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Biomedical subjects

J S Cameron

Publications and source records attributed to J S Cameron.

At least 217 records · Page 12Linked to original sources
PubMed1985

Enhanced relaxation and reduced positive inotropic effects of amrinone in ventricular muscle from cats with subacute heart failure. Implications for drug therapy.

Previously, we reported that amrinone increases isometric twitch force but relaxes K+-induced contracture in muscles from normal cat right ventricle. This study evaluated its effects on diseased cardiac tissue. Right-ventricular papillary muscles were obtained from cats with subacute right-ventricular failure (3-14 days after partial pulmonary-artery ligation) and studied in vitro during stimulation (0.5 Hz) and exposure to high-K+ Tyrode solution. Active isometric twitch force and rate of force development (dP/dt) were significantly lower in muscles from hearts with right-ventricular failure compared to control muscles. In addition, while time to peak force was not different, duration of the twitch was significantly longer. In contrast to its positive inotropic actions in control muscles, amrinone (5.3 X 10(-4) M) had no significant effects on twitch force and dP/dt in muscles from failed ventricles. Time to peak force was not changed by amrinone in either group, but unlike its action in control muscle, duration of the twitch was reduced in failed muscle. Amrinone reduced K+-contracture force similarly in both control and failed muscles. Isoproterenol (10(-6) M) significantly increased twitch force and dP/dt and reduced K+-contracture force in both muscle groups. Since amrinone appears to be a phosphodiesterase inhibitor, our data indicate that cyclic AMP (cAMP)-related relaxation processes, but not cAMP-related contractile processes, can be enhanced by phosphodiesterase inhibitors in experimental heart failure. Furthermore, amrinone's reduced positive inotropic effect in failed myocardium suggests that its improvement of ventricular function in patients reflects, in part, enhancement of relaxation.

Aminopyridines↗
PubMed1985

Enhanced adverse electrophysiologic effects of histamine after myocardial infarction in guinea pigs.

To evaluate the electrophysiological sensitivity of infarcted myocardium to histamine, we used microelectrodes to study its effects in isolated guinea-pig left ventricles 1 hr (acute), 24 hr (subacute) and 4 to 6 weeks (chronic) after multiple (6-8) ligations of the left coronary artery system. In both control and infarcted preparations, histamine (10(-8) to 10(-5) M) caused marked concentration-dependent increases in automaticity. Histamine also induced rhythm disturbances, including premature depolarizations, irregular patterns of spontaneous depolarization and spontaneous bursts of rapid ventricular activity. In each case, threshold concentrations for these effects were lowest in the preparations with infarcts. Cimetidine (10(-5) M) abolished the arrhythmogenic effects of histamine, whereas chlorpheniramine (10(-5) M) did not; beta adrenergic blockade induced by propranolol also had no effect. The effects of histamine were mimicked in normal hearts by the H2-agonist dimaprit. These data indicate that threshold concentrations of histamine induce rhythm disturbances in the setting of experimental myocardial infarction. We suggest histamine plays some role in arrhythmias associated with myocardial infarction in humans.

Action Potentials↗
PubMed1985

Interstitial foam cells in the nephrotic syndrome belong to the monocyte/macrophage lineage.

Interstitial foam cells are occasionally seen in patients with the nephrotic syndrome. In a group of patients with the nephrotic syndrome we were able to demonstrate that these cells express markers characteristic of the monocyte/macrophage lineage. Their presence was related to the previous duration of proteinuria, but they had no apparent influence on the subsequent evolution of renal function. The mechanisms leading to their presence are unknown.

Adult↗
PubMed1985

Five hundred years of the nephrotic syndrome: 1484-1984.

The nephrotic syndrome has emerged over several centuries as the consequence of continued profuse proteinuria, arising in turn from a variety of lesions affecting the glomerulus which impair glomerular ability to retain plasma proteins, in particular, albumin. As a syndrome, it has its own complications and requires its own management irrespective of the underlying lesions. Dissection of these by renal biopsy and by clinical investigation reveals a variety of systemic diseases which affect the kidney, but a majority of primary immune-based diseases appear unique to the glomerulus. Whether the lesion called by Müller and Munk 'nephrosis', and now called minimal change disease and focal segmental glomerulosclerosis is one disease or many, is the subject of intense debate at the moment, as is the relationship between two types of lesion. Only a better understanding of their pathogenesis, and of how the glomerulus normally retains plasma protein, will solve this knotty problem.

Acute Kidney Injury↗
PubMed1985

Adult-onset nephrotic syndrome with minimal changes: response to corticosteroids and cyclophosphamide.

Eighty-nine patients with onset of nephrotic syndrome over the age of 15 years and minimal changes on renal biopsy have been studied. Seventy-five patients were given a course of prednisone in an initial dosage of 60mg/24hr, tapering over the following 8-16 weeks. Only 45 were in remission after eight week's treatment, 55 after 16 weeks; eventually, a total of 58 lost their proteinuria completely. Of these, 24 per cent never relapsed, 56 per cent relapsed on a single occasion or infrequently, and only 21 per cent were frequent relapsers. Cyclophosphamide, used in 36 patients, had a similar time to response. Stability of remission was better than in similar children, 66 per cent being in remission at five years, after which no further relapses were seen.

Adolescent↗
PubMed1985

Platelet involvement in the nephritis of acute serum sickness in rabbits: protection by dipyridamole and FUT-175.

In the acute serum sickness model in rabbits, we investigated platelet release of 5-HT, platelet surface immunoglobulins, and platelet aggregation in response to ADP, together with the effect of dipyridamole and the Clr antagonist FUT-175. The immune release of 5-HT from platelets occurred between 4 and 6 days after injection of bovine serum albumin (BSA), before immune elimination and proteinuria, but coincident with the appearance of immune complexed BSA in the circulation. Nevertheless, platelet turnovers were not detectably accelerated. Treatment with dipyridamole 50 mg/kg/24 h prevented the release of 5-HT and inhibited proteinuria, glomerular hypercellularity and immune complexes in the glomeruli. Using the Clr antagonist FUT-175, similar abrogation of the disease was obtained. We conclude that in the nephritis of acute serum sickness in rabbits, some of the immune release from platelets may be the result of immune complex binding to the platelet, perhaps through the receptor for C3b.

Adenosine Diphosphate↗
PubMed1984

Renal transplantation after removal and prevention of resynthesis of HLA antibodies.

Plasma exchange and immunosuppression with prednisolone and cyclophosphamide were used to remove HLA antibodies and prevent their resynthesis in five patients awaiting renal transplantation. After treatment HLA antibody titres and reactivities against a panel of donor lymphocytes were considerably reduced and, as a result, these patients received transplants. Four of these patients have successfully functioning transplants; the other patient died as a result of septicaemia with a poorly functioning allograft.

Adolescent↗
PubMed1984

Histamine modification of spontaneous rate and rhythm in infarcted canine ventricle.

Histamine (10(-3) M) increased the spontaneous rate similarly in isolated preparations of normal left ventricular tissue from control, i.e. normal and sham-operated, dogs (control preparations) and in preparations consisting of normal and contiguous infarcted left ventricular tissue from dogs with subacute, i.e. 24 hours after left coronary artery ligation, myocardial infarction (infarcted preparations). Histamine (10(-3) M) markedly enhanced the irregular rhythm of infarcted preparations. The H1-receptor antagonist, chlorpheniramine (10(-4) M), and the H2-receptor antagonist, cimetidine (10(-3) M), antagonized the effects of histamine (10(-3) M) on the spontaneous rate of both control and infarcted preparations. The H1-receptor agonist, 2-pyridyl ethylamine (PEA, 10(-4) M), increased the spontaneous rate of control and infarcted preparations; these effects were antagonized by chlorpheniramine (10(-4) M). The H2-receptor agonist, dimaprit, had no effect. Similar to histamine (10(-3) M), PEA (10(-4) M) enhanced the irregular rhythm of infarcted preparations; dimaprit had no effect. High local concentrations of histamine may occur in poorly perfused ischemic tissue. The enhancement of irregular rhythm produced by histamine, and the specific H1-receptor agonist, PEA, leads us to suggest its involvement in arrhythmias associated with subacute myocardial infarction.

Animals↗
PubMed1984

Regional distribution of action potential abnormalities induced by subacute right ventricular pressure overload.

Right ventricular pressure overload of 3 days' duration was established in cats by banding of the pulmonary artery. To characterize the regional distribution of the resulting electrophysiologic changes, the right ventricular free wall, adjacent pulmonary outflow tract and septum were mounted in tissue bath and examined by conventional microelectrode techniques. Abnormal action potentials, identified by a negative shift of the voltage level of phase 2 with a corresponding accentuation of phase 1, were recorded from sites contiguous to the tricuspid valve and pulmonary outflow tract and in limited adjacent areas. No abnormal action potentials were recorded on the septal surface, apical end of the free wall, or at any right ventricular location in normal or sham-operated cats. Abnormal potentials could be recorded from sites sampled 5 cell layers deep in the endocardium. The number and extent of distribution of cells demonstrating altered action potentials correlated best with increased right ventricular wet weight at time of sacrifice. Abnormal cells responded to epinephrine or elevated extracellular calcium by a shift in plateau voltage towards zero and by an increase in action potential duration prior to usual plateau shortening. Responsiveness of these cells to agents which influence slow inward current suggests pressure overload-induced changes in the cell membrane that limit or otherwise affect availability of calcium. Regional distribution of plateau potential abnormalities may reflect differential physical stress within the myocardium provoked by sudden pressure overload.

Action Potentials↗
PubMed1984

Regional variations in myosin heavy chain concentration after healing of experimental myocardial infarction in cats.

Densitometric scanning of SDS-polyacrylamide gels was used to measure myosin heavy chain concentration in left ventricular specimens obtained from cat hearts 3 to 12 months after healing of small experimental myocardial infarctions. The study was designed to test the hypothesis that myosin concentration varies as a function of anatomic proximity to the infarct scar. Myosin heavy chain concentration was elevated in non-scarred areas adjacent to a healed infarct and normal in areas remote from the scar. The scar itself had reduced concentrations, reflecting the loss of muscle mass in this area. The increased myosin heavy chain concentration in regions adjacent to the scar may be an attempt to regulate or compensate for the decrease in mechanical function of the scarred area.

Animals↗
PubMed1984

Successful removal and prevention of resynthesis of anti-HLA antibody.

The successful removal and prevention of the resynthesis of an anti-HLA antibody by plasma exchange and immunosuppression in a patient awaiting renal transplantation is described. Before treatment, the patient's serum contained a high titer (greater than 1/50) anti-HLA antibody that reacted with 94% of our lymphocyte donor panel and produced positive cross matches with the lymphocytes from 40 cadaver kidneys. Following treatment, her anti-HLA titers fell to less than 1/10 and her sera reacted with 43% of our lymphocyte donor panel and produced negative crossmatches with lymphocytes from the first two cadaver kidney donors she was tested against. She was successfully transplanted with the second of these kidneys and is now well eight months later, with good graft function.

Adult↗
PubMed1984

Immunoglobulin (Gm) allotype frequencies in idiopathic membranous nephropathy and minimal change nephropathy.

40 Caucasoid patients with idiopathic membranous nephropathy (IMN) and 49 Caucasoid patients with minimal change nephropathy (MCN) were immunoglobulin allotyped for the Gm markers G1m (1, 2, 3) and G3m (5, 11, 21). Compared with normal controls the IMN group had a significantly decreased incidence of the G1m (3); G3m (5, 11) phenotype (P = less than 0.005). This decrease was accompanied by concommitant increase in both the G1m (1, 3); G3m (5, 11, 21) and the G1m (1, 2, 3); G3m (5, 11, 21) phenotypes. The result was most pronounced in IMN patients with deteriorating renal function. In contrast no significant differences were observed between the Gm phenotype frequencies of the MCN patients and controls.

Adolescent↗
PubMed1984

Platelets in glomerular disease.

Platelets are inflammatory cell fragments derived from the same stem cells as polymorphs and macrophages. They can induce inflammation and release chemotactic and mitogenic substances. There is evidence from both experimental and clinical nephritis that they are involved in mediating or amplifying glomerular injury by increasing vascular permeability and by promoting glomerular cell proliferation and infiltration. The nephrotic state renders platelets hyperaggregable.

Animals↗