Control of communicable disease. A problem shared.
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Communicable Disease Control↗
Biomedical subjects
J Chalmers
Publications and source records attributed to J Chalmers.
Stress-induced activation of CRF and c-fos mRNAs in the paraventricular nucleus are not affected by serotonin depletion.
The role of serotonin in regulating the stress response is controversial. We have investigated the effects of serotonin depletion by p-chlorophenyl-alanine (PCPA) on corticotrophin-releasing factor (CRF) mRNA and c-fos mRNA responses in the paraventricular nucleus (PVN) together with circulating levels of ACTH and corticosterone to both physical and psychological stressors in the rat. PCPA pretreatment, which resulted in a 95% depletion in hypothalamic serotonin, had no effect on basal levels of ACTH or the increase in response to the physical stress of hypertonic saline. Plasma ACTH concentrations were also not affected by serotonin depletion in response to the predominantly psychological stress of restraint. Both basal and restraint stress-induced circulating corticosterone levels were however further stimulated in the PCPA-pretreated rats suggesting a possible inhibitory serotoninergic tone at the adrenal level. C-fos mRNA was undetectable in control animals. Activation of c-fos mRNA in response to stress was unaffected by serotonin depletion and the activation of magnocellular PVN and supraoptic nucleus cells was demonstrated to be stressor dependent. Basal and stress-induced levels of CRF mRNA were unaffected by PCPA pretreatment. It appears therefore that under these experimental conditions there is little if any involvement of serotonin in either basal levels or the stress-induced activation of the hypothalamo-pituitary-adrenal axis in vivo.
Adrenocorticotropic Hormone↗
Vasodepressor neurons in medulla alter cardiac contractility and cardiac output.
We injected neuroexcitatory and neuroinhibitory agents into the depressor region of the caudal ventrolateral medulla of anesthetized rabbits and determined the effect on arterial pressure, myocardial contractility, cardiac output, and plasma catecholamines and neuropeptide Y. Brief excitation of the sympathoinhibitory neurons with medullary injection of L-glutamate reduced arterial pressure, peripheral vascular resistance, and myocardial contractility. Cardiac output was unaffected. Prolonged inhibition of the sympathoinhibitory neurons with medullary injection of muscimol increased arterial pressure, peripheral vascular resistance, and myocardial contractility. There was a progressive fall in cardiac output. These changes were accompanied by an increase in plasma neuropeptide Y and plasma norepinephrine, but no change in plasma epinephrine. Our findings indicate that the sympathoinhibitory vasomotor neurons in the caudal ventrolateral medulla tonically suppress the activity of sympathetic preganglionic neurons controlling myocardial contractility as well as peripheral vasomotor tone. Dysfunction of these medullary neurons could underly some forms of experimental hypertension.
Animals↗
Riedel's thyroiditis complicated by hypoparathyroidism and hypothyroidism.
Riedel's thyroiditis is a rare condition in which the thyroid gland is replaced by fibrous tissue. The case reported is one of Riedel's thyroiditis complicated by hypoparathyroidism and hypothyroidism. There would appear to have been only five earlier reports in the literature of hypoparathyroidism complicating Riedel's thyroiditis.
Female↗
The place of combination therapy in the treatment of hypertension in 1993.
"Step Care" fell into disuse following the advent of the ACE inhibitors and calcium antagonists. This was partly because the potency of these agents encouraged their use in monotherapy, and partly because of dissatisfaction with ritual treatment using multiple drugs. However monotherapy too has its problems, not the least of which is ritual increase in the dose of the first drug prescribed, leading to prolonged treatment with high doses and hence an increase in side effects. It is therefore important to consider changing to an alternative drug rather than automatically increasing the dose, or adding a second drug. Combination therapy still has a major place in the treatment of hypertension. It is necessary in patients with severe hypertension, with clinical manifestations of target organ damage, or with associated conditions that often help the doctor to choose a rational combination. Even in patients with uncomplicated mild hypertension, the achievement of goal blood pressure requires combination therapy in around half the cases. By choosing two drugs from appropriate classes of agent, it is possible to add the primary actions of drugs acting through different mechanisms, while opposing the homeostatic compensations that limit the fall in blood pressure. Effective combinations therefore maximise hypotensive efficacy while minimising side effects. Effective combinations for the treatment of classical and of systolic hypertension, are discussed.
Aged↗
Enthesopathy as the presenting feature of X-linked hypophosphatemia. A case report.
X-linked hypophosphatemia has a wide spectrum of clinical presentation. I describe a woman in whom diffuse enthesopathy was the only manifestation. The diagnosis was established from the family history. The severity of the enthesopathy did not relate to the severity of the biochemical changes.
Family↗
Round table 2. First-line drugs: the position of the World Health Organization-International Society of Hypertension.
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Antihypertensive Agents↗
Are the ventrally projecting dendrites of respiratory neurons a neuroanatomical basis for the chemosensitivity of the ventral medulla oblongata?
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Animals↗
Removal of metal implants after fracture surgery--indications and complications.
In a study of 297 internal fixation operations for fractures or joint injuries performed during 1982, a second operation for implant removal was undertaken in 42% of cases. Significant complications occurred following the second procedure in 19%. Implants which were retained did not give rise to appreciable problems. It is suggested that implants should only be removed when there are clear clinical indications for doing so.
Arm Injuries↗
Sympathetic preganglionic neurons projecting to the adrenal medulla and aorticorenal ganglion in the rabbit.
The distribution of sympathetic preganglionic neurons (SPN) projecting to the adrenal medulla and the aorticorenal ganglion in the rabbit was studied using a dual retrograde transport technique. The B subunit of cholera toxin (CTB) was injected into the left adrenal medulla and wheatgerm agglutinin-apo-horseradish peroxidase-7 nm gold (WGA-apo-HRP-gold) was injected into the left aorticorenal ganglion. Retrogradely transported CTB was detected by immunohistochemistry, while gold particles were detected by silver intensification. SPN projecting to the adrenal medulla were observed in segments T2-L2 of the spinal cord in 5 rabbits, with the majority of cells within segments T6-T11 (79%). SPN projecting to the aorticorenal ganglion were seen in segments T2-L1 of the spinal cord in 5 rabbits, with the greatest number of the cells within T6-T11 (81%). Only a small number of doubly labelled cells (1%) were found in two rabbits. The results suggest that despite their similar segmental distribution SPN projecting to the adrenal medulla or the aorticorenal ganglion belong to separate populations and few, if any, individual SPN have axonal projections to both locations.
Adrenal Medulla↗
Substance P immunoreactive boutons form synapses with feline sympathetic preganglionic neurons.
In this study, the relationship between substance P-immunoreactive boutons and antidromically activated sympathetic preganglionic neurons was examined by light and electron microscopy. Sympathetic preganglionic neurons in the T2-T4 spinal segments of the cat were identified by intracellular recording and antidromic activation from the corresponding white ramus. Neurons were filled with lucifer yellow and then stained to reveal, simultaneously, substance P and lucifer yellow immunoreactivity. All of the neurons examined with the light microscope (n = 13) received appositions from substance P-immunoreactive boutons. Appositions were found on all parts of the neuron, including the somata, dendrites, and axon initial segment. In most cases (11/13) few close appositions were seen; however, two neurons received large numbers of appositions from substance P-immunoreactive boutons. On one neuron, 16 substance P-immunoreactive varicosities that were identified as being closely apposed at the light microscope level were serially sectioned and examined with the electron microscope. Of these 16 varicosities, eight either directly contacted the neuron or formed morphologically identifiable synapses. The remaining eight varicosities were separated from the neuron by thin glial processes. Two other sympathetic preganglionic neurons that were examined ultrastructurally also received substance P-immunoreactive synapses and close contacts. These findings suggest that substance P-containing nerve fibres could affect all sympathetic preganglionic neurons but are likely to be important in regulating the activity of only a small proportion of these neurons.
Animals↗
Sympathetic preganglionic neurons in rabbit spinal cord that project to the stellate or the superior cervical ganglion.
The segmental distribution of sympathetic preganglionic neurons in the rabbit spinal cord that project to the stellate or the superior cervical ganglion was determined using retrograde tracing with cholera toxin B subunit from the stellate ganglion and wheat germ agglutinin-apo-horseradish peroxidase-gold from the superior cervical ganglion. Sympathetic preganglionic neurons that projected to the stellate ganglion were located in spinal segments T1 to T10. Sympathetic preganglionic neurons projecting to the superior cervical ganglion were found in segments T1 to T8. Both types of neuron had somata that were elongated in the rostrocaudal direction, and dendrites that were mainly confined to the intermediolateral cell column. Almost 95% of the neurons supplying the superior cervical ganglion had axons that passed through the stellate ganglion.
Animals↗
The metabolism of aminoacetone to methylglyoxal by semicarbazide-sensitive amine oxidase in human umbilical artery.
The aliphatic amine aminoacetone has been described previously as a product of mitochondrial metabolism of threonine and glycine. Here, aminoacetone is shown to be deaminated to methylglyoxal by supernatants obtained by low speed centrifugation (600 g/10 min) of human umbilical artery homogenates, and also by membrane fractions isolated by high speed centrifugation (105,000 g/60 min) of these supernatants. Metabolism of 100 microM aminoacetone was completely inhibited by 1 mM propargylamine and MDL 72145, drugs which are capable of inhibiting the membrane-bound semicarbazide-sensitive amine oxidase (SSAO) activity found in vascular smooth muscle cells, whereas 1 mM pargyline and deprenyl which are inhibitors of monoamine oxidase, were without inhibitory effect. Estimated kinetic constants (at pH 7.8) for aminoacetone metabolism were Km = 92 microM; Vmax = 270 nmol/hr/mg protein. In addition, aminoacetone was a competitive inhibitor (Ki = 83 microM and 128 microM in low speed supernatants and high speed membrane fractions, respectively) of [14C]benzylamine metabolism by SSAO in this tissue. Aminoacetone would appear to be an endogenously occurring amine with a Km for metabolism by SSAO far lower than other aliphatic and aromatic biogenic amines examined previously as potential physiological substrates for the human vascular enzyme and possible implications of this are discussed.
Acetone↗
Setting a strategy for health.
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Health Care Rationing↗
Interactions of endogenous opioid and excitatory amino acid inputs to the caudal ventrolateral medulla of the rat.
This study investigated the cardiovascular consequences of interactions between endogenous opioid and excitatory amino acid inputs to the caudal ventrolateral medulla of the anaesthetised rat. Drugs were injected bilaterally into the functionally identified depressor region of the caudal ventrolateral medulla. The opioid antagonist, naloxone (2.5-8.0 nmol/side) elicited a dose-dependent decrease in blood pressure and a bradycardia. The NMDA-receptor antagonist, 2-amino, 5-phosphonovaleric acid (2-APV; 1.25-500 pmol/side), dose-dependently increased blood pressure but had little effect on heart rate. After the maximum dose of naloxone, the pressor response to both 1.25 and 25 pmol/side of 2-APV was attenuated by 89 and 66%, respectively. By contrast, the pressor response, elicited by injection of the GABA agonist, muscimol (1 pmol/side), was not affected. After 2-APV (500 pmol/side), the depressor response to 2.5 nmol/side of naloxone was enhanced by 84%, although this effect was lost when a larger dose of naloxone (5 nmol/side) was used. 2-Amino,5-phosphonovaleric acid also potentiated the depressor response to a submaximal dose of the GABA antagonist, bicuculline (2 pmol/side). The results suggest firstly that, in the caudal ventrolateral medulla, excitatory amino acid inputs are functionally less important when tonic opioid effects are blocked. This interaction appears to be pharmacologically specific. Secondly, tonic inhibitory inputs, whether due to opioids or to GABA, are functionally more effective after excitatory amino acid inputs are antagonized.
2-Amino-5-phosphonovalerate↗
Haemodynamic and neurohumoral response in heart failure produced by rapid ventricular pacing.
OBJECTIVE: The aim was to determine the exact sequence of hormone changes during the progression of fluid retention in a canine model of "congestive cardiac failure" induced by rapid right ventricular pacing, and during recovery when pacing is stopped. METHODS: Rapid ventricular pacing at a rate of 250 pulses.min-1 was used in six mongrel dogs with implanted right ventricular pacemakers. Right heart haemodynamics were measured by means of Swan Ganz catheterisation, allowing flow measurement by thermodilution and pressure measurement by external manometry. Plasma renin activity, arginine vasopressin, and atrial natriuretic factor were assayed on venous blood samples by radioimmunoassay. Noradrenaline was assayed by high pressure liquid chromatography. RESULTS: The onset of rapid pacing was accompanied by a fall in cardiac output and a rise in pulmonary arterial, pulmonary capillary wedge, and right atrial pressures. Noradrenaline and atrial natriuretic factor rose. Plasma renin activity showed an initial fall followed by a rise, and arginine vasopressin was unchanged in the first 8 h. When rapid pacing was continued for a further 35 d, clinical signs of fluid retention appeared by day 28, by which time cardiac output had fallen, and central pressures risen further. Atrial natriuretic factor peaked at around 14 d whereas plasma renin activity, arginine vasopressin, and noradrenaline tended to reach a plateau at about d 20 and then to show further increases as clinical signs of fluid retention appeared; this was most marked with plasma renin activity. Cessation of pacing at d 35 caused a rapid reversal (increase) of cardiac output but a more gradual reversal (decrease) of right heart pressures over 5 d; only wedge pressure returned to base line. Arginine vasopressin and plasma renin activity fell rapidly to around 40% of the final pacing levels and reached basal values after 8 h and 48 h respectively. Noradrenaline fell after 8 h and reached basal levels in 5 d. Atrial natriuretic factor fell quickly by 60% after 8 h but remained above basal levels for 5 d. At the end of pacing, body weight fell rapidly in conjunction with a large diuresis. CONCLUSIONS: These findings are compatible with a major role of one or more of renin, vasopressin, and noradrenaline in the pathophysiology of the fluid retention of heart failure; the manifestations are not counteracted by the rise in atrial natriuretic factor.
Animals↗
Ventral medulla stimulation increases blood pressure and spinal cord amino acid release.
Microdialysis in combination with HPLC and fluorescence detection was used to measure the release of endogenous amino acids from the region of the intermediolateral cell column of rat thoracic spinal cord in response to electrical stimulation of the rostral ventrolateral medulla (RVLM). Stimulation of the RVLM led to a marked rise in blood pressure (74 +/- 6 mm Hg) accompanied by an immediate increase in the release of glutamate (80%) and aspartate (50%). Small increases in the release of glycine and taurine were found, but there were no changes in alanine and serine release. These results suggest that the RVLM pressor pathway to the thoracic spinal cord may use, at least in part, excitatory amino acids as neurotransmitters, supporting previous pharmacological and neuroanatomical investigations of this bulbospinal pathway.
Alanine↗
Kainic acid injection in NTS evokes hypertension and c-fos expression in spinal cord.
Kainic acid injected into rat nucleus tractus solitarius (NTS) caused a slowly developing hypertension, with a 2-fold increase in Fos-immunoreactive (Fos-IR) nuclei in the area of the presympathetic bulbospinal neurons in the rostral ventrolateral medulla (RVLM) and a widespread activation of sympathetic preganglionic neurons (SPN) in the spinal cord, particularly in the mid to lower thoracic cord. The highest segmental concentration of Fos-IR SPN was in T8, with Fos-IR nuclei increased 12-fold compared with the vehicle injected group. More than 60% of retrogradely labelled sympathoadrenal neurons in T8 were Fos-IR after kainic acid injection, consistent with the 60-fold increases in plasma adrenaline levels observed in these rats.
Animals↗