Biomedical subjects

L C Anderson

Publications and source records attributed to L C Anderson.

At least 55 records · Page 3Linked to original sources

PubMed1992

Changes in the lectin-binding of capillaries in rat salivary glands after streptozotocin-induced diabetes.

The lectin-horseradish peroxidase conjugate of GSA I-B4 (Griffonia simplicifolia isolectin) has some binding affinity with capillary walls in sections of the major salivary glands from normal rats. After inducing diabetes with streptozotocin a conspicuous increase in the staining intensity with GSA I-B4 was already evident in parotid capillaries at 3 weeks and this increase persisted at 3 and 6 months. In submandibular capillaries, however, an increased uptake of GSA I-B4 was evident only at 6 months after inducing diabetes. The reasons for these different time scales in the two glands are not known but the increased uptake of GSA I-B4, which is due to an increase in carbohydrate-containing sites with available terminal alpha-D-galactose, is considered to reflect a pathological change.

Animals↗

PubMed1992

Lipid analysis of the major salivary glands in streptozotocin-diabetic rats and the effects of insulin treatment.

Two separate sets of experiments were performed on female Wistar rats made diabetic with streptozotocin: (1) a time-course study where groups of three animals were removed at weekly intervals, up to 4 weeks after induction of diabetes, with an age-matched group of control (normal) animals kept for 4 weeks; (2) six further animals were made diabetic and kept for 7 weeks; three of these were given insulin in the final week. At the required time the animals were anaesthetized and the salivary glands removed and preserved by fixation or freezing. The frozen tissues were later homogenized and the protein and lipid content analysed. Histologically, intracellular lipid droplets had accumulated in the majority of the diabetic salivary glands. In the time-course experiment, the visible amount of intracellular lipid reached a maximum after 2 weeks and then decreased, with a concomitant disappearance of interstitial lipid. The increased lipid content was not attributable to any one class. The fatty acid profiles of the glands showed an increase in the percentages of C18:0 (stearic acid) and C18:2w6 (linoleic acid) and a decrease in the percentages of C18:1w9 (oleic acid) and C20:4w6 (arachidonic acid). After 1 week of insulin treatment the lipid content and the fatty acid profiles returned to normal. Thus the effect of insulin on salivary gland lipid metabolism is rapid both in its occurrence and reversibility. The effects seen in the diabetic rats are considered to be due to a lack of insulin and not to the presence of streptozotocin.

Animals↗

PubMed1992

Secretory oedema in diabetic submandibular glands during parasympathetic nerve stimulation: relationship to microvascular abnormalities in streptozotocin-treated rats.

1. Submandibular secretion during parasympathetic stimulation (5 Hz) was examined in streptozotocin-diabetic and age-matched control rats. 2. At 3 weeks, but not 3 and 6 months, flow rate was initially greater than in controls, but it declined rapidly after 30 min. 3. The reduction in flow rate was associated with oedema of the gland. 4. At 3 months, graded stimulation revealed a tendency to oedema at frequencies of 10 Hz and above. 5. Morphologically, submandibular capillary density was increased in diabetic rats. 6. Thus, in diabetes the submandibular gland appears less able to withstand continuous parasympathetic stimulation, due in part to an increase in tissue capillary area.

Animals↗

PubMed1991

Secretory responses in granular ducts and acini of submandibular glands in vivo to parasympathetic or sympathetic nerve stimulation in rats.

The roles of sympathetic and parasympathetic nerves in the secretion of saliva from submandibular glands of rats have been tested by electrical stimulation of either nerve for 1 h unilaterally in separate animals. The flows of saliva thereby induced and their protein content were monitored. Structural changes in each gland were assessed by light- and electron microscopy and compared with the unstimulated contralateral control gland, and the extent of the changes was determined morphometrically. Sympathetic nerve stimulation induced a relatively low flow of saliva that was rich in protein and was accompanied by extensive degranulation from both acinar and granular duct cells. In contrast parasympathetic nerve stimulation induced a considerable flow of saliva that had a low protein content and no detectable degranulation occurred from the secretory cells. It is possible, therefore, that some protein in parasympathetic saliva may have arisen from a non-granular pathway.

Animals↗

PubMed1991

Rat sublingual salivary glands: secretory changes on parasympathetic or sympathetic nerve stimulation and a reappraisal of the adrenergic innervation of striated ducts.

Sublingual glands were examined by light and electron microscopy after stimulating the parasympathetic nerve (5 Hz continuously) or the sympathetic nerve (50 Hz in bursts 1 s every 10 s) and compared with contralateral, unstimulated, normal glands from each animal. Parasympathetic stimulation caused secretion of mucin from the tubulo-acini and possibly a small amount of degranulation from the demilunes but no changes were detected in the striated ducts. Sympathetic stimulation, on the other hand, had no effect on the tubulo-acini or demilunes but caused a surprisingly extensive degranulation of the striated ducts plus loss of glycogen from their cells. Reassessment of the adrenergic innervation in the glands was therefore undertaken, by means of catecholamine fluorescence. This identified a regular association between adrenergic nerves and the striated ducts not only in sublingual but also in submandibular glands; features that have not previously been recognized. There was, however, only a sparse adrenergic innervation of the other parenchymal elements in the sublingual glands.

Animals↗

PubMed1991

Effects of diabetes and dietary manipulation on rat parotid gland secretory response to sympathetic nerve stimulation.

1. The effects of streptozotocin-diabetes, bulk-diet, low protein diet (8%) and protein-calorie malnutrition on parotid gland response to sympathetic nerve stimulation were studied in male Wistar rats. 2. Mean body weights were considerably less in diabetic and protein-calorie malnourished rats than in the other groups, but parotid gland weight was reduced only in animals placed on a low-protein diet. 3. Salivary flow rate (microliter/min/g tissue) and total protein output (mg secreted/g tissue) were reduced in diabetic rats. 4. Salivary composition was altered in diabetes and protein-calorie restriction, and the specific changes were unique to each condition. 5. Thus, with the possible exception of gland weight the effects of diabetes on parotid gland structure and function are not related to either hyperphagia or nutritional status.

Animals↗

PubMed1991

A review of the intraosseous course of the nerves of the mandible.

A review of the literature revealed that a common feature of all human mandibles is a large nerve (inferior alveolar nerve, IAN) between the mandibular and mental foramina. This nerve sends branches directly to the teeth or contributes a variable number of branches to a plexus of nerves which does the same. The plexus originates from a separate nerve that enters the mandibular foramen. The nerve plexus has been demonstrated by dissections and not by radiology. The buccal-lingual and superior-inferior positions of the IAN were not consistent among mandibles. The intramandibular IAN frequently ran a concave curve with a posterior segment descending as it progressed anteriorly and an anterior segment that ascended to the mental foramen. A bony canal was not always observed between the mandibular and mental foramina. The canal frequently lacked definite walls, especially near the mental foramen. Bilateral symmetry (location of the canal in each half of the mandible) was common, whereas duplications of the canal were rare. Nutrient canals and other branches of the mandibular nerve have been observed within the mandible. These may have been confused for the IAN or may contribute to the plexus of nerves.

Humans↗

PubMed1990

Time delays in the diagnosis and treatment of acute myocardial infarction: a tale of eight cities. Report from the Pre-hospital Study Group and the Cincinnati Heart Project.

To establish the magnitude of prehospital and hospital delays in initiating thrombolytic therapy for acute myocardial infarction, the time from telephone 911 emergency medical system (EMS) activation to treatment and its components were analyzed from eight separate ongoing trials. This included estimates of ambulance response time, prehospital evaluation and treatment time, and time from admission to the hospital to initiation of thrombolytic therapy. The average time from EMS activation to patient arrival at the hospital was prospectively determined to be 46.1 +/- 8.2 minutes in 3715 patients from eight centers. The time from admission to the hospital to initiation of thrombolytic therapy was retrospectively determined to be 83.8 +/- 55.0 minutes in a separate group of 730 patients from six centers. Both the prehospital and hospital time delays were much longer than those perceived by paramedics and emergency department directors. Shorter hospital time delays were observed in patients in whom a prehospital ECG was obtained as part of a protocol-driven prehospital diagnostic strategy and a diagnosis of acute infarction made before arrival at the hospital (36.3 +/- 11.3 minutes in 13 patients). These results show that the magnitude of time required to evaluate, transport, and initiate thrombolytic therapy will preclude initiation of treatment to most patients within the first hour of symptoms. Implementation of a protocol-driven prehospital diagnostic strategy may be associated with a reduction in time to thrombolytic therapy.

Electrocardiography↗

PubMed1990

Morphological effects of sympathetic nerve stimulation on rat parotid glands 3-4 weeks after the induction of streptozotocin diabetes.

Male Wistar rats were fasted overnight and anaesthetized 3-4 weeks after the induction of streptozotocin diabetes. The right parotid ducts were cannulated, and parotid salivary flow was induced by stimulating the sympathetic trunk in bursts (50 Hz, 1:10). Stimulated and unstimulated glands were weighed, fixed for morphometric analysis, and assayed for total protein and amylase. Gland weights did not differ between diabetic and control rats. Nevertheless, total protein (6.17 +/- 5.40 mg) and amylase (1.32 +/- 0.49 mg) output from the gland were reduced in diabetic animals compared with controls (13.73 +/- 2.81 and 3.41 +/- 0.51 mg, respectively). Morphometric analysis of unstimulated glands showed no differences in either acinar cell profile area, or in the number of secretory granule profiles/cell in unstimulated glands. Upon sympathetic stimulation, however, the depletion of granule profiles was significantly less in diabetic than in control rats. Finally, the mean diameter of secretory granules was significantly less in diabetic (0.89 +/- 0.05 microM) than in control (1.04 +/- 0.06 microM) glands.

Amylases↗

PubMed1990

Fate of patients with acute myocardial infarction with patency of the infarct-related vessel achieved with successful thrombolysis versus rescue angioplasty.

Patients with failure of infarct-related artery recanalization after thrombolytic therapy have a poor clinical outcome. These patients have been considered for rescue angioplasty 90 min after thrombolytic therapy at the time of emergency catheterization in the course of five Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) trials. The outcome of 776 patients with patent infarct-related vessels after emergency catheterization was analyzed--607 with thrombolysis-mediated patency of the infarct-related vessel and 169 with patency achieved by angioplasty. Baseline characteristics of the thrombolysis and angioplasty patency groups were similar except for a higher acute left ventricular ejection fraction (51.3% versus 48.2%) in the thrombolysis group (p = 0.003). Seven to 10 day left ventricular ejection fraction was higher (52.3% versus 48.1%), infarct zone functional recovery was greater (0.44 versus 0.21 standard deviation/chord, or 18% versus 7%, p = 0.001) and reocclusion was less (11% versus 21%) in the thrombolysis compared with the angioplasty group. Despite these differences, angioplasty patency was associated with the same low in-hospital mortality rate (5.9% versus 4.6%) and long-term mortality rate (3% versus 2%) as thrombolysis patency. Reocclusion adversely affected the mortality rate and ventricular functional recovery. Technical failure of rescue angioplasty was associated with a much higher mortality rate than was technical success (39.1% versus 5.9%). Thrombolysis patency was preferable to angioplasty patency after thrombolytic therapy in acute myocardial infarction, but both were associated with the same low in-hospital and long-term mortality rates, suggesting that rescue angioplasty is beneficial in some patients with failure of infarct-related artery recanalization after thrombolytic therapy.

Angioplasty, Balloon, Coronary↗

PubMed1989

Favorable early and long-term prognosis following coronary bypass surgery therapy for myocardial infarction: results of a multicenter trial. TAMI Study Group.

Coronary bypass surgery was performed before hospital discharge on 82 (21%) of 386 consecutive patients enrolled in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) multicenter trial of intravenous tissue plasminogen activator and coronary angioplasty for acute myocardial infarction. Time from infarct symptom onset to coronary bypass surgery was 7.3 +/- 1.9 hours for 24 patients operated upon on an emergency basis and 9.3 +/- 5.2 days for 58 patients having late in-hospital surgery. There were no operative deaths and five in-hospital deaths in the surgical group, all of which occurred in patients with preoperative cardiogenic shock. Although patients in the surgical group were older (59.7 +/- 10.4 years versus 54.9 +/- 10.2 years; p = 0.03), had more extensive coronary artery disease (42% three-vessel disease versus 11%; p = 0.001), and had a higher incidence of anterior wall myocardial infarction (48% versus 39%; p = 0.02), in-hospital mortality for the surgical group (6%) was similar to that in 301 patients not undergoing surgery (7%) in this trial. For patients discharged from the hospital, mortality at 1 year was 2.5% in the surgical group and 1.8% in patients not having coronary bypass surgery before hospital discharge. At a 1 year follow-up, there were no significant differences in the frequency of cardiac or noncardiac-related hospitalizations or in event-free survival between surgical and nonsurgical groups. The majority of patients in both groups considered themselves to be in excellent or good condition. Coronary bypass surgery can be performed with low morbidity and mortality rates in close temporal association to acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon↗

PubMed1989

Alpha-aminoisobutyric acid transport in isolated rat submandibular salivary acinar cells.

Na+-dependent alpha-aminoisobutyric acid (AIB) transport by isolated submandibular cell aggregates (pmol min-1 mg protein-1) was greater in the presence than in the absence of insulin, Vmax (5220 compared with 2900). Km (1.78 and 1.40 mM, respectively) was unaffected by insulin. Na+-dependent methyl-aminobutyric acid (MeAIB) transport was also greater in the presence of insulin (V max, 3120 compared with 2010 pmol min-1 mg protein-1; Km, 1.03 and 0.93 mM). In the presence of 10 mM MeAIB, Na+-dependent AIB transport was reduced to 76 pmol min-1 mg protein in both control and insulin-treated cells. The remaining Na+-dependent uptake of AIB was inhibited by 10 mM serine. Na+-independent AIB transport was unaffected by insulin, and in the presence of 5 mM 2-aminobicyclo-[2,2,1]-heptane-carboxylic acid (BCH) AIB uptake was reduced to 10% of that observed under Na+-replete conditions. In the absence of insulin, the rate of Na+-dependent AIB uptake rapidly decayed; however, following the addition of hormone the rate of transport was maintained. Thus in the rat submandibular gland AIB uptake is mediated by at least three transport systems (A, L and ASC), and maintenance of normal system A activity requires insulin.

Aminoisobutyric Acids↗

PubMed1989

Effects of streptozocin-induced diabetes on sympathetic and parasympathetic stimulation of parotid salivary gland function in rats.

Diabetes was induced with streptozocin in male Wistar rats. After 4-6 mo, parotid salivary flow was induced by stimulating bipolar electrodes (3-5 V for 2 ms) on either the auriculotemporal nerve (5 Hz) or the cervical sympathetic trunk (10 Hz). During parasympathetic stimulation, flow rates were 443 +/- 287 microliters/30 min in diabetic animals compared to 657 +/- 134 microliters/30 min in controls (P less than .01). Although parotid flow rates during parasympathetic stimulation were well maintained in controls, they decreased rapidly in most diabetic rats. Parotid secretory response to sympathetic stimulation was also reduced in diabetic compared with control animals (40 +/- 16 microliters/30 min and 82 +/- 50 microliters/30 min, respectively, P less than .01). In contrast to results obtained with direct neural stimulation, no differences in threshold dose or total saliva were observed when cholinergic (methacholine) and peptidergic (physalaemin) agonists were administered intravenously. Response threshold for an adrenergic agonist (epinephrine) was significantly increased in diabetes. Electron microscopy showed axoplasmic abnormalities in nonmyelinated axons in diabetic glands but not in control glands. Although most nerve profiles appeared normal, neuroaxonal abnormalities were found in every diabetic animal. The ultrastructural findings and the similar responses to methacholine and physalaemin suggest that autonomic neuropathy may be a factor in the abnormal response of the parotid gland to parasympathetic nerve stimulation.

Amylases↗

PubMed1988

Insulin-stimulated protein synthesis in submandibular acinar cells: interactions with adrenergic and cholinergic agonists.

The effects of insulin and secretory agonists on amino acid incorporation into submandibular gland proteins were studied using isolated acinar cell aggregates. Insulin stimulated the incorporation of 3H-leucine into TCA-precipitable proteins in a rapid, dose-dependent manner (half-maximal response at 1 nM). Isoproterenol, a beta-adrenergic agonist, also stimulated amino acid incorporation, and this effect was mimicked by both dibutyryl cAMP and IBMX, a phosphodiesterase inhibitor. Although insulin further stimulated incorporation in the presence of isoproterenol and IBMX, no additional increase in the rate of synthesis was observed after stimulation by dibutyryl cAMP. High concentrations of carbamylcholine, a cholinergic agonist, inhibited both basal and insulin-stimulated incorporation. At low concentrations, however, carbamylcholine stimulated synthesis, and the effects of insulin and carbamylcholine were additive. A23187, a calcium ionophore, also inhibited 3H-leucine incorporation and insulin stimulation, but in contrast to carbamylcholine, low concentrations of A23187 neither inhibited nor enhanced the rate of synthesis. Thus, protein synthesis in the rat submandibular gland is regulated by both insulin and neurotransmitters. Whereas beta-adrenergic stimulation appears to be mediated through cAMP, the intracellular signals mediating the actions of insulin and cholinergic agonists remain to be elucidated.

Adrenergic beta-Agonists↗

PubMed1988

Advantages of burst stimulation for inducing sympathetic salivary secretion in rats.

Electrical stimulation of the cervical sympathetic nerve trunk delivered at 50 Hz in bursts of 1 s every 10 s, evoked a more copious, uniform and reproducible flow of saliva than when delivered at 10 Hz continuously. This advantage of burst stimulation occurred with parotid secretion and was especially evident with secretion from submandibular glands, where the oedema, commonly seen after stimulating the sympathetic nerve continuously, was avoided. Therefore stimulation in bursts is recommended for obtaining sympathetic salivary responses in rats.

Animals↗

PubMed1987

The effect of nifedipine on cystoscopy-induced autonomic hyperreflexia in patients with high spinal cord injuries.

We evaluated the ability of the calcium channel blocker nifedipine to control autonomic hyperreflexia during cystoscopy in 7 patients with cervical spinal cord injuries. Nifedipine (10 mg.) alleviated autonomic hyperreflexia when given sublingually during cystoscopy and prevented autonomic hyperreflexia when given orally 30 minutes before cystoscopy. No adverse drug effects were observed.

Administration, Oral↗

PubMed1987

Guinea pig husbandry and medicine.

Guinea pigs are hardy, gentle, virtually odor-free rodents. Their adverse, often lethal response to antibiotics requires an appropriate program of nutrition, husbandry, and handling, which are reviewed in this article. A summary of anatomical characteristics, basic biology, and reproductive data is provided. Diseases of practical clinical significance, primarily those of bacterial or nutritional origin, are also reviewed.

Animal Diseases↗

PubMed1987

Parotid gland function in streptozotocin-diabetic rats.

The in vivo response of parotid glands to adrenergic, cholinergic, and peptidergic agonists was studied in control, streptozotocin- (one month's duration), and insulin-treated (three hr) diabetic rats. Neither diabetes nor insulin had an effect on the response to physalaemin. In contrast, physalaemin threshold-dose was lower and maximal response greater in control rats placed on a bulk diet. As previously described, diabetes resulted in nonparallel changes in parotid protein composition, including a production in amylase and an increase in peroxidase concentrations (mg/mg protein). In contrast to the results observed with physalaemin, response to methacholine was significantly reduced in diabetic animals, and could be restored to control levels by insulin. Placement of animals on a bulk-diet, however, had no effect on threshold response to methacholine. Finally, response threshold for epinephrine was unaffected by diabetes, insulin, or bulk diet. Thus, insulin appears, directly and specifically, to alter the response of parotid acinar cells to cholinergic stimulation.

Amylases↗