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Biomedical subjects

J R Oliver

Publications and source records attributed to J R Oliver.

At least 37 records · Page 2Linked to original sources
PubMed1991

Correction of incontinent ileocolic urostomy with Kock's nipple valve.

Continent urostomy procedures may be replacing the incontinent ileal or colon conduit as the preferred method of urinary diversion in gynecologic cancer patients. One method of continent urinary diversion utilizes the detubularized ascending and transverse colon as a reservoir with a tapered segment of distal ileum as the stoma through which the patient catheterizes the pouch (Miami pouch). Failures of this procedure have been reported. A case report of such a failure is presented. This patient was managed by replacing the tapered ileal stoma with a Kock intussuscepted nipple valve made from proximal ileum. The patient is now continent. This technique warrants further investigation as a method of treating patients with continent urostomies of various types (Kock, Indiana, Miami, Mainz) that become partially or completely incontinent.

Aged↗
PubMed1991

Afferent vascular resistance control during hemorrhage in normal and autonomically blocked rabbits.

We examined the role of the arterial and cardiac baroreceptors on the hindquarter conductance and heart rate responses of conscious rabbits bled at approximately 3% blood volume (BV)/min to 80% BV (i.e., 20% BV removed). We used rabbits with both sets of baroreceptors working and when only one or neither sets was working. Each animal was studied with normal effector function and during autonomic blockade (hormonal + local effectors), where release of arginine vasopressin (AVP) and renin (angiotensin II, ANG II) were enhanced. The local response (LR) to hemorrhage was determined in a separate group of neurohumorally blocked rabbits. The estimated constrictor response (ECR) was the difference between the LR and net conductance response. In normal rabbits, the ECR was 49 units, with the estimated arterial-to-cardiac barorecptor drive ratio approximately 2.8:1 and with the two receptor groups acting by simple addition. Both barorecptors contributed to the rise in heart rate, with the relative arterial-to-cardiac baroreceptor drive ratio approximately 4:1. When hemorrhage was performed during autonomic blockade, ECR was 84 units (compared with normal rabbits, P less than 0.01), but blood pressure was poorly maintained and the constrictor effect was not under baroreceptor control. Although the baroreceptors were critical for AVP release during autonomic blockade, they played no role in renin release (ANG II production); the latter was released in large amounts, producing near-maximum constriction, which was unrelated to the afferent input. Thus neurally mediated regulation during hemorrhage has substantial advantages over that mediated primarily through the pressor hormones.

Afferent Pathways↗
PubMed1991

Platelet-activating factor stimulates the release of atrial natriuretic factor from the rat heart.

Atrial natriuretic factor (alpha-ANF (99-126), ANF) is released from atrial cells following atrial distension, myocardial infarction and periods of ischaemic or tachyarrhythmias. In this report we demonstrate that platelet-activating factor (PAF) stimulates ANF release from the isolated perfused rat heart and following i.v. injection to conscious unrestrained rats. ANF release peaked at 145% above baseline following injection of 2.5 nmol PAF into the isolated heart while administration of 2 nmol in vivo produced a 135% increase in plasma ANF levels. The PAF receptor antagonist BN52021 (10 mumol/l) attenuated this stimulated release, with the results suggesting a role for PAF in ANF secretion following release from damaged myocardium or as a humoral factor originating from the kidney.

Animals↗
PubMed1990

Neuropeptide Y-immunoreactive synapses in the intermediolateral cell column of rat and rabbit thoracic spinal cord.

Neuropeptide Y (NPY)-immunoreactive nerve fibers in the intermediolateral cell column of rat spinal cord segments T2-T3 and T8-T10 and rabbit segments T3-T6 were studied with light and electron microscopic immunocytochemistry. Plexuses of NPY-immunoreactive nerve fibers were found by light microscopy. NPY-positive synapses were present electron microscopically but non-immunoreactive synapses greatly outnumbered NPY-immunoreactive ones. In the lateral horn of rat T9, 30% of the vesicle-containing NPY-positive axon profiles formed synapses, 95% of which were axodendritic. These synaptic connections may mediate the effects of brainstem NPY neurons on the activity of sympathetic preganglionic neurons.

Animals↗
PubMed1990

Concentrations of plasma atrial natriuretic factor during and after reversion of ventricular tachycardia.

Plasma concentrations of immunoreactive atrial natriuretic factor were considerably increased (mean 745 (376) pg/ml) in 15 patients during spontaneous ventricular tachycardia. There was no significant relation, however, between concentrations of plasma atrial natriuretic factor and systolic arterial blood pressure during tachycardia. Samples taken 30 minutes and 24 hours after reversion of ventricular tachycardia to sinus rhythm showed that, although plasma concentrations of atrial natriuretic factor had fallen significantly, they were still raised after 24 hours. Raised concentrations of atrial natriuretic factor during ventricular tachycardia did not seem to contribute significantly to the hypotension that is often associated with the arrhythmia.

Aged↗
PubMed1990

Reflex release of vasopressin and renin in hemorrhage is enhanced by autonomic blockade.

We determined the relationships during hemorrhage between nominal blood volume (BV) and 1) plasma arginine vasopressin (AVP), 2) plasma renin activity (PRA), and 3) mean arterial pressure (MAP). Conscious rabbits were studied under normal conditions and during total autonomic blockade (TAB) at bleeding rates of 2 and 4 ml/min. Normally, MAP was well maintained until BV had been reduced to approximately 65% of control (termed 65% BV) after which it fell abruptly. The threshold for a rise in AVP was 80-75% BV, followed by exponential rises to levels of 14 and 24 times control at the slow and fast rate of bleeding. PRA rose earlier in hemorrhage, but this rise was more gradual, to values at 60% BV of 5.5 and 7 times control at the two rates of bleeding. During TAB, MAP fell rapidly and both BV concentration curves were shifted to the left with the rises in AVP and PRA/unit delta BV greater than normal; at 75% BV at each rate of hemorrhage, AVP and PRA had risen, respectively, to approximately 40 and 8 times control. Normally, the rises in the AVP and PRA (i.e., angiotensin II) concentrations were modest during the nonhypotensive phase, consistent with their minimal constrictor action observed in a parallel study. During the hypotensive phase, both reached high levels in the constrictor range. During TAB, high concentrations were reached with small BV loss, representing a model of near-maximum release of PRA and AVP.

Animals↗
PubMed1990

Autonomic, hormonal, and local circulatory effects of hemorrhage in conscious rabbits.

Conscious instrumented rabbits were bled at a constant rate of congruent to 3% of the blood volume (BV) per minute. We determined the BV-response relationships for mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), mesenteric and hindlimb blood flows, and for the corresponding conductances. We studied the responses 1) under normal conditions; 2) after pretreatment with captopril, arginine vasopressin (AVP) antagonist, or both; 3) during total autonomic blockade (TAB); and 4) during neurohumoral blockade (NHB, i.e., TAB + captopril + AVP antagonist). We determined the direct local response component from the responses obtained during NHB. The local chronotropic effects congruent to 0, so that the reflex rise in HR was entirely autonomically mediated. The local vascular response consisted of vasodilatation and provided the base line for assessing the estimated constrictor component from the net response from control, with the former ranging from 2 to 16 times the conventional estimates based on the net responses. In normal rabbits, the phase of good maintenance of MAP was entirely governed by autonomic mechanisms, which minimized the fall in CO and offset the local vasodilator component. During the hypotensive phase immediately after hemorrhage, when congruent to 30-35% BV had been removed, the constrictor effects of AVP and angiotensin II (ANG II) became important, whereas the role of autonomic mechanisms diminished. During TAB, the constrictor effects of AVP and ANG II were prominent even with small BV losses.

Animals↗
PubMed1990

The depletion of plasma prolactin by pantethine in oestrogen-primed hyperprolactinaemic rats.

Pantethine was investigated for its potential to deplete prolactin in the plasma and pituitary cells of oestrogen-primed hyperprolactinaemic rats. This compound has been used in the past to deliver cysteamine systemically, through its congener pantetheine, a metabolic precursor for cysteamine. Cysteamine itself, specifically reduces plasma and pituitary prolactin. The addition of pantethine (2-10 mmol/l) to the media of isolated pituitary cells over 4 h did not appreciably alter the intracellular content of immunoreactive prolactin. Moreover, oral administration of pantethine at 0.5 and 1.0 g/kg body weight did not influence the concentration of immunoreactive plasma prolactin. However, the concentration of plasma prolactin fell by 48 and 67%, when pantethine was injected i.p. at 0.5 and 1.0 g/kg body weight, after 4 h. Intravenous administration of pantethine resulted in even greater losses of prolactin, in the order of 50 and 81% depletion for 0.5 and 1.0 g/kg body weight respectively and within 2 h of administration. However, cysteamine was found to be more efficacious than pantethine on a molar basis with regard to depleting the plasma concentration of prolactin in hyperprolactinaemic rats.

Administration, Oral↗
PubMed1990

Effect of cysteamine on the lysosomal enzymes of the hyperprolactinaemic rat pituitary.

The effect of cysteamine on the activity of lysosomal enzymes and the prolactin content of isolated hyperprolactinaemic cells has been investigated. In broken cell preparations, cysteamine markedly stimulated acid prolactin protease activity. In intact cells, however, cysteamine inhibited acid prolactin protease activity and beta-galactosidase. Moreover, the activities of alpha-mannosidase, acid phosphatase, beta-glucuronidase, total arylsulphatase and hexosaminidase were not changed by the addition of cysteamine. Cysteamine significantly depleted the cells of prolactin, and this action was not compromized by the inclusion of either leupeptin, chloroquine or NH4Cl in the incubation media. Taken together, these results indicate that cysteamine does not promote degradation of prolactin and hence depletion of prolactin from the pituitary through a mechanism involving lysosomal enzyme degradation.

Animals↗
PubMed1990

Possible oncostatic action of cysteamine on the pituitary glands of oestrogen-primed hyperprolactinaemic rats.

Cysteamine was investigated for its potential to reduce the size and secretion of oestrogen-primed hyperprolactinaemic rat pituitary glands. Subcutaneous administration of 80 and 120 mg cysteamine/kg significantly reduced plasma prolactin concentrations by 58 and 91% respectively, after 4h. Administration of cysteamine (60 mg s.c./kg body weight per day) for 10 days, to rats which had received an injection of 2 mg oestradiol benzoate on day 1, resulted in a significant reduction in pituitary mass (19%) and GH concentration (21%). Oral administration of 60 mg cysteamine/kg body weight to hyperprolactinaemic rats also produced a significant reduction in plasma prolactin of 94% after 2h. Oral administration of 60 mg cysteamine/kg body weight per day to rats for a 20-day period, during which they had received two injections of 2 mg oestradiol benzoate on day 1 and day 14 of treatment, resulted in a significant reduction in pituitary mass (29%) and the concentration of trunk blood prolactin concentration (35%). However, when oral cysteamine (60 mg cysteamine/kg body weight per day) was given for 20 days to rats which had been treated with 2 mg oestradiol benzoate once every 14 days over a 90-day period, it caused no change in pituitary weight, prolactin or GH concentration, or the concentration of prolactin in trunk blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Growth kinetics of the Lyme disease spirochete (Borrelia burgdorferi) in vector ticks (Ixodes dammini).

Lyme disease spirochetes (Borrelia burgdorferi) multiplied rapidly in larval Ixodes dammini, reaching a mean density of 2,735 spirochetes/tick on day 15 post-repletion. A 5-fold drop in spirochete levels occurred during the subsequent premolting period. Recently molted nymphs contained a mean of less than 300 spirochetes/tick. Following nymphal repletion, spirochete multiplication renewed, reaching a mean abundance of 61,275 spirochetes/nymph on day 75 post-repletion. A 10-fold drop in spirochete abundance occurred again when ticks molted to the adult stage. Tick-derived spirochetes proved to be infectious when greater than 10(4) spirochetes were inoculated ip into hamsters (4 of 4 animals infected). Inocula of 10(3-4) spirochetes were not always infectious (8 of 23 animals infected), and inocula of less than 10(3) spirochetes were insufficient for establishing infection (0 of 8 animals infected).

Animals↗
PubMed1989

Direct and neurohumoral cardiovascular effects of atrial natriuretic peptide.

We studied the hemodynamic changes produced in conscious, chronically instrumented rabbits during steady-state administration of atrial natriuretic peptide (ANP). We administered synthetic alpha-human ANP intravenously (i.v.) at progressively increasing doses of 1, 2, and 4 micrograms/min, each for 30 min. In different experiments in each rabbit, we determined the effects of the peptide under closed-loop conditions in the intact animal and the "direct" circulatory effects of the peptide after "total" blockade of the autonomic nervous system (TAB) and after combined neurohumoral blockade (NHB), where in addition the vascular effects of vasopressin and angiotensin II were also prevented. In intact rabbits, ANP produced a dose-related reduction in mean arterial pressure (MAP, -3 to -14%), which was entirely due to a fall in cardiac output (CO, -14 to -20%), and there was a small rise in total peripheral resistance (TPR 5-12%). Heart rate remained unchanged. In rabbits subjected to TAB and NHB, all hemodynamic effects of ANP were attenuated. There were dose-related falls in left and right atrial pressures which reached maxima of -3.3 +/- 0.9 and -1.8 +/- 0.2 mm Hg, respectively. There was a reversible rise in hematocrit, probably owing to a shift of approximately 8% in blood volume. These effects occurred mainly through direct actions of the peptide, and there was no evidence of systemic vasodilatation. The magnitude of reflex autonomic effects appeared to be less than expected for the observed fall in MAP, suggesting that ANP also inhibited cardiovascular reflexes.

Angiotensin II↗
PubMed1988

The distribution of neuropeptide Y-like immunoreactive neurons in the human medulla oblongata.

We have described the distribution of neuropeptide Y-like immunoreactive neurons in the medulla oblongata of the adult human. The majority of neuropeptide Y-like immunoreactive cells were found in four regions of the medulla: the ventrolateral reticular formation, the dorsomedial medulla, the secondary sensory nuclei and the rostral raphe nuclei. The morphology of neuropeptide Y-like immunoreactive cells varied in each of these regions. In the ventrolateral reticular formation, the labelled neurons were round and pigmented caudal to the obex but elongated and non-pigmented rostral to the obex; in the dorsomedial medulla, they were triangular and pigmented caudal to but not rostral to the obex; in the secondary sensory nuclei, they were multipolar, non-pigmented and significantly smaller than in the other areas; in the rostral raphe nuclei, they were bipolar and non-pigmented. Colocalization studies revealed that many neuropeptide Y-like immunoreactive cells also synthesize monoamines, consistent with conclusions based on a quantitative comparison of their distributions. Neuropeptide Y-like immunoreactivity was present in about 25% of presumed noradrenaline-synthesizing cells in the caudal ventrolateral medulla (corresponding to the A1 region); about 50% of adrenaline- and 70% of presumed serotonin-synthesizing cells in the rostral ventrolateral medulla (C1 and B2-3 regions); 90-100% of presumed noradrenaline-synthesizing cells in the dorsomedial medulla at and above the obex (A2 region); about 50% of adrenaline-synthesizing cells in the rostral dorsomedial medulla (C2 region); about 5% of presumed serotonin-synthesizing cells in the rostral raphe nuclei (B2-3 region). The largest of these groups was the presumed serotonin-synthesizing cells that contained neuropeptide Y-like immunoreactivity in the rostral ventrolateral medulla. This is the first report of such a cell group in the medulla of any mammal, and emphasizes the neuroanatomical differences between humans and other species.

Aged↗
PubMed1988

Plasma atrial natriuretic polypeptide concentrations during and after reversion of paroxysmal supraventricular tachycardias.

Plasma concentrations of immunoreactive atrial natriuretic polypeptide were raised in 22 of 23 patients with paroxysmal supraventricular tachycardia and in all seven patients with atrial flutter. Plasma concentrations of atrial natriuretic polypeptide rose soon after the onset of supraventricular tachycardia. A sample taken 30 minutes after reversion to sinus rhythm (pharmacological or non-pharmacological) showed a significant fall in 19 of the 23 patients with paroxysmal supraventricular tachycardia and all seven patients with atrial flutter. Because atrial natriuretic polypeptide has powerful natriuretic and diuretic properties, an increase may contribute considerably to the polyuria that is often associated with episodes of supraventricular tachycardia.

Adolescent↗
PubMed1987

Somatostatin and neuropeptide Y are almost exclusively found in the same neurons in the telencephalon of turtles.

In mammals, somatostatin and neuropeptide Y (NPY) are largely found in the same neurons of the telencephalon. To determine if this is a phylogenetically ancient feature of telencephalic organization, the brain of red-eared turtles was examined using immunofluorescence double-labeling procedures. The results showed that somatostatin and NPY are found almost exclusively in the same neurons in the telencephalon of turtles, but these neuropeptides rarely co-occur in neurons outside the telencephalon. Thus, the extensive co-occurrence of NPY and somatostatin appears to be a feature of telencephalic organization that was present in the reptilian common ancestors of mammals and modern reptiles.

Animals↗
PubMed1987

Neuropeptide Y-like immunoreactive C1 neurons in the rostral ventrolateral medulla of the rabbit project to sympathetic preganglionic neurons in the spinal cord.

After injection into the thoracic spinal cord of the rabbit, gold particles coupled to concanavalin A were found in the rostral ventrolateral medulla in neurons which contained neuropeptide Y-like immunoreactivity. These cells have previously been shown to belong to the C1 catecholamine (presumably adrenaline)- synthesizing group. Nerve terminals in the intermediolateral column contained both tyrosine hydroxylase and neuropeptide Y-like immunoreactivity. When fast blue was injected into the adrenal gland the retrogradely labeled preganglionic neurons were shown to be surrounded by nerve terminals containing neuropeptide Y-like immunoreactivity. Our results indicate that at least some of these terminals derive from C1 neurons which also synthesize neuropeptide Y.

Animals↗
PubMed1987

The effect of cysteamine, cystamine, and the structurally related compounds taurine, N-acetyl-cysteine, and D-penicillamine on plasma prolactin levels in normal and estrogen-primed hyperprolactinemic rats.

Studies were undertaken to evaluate the effects of cysteamine (CSH), cystamine (CS-S), N-acetyl-cysteine, D-penicillamine, and a major metabolite of CSh, taurine, on plasma PRL levels in normal and estrogen-primed hyperprolactinemic rats. Both CSH and CS-S caused a marked decrease in plasma PRL concentration in hyperprolactinemic rats. The effects of CSH and CS-S lasted for at least 6 h but returned toward pretreatment levels 24 h later. In normal rats a fall in basal plasma PRL concentration was not readily observed but after stimulation with TRH or metaclopramide, PRL secretion elicited by these stimuli was markedly inhibited by CSH and CS-S. The response to TRH or MCP 24 h after treatment with CSH was variable with CS-S appearing to cause an unexpected increase in PRL release in response to TRH or metaclopramide. The structurally related compounds, taurine, N-acetyl-cysteine, and D-penicillamine did not cause any reduction of plasma PRL levels in hyperprolactinemic rats. This may be due, in the case of taurine, to a loss of the free sulfydryl group, in the case of N-acetyl-cysteine, a change in basicity because of a carboxyl group and derivatization of the amino group and D-penicillamine, again a change in basicity due to a free carboxyl group as well as an altered structural relationship between the free amino and sulfydryl groups. These studies indicate that CSH and CS-S by possible reduction to CSH cause a reversible depletion in plasma PRL in normal and hyperprolactinemic rats. Because both substances inhibit different receptor-mediated stimuli, their mechanism of action is likely to be mediated at a common locus involved with the synthesis and release of PRL.

Acetylcysteine↗