Among the 11 established clones reported here, nine produce anti-H-2 antibodies and two produce anti-Ia antibodies. The specificities and cross-reactions of these monoclonal antibodies have been studied in detail. One hybridoma antibody reacted only to Kk antigens without any detectable cross-reactions, thus suggesting reaction to a private specificity of the Kk molecule. All other anti-H-2 hybridoma antibodies appeared to detect public specificities as defined either by reactions with products of more than one H-2 locus or with different alleles at one or more loci. The two anti-Ia antibodies both reacted with I-E/C products, but exhibited different cross-reactivity patterns. Strain distribution analyses so far indicate that the public specificities detected by these monoclonal antibodies are considerably different from those that had been established by traditional serology. Since public specificities defined by the hybridoma antibodies must by definition represent cross-reactions, these findings may have important implications relating to the structure and evolution of MHC gene products.

Animals↗
PubMed1979

Substance P: model studies of its binding to phospholipids.

1. The partition of substance P (SP) between buffer solutions (pH 1.6--7.8) and an organic, phospholipid (phosphatidyl serine, phosphatidyl ethanolamine, phosphatidyl inositol and phosphatidyl choline) containing phase (chloroform:methanol 2:1) was studied. 2. The binding of SP to phosphatidyl serine, phosphatidyl ethanolamine and phosphatidyl inositol was lowest at pH 2 and increased with pH. The binding to phosphatidyl choline was much smaller and less dependent on pH. 3. In contrast to the basic peptide SP (pI 10.5), physalaemin (pI 7.0) did not show any binding to phospholipids at any investigated pH value which underlines the importance of a basic group in the peptide for its binding. 4. The high affinity (KD = 0.1 microM) and capacity of 44 pmol SP/microgram phosphatidyl serine and 48 pmol SP/microgram phosphatidyl ethanolamine at pH 7.2 under conditions of saturation contrasted with the very low binding of SP to phosphatidyl inositol or phosphatidyl choline. Ionic bindings between the basic peptide and phosphatidyl serine or phosphatidyl ethanolamine are regarded to be predominant, although other binding forces cannot be excluded. 5. There was a concentration-dependent reduction in the binding of SP to phosphatidyl serine or phosphatidyl ethanolamine by Na+ and Ca2+, whereas K+ showed hardly any effect at physiological concentrations. 6. The model studies served to consider the possibilities of the binding of a basic peptide to lipid storage or receptor sites.

Animals↗
PubMed1979

Substance P: characteristics of binding to synaptic vesicles of rat brain.

1. The binding of substance P (SP) to synaptic vesicles from rat brain was studied by use of the 125I-Tyr8-analogue of SP. 2. The pH dependence of the binding of both peptides to the lipid extractable fraction of synaptic vesicles was shown to be comparable. 3. The binding of 125I-Tyr8-SP shows a rate constant of association (k1 = 6.6 x 10(6) M-1 S-1), a rate constant of dissociation (k-1 = 6.4 x 10(-4) S-1) and gives a KD of 1 x 10(-10) M. Kd derived from equilibrium studies was 3.2 x 10(-10) M. 4. The binding of 125I-Tyr8-SP to lipids of synaptic vesicles was shown to be reversible, saturable and highly specific. 5. The kinetic data suggest one population of binding sites with a maximal number of 0.8 pmol per mg protein of the synaptic vesicle preparation. 6. Unlabeled SP and the (2--11)-, (3--11)- and (4--11)-analogues of SP inhibit the binding of 125I-Tyr8-SP in a decreasing order in a competitive way when added in excess. Tyr8-SP and eledoisin did not interfere with the binding of 125I-Tyr8-SP whereas uperolein and neurotensin caused a partial inhibition. Physalaemin and D-Ala2-D-Met5-enkephalin enhance the binding of 125I-Tyr8-SP in a cooperative way.

Animals↗
PubMed1978

Substance P: binding to lipids in the brain.

1. Substance P (SP) could be extracted from brain homogenates with chloroform-methanol by a method which extracts all lipids. 2. SP could be transferred form this total lipid extract (TLE) into an aqueous solution at low pH values (2.0--3.0). 3. At higher pH values (5.5) SP could be transferred from an aqueous phase into an organic phase (chloroform:methanol, 2:1) and recombined with TLE (which was previously freed from endogenous SP) contained in this phase. The binding capacity of TLE for SP exceeded by far the amount of endogenous SP bound originally in the brain extracts. 4. Among the lipids present in TLE, phosphatidylserine was able to bind and release SP in a pH dependent manner. 5. It is suggested that SP bound to phosphatidylserine is the storage form of SP in the brain. The mechanisms by which it is released are still unknown. The possibility that the SP-receptor is also a phospholipid is considered.

Animals↗
PubMed1978

The Baron revisited: a case report.

The Munchausen patient seeks hospital care to satisfy a masochistic streak and is willing to undergo operations and painful hospital procedures while at the same time being abusive and aggressive. He often uses an argument with hospital personnel as an excuse to leave against medical advice. The diagnosis is rarely made in the emergency department but might be made more frequently if lists of known "Munchausens" were circulated through emergency department and if emergency physicians were more aware of the problem. The physician in doubt, however, will do better to risk being fooled and manage the patient as if his complaints were real. One such case is reported.

Emergency Service, Hospital↗
PubMed1977

Substance P in rat brain synaptosomes.

1. Rat brain synaptosomes were incubated under different conditions to study the release of substance P (SP). 2. Potassium ions and electrical field stimulation induced a loss of SP from synaptosomes. The release of SP by potassium in high concentrations (23.8 mM) was shown to be calcium dependent. 3. Substance P was retained in synaptosomes during incubation in 0.32 M sucrose at +4 degrees C up to 120 min. During incubation at 30 degrees C the SP content fell initially (30 min) but was gradually restored (120 min). 4. If these pre-incubated synaptosomes were reincubated for 45 min at 30 degrees C in potassium free Krebs-Ringer-phosphate buffer a further rise in their SP content occurred which was taken as indication that SP is being synthesized in synaptosomes. 5. The newly synthesized SP is presumably stored by binding to phosphatidyl serine until a sudden release is initiated by depolarization.

Animals↗