Biomedical subjects

G Varga

Publications and source records attributed to G Varga.

At least 19 recordsLinked to original sources

PubMed2001

Bicarbonate and fluid secretion evoked by cholecystokinin, bombesin and acetylcholine in isolated guinea-pig pancreatic ducts.

1. HCO3- secretion was investigated in interlobular duct segments isolated from guinea-pig pancreas using a semi-quantitative fluorometric method. Secretagogue-induced decreases in intracellular pH, following blockade of basolateral HCO3- uptake with a combination of amiloride and DIDS, were measured using the pH-sensitive fluoroprobe BCECF. Apparent secretory HCO3- fluxes were calculated from the initial rate of intracellular acidification. 2. In the presence of HCO3-, stimulation with secretin (10 nM) or forskolin (5 microM) more than doubled the rate of intracellular acidification. This effect was abolished in the absence of HCO3-. It was also abolished in the presence of HCO3- when DIDS and NPPB were applied to the luminal membrane by microperfusion. We therefore conclude that the increase in acidification rate is a useful index of secretagogue-induced HCO3- secretion across the luminal membrane. 3. Secretin, cholecystokinin (CCK) and bombesin each stimulated HCO3- secretion in a dose-dependent fashion. They evoked comparable maximal responses at about 10 nM and the EC50 values were 0.5 nM for secretin, 0.2 nM for CCK and 30 pM for bombesin. Acetylcholine (ACh) was also effective, with a maximum effect at 10 microM. 4. The stimulatory effect of CCK was blocked completely by the CCK1 receptor antagonist devazepide but not by the CCK2 receptor antagonist L365,260. The CCK analogue JMV-180 (Boc-Tyr(SO3H)-Nle-Gly-Trp-Nle-Asp-phenylethyl ester), which is an agonist of the high-affinity CCK1 receptor but an antagonist of the low-affinity receptor, also stimulated HCO3- secretion but with a smaller maximal effect than CCK. JMV-180 partially inhibited the response to a high concentration of CCK but not to a lower concentration, suggesting that both high- and low-affinity states of the CCK1 receptor evoke HCO3- secretion. 5. The stimulatory effect of bombesin was blocked completely by the gastrin-releasing peptide (GRP) receptor antagonist D-Phe6-bombesin(6-13)-methyl ester (BME) but not by the neuromedin B (NMB) receptor antagonist D-Nal-cyclo[Cys-Tyr-D-Trp-Orn-Val-Cys]-Nal-NH2 (BIM-23127). 6. Secretagogue-evoked fluid secretion was also examined using video microscopy to measure the rate of swelling of ducts whose ends had sealed during overnight culture. Secretin, CCK, bombesin and ACh all evoked fluid secretion with maximal rates of approximately 0.6 nl x min(-1) x mm(-2), and with concentration dependences similar to those obtained for HCO3- secretion. 7. We conclude that CCK, bombesin and ACh stimulate the secretion of a HCO3--rich fluid by direct actions on the interlobular ducts of the guinea-pig pancreas and that these responses are mediated by CCK1 receptors, GRP receptors and muscarinic cholinoceptors, respectively.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed2001

Overexpression of CD40 ligand in murine epidermis results in chronic skin inflammation and systemic autoimmunity.

CD40-CD40 ligand (L) interactions play a pivotal role in immune-mediated inflammatory responses via the activation of antigen-presenting cells (APCs). To investigate the effects of continuous activation of resident tissue APCs, in this case the Langerhans cells (LCs) of the skin, CD40L expression was targeted to the basal keratinocytes of the epidermis of mice using the keratin-14 promoter. Approximately 80% of the transgenic (Tg) mice spontaneously developed dermatitis on the ears, face, tail, and/or paws. Compared with littermates, Tgs had a >90% decrease in epidermal LCs yet increased numbers within the dermis suggestive of enhanced emigration of CD40-activated LCs. Tgs also displayed massive regional lymphadenopathy with increased numbers of dendritic cells and B cells. Moreover, a decrease in IgM and an increase in IgG1/IgG2a/IgG2b/IgE serum concentrations was detectable. Screening for autoantibodies revealed the presence of antinuclear antibodies and anti-dsDNA antibodies implicative of systemic autoimmunity. Accordingly, renal Ig deposits, proteinuria, and lung fibrosis were observed. Adoptive transfer of T cells from Tgs to nonTg recipients evoked the development of skin lesions similar to those found in the Tgs. Dermatitis also developed in B cell-deficient CD40L Tg mice. These findings suggest that in situ activation of LCs by CD40L in the skin not only leads to chronic inflammatory dermatitis but also to systemic mixed-connective-tissue-like autoimmune disorders, possibly by breaking immune tolerance against the skin.

Animals↗

PubMed2001

[Analgesics-induced chronic renal failure in patients on dialysis therapy in Hungary].

In recent years elaboration of the diagnosis of analgesic-nephropathy (ANP) with the help of imaging techniques significantly increased the possibility of diagnosing the disease. Therefore, evaluating the prevalence of ANP has become more accurate in our country as well. The prevalence of ANP has been investigated in patients who have newly been taken into the dialysis program due to renal disease of unknown aetiology in 22 dialysis centers between December 1994-December 1997. The diagnosis of ANP has been based on revealing chronic drug abuse in the history and positive results of renal imaging (decrease in length of both kidneys combined with either bumpy contours and/or papillary calcification). Among 284 patients dialysed with unknown diagnosis 42 (14.8% of all cases) proved to have ANP. All patients except 2 took analgesic mixtures containing phenacetin/paracetamol, phenason derivatives, acetilsalysilic acid, caffeine and/or codeine. According to their investigations, ANP is a common disease resulting in end-stage renal failure in Hungary as well.

Acetaminophen↗

PubMed2001

Regulation by rho family GTPases of IL-1 receptor induced signaling: C3-like chimeric toxin and Clostridium difficile toxin B inhibit signaling pathways involved in IL-2 gene expression.

In this study the participation of Rho family GTPases in the regulation of IL-1-activated protein kinase cascades controlling IL-2 synthesis was investigated in murine EL-4 thymoma cells. The recombinant C3-like chimeric toxin, which consists of the C3 toxin of Clostridium limosum and the N-terminal part of Clostridium botulinum C2 toxin (C2IN-C3) interacting with the C2II binding subunit to facilitate uptake into cells, and selectively inactivates Rho A by ADP-ribosylation, prevented IL-1-stimulated activation of Jun-NH2-terminal-kinases (JNK) and p38 mitogen-activated-protein kinases (MAPK). UDP-monoglucosylation and concomitant inactivation of Rho A and of Rac-2 by Clostridium difficile toxin B also inhibited IL-1-induced activation of JNK and p38 MAPK, but additionally inhibited activation of the extracellular-regulated-kinase pathway and DNA binding of the transcription factor NFkappaB. Accordingly, pre-treatment of cells with C21N-C3 fusion toxin only decreased IL-1-stimulated IL-2 synthesis by 50%, while in C. difficile toxin B-treated cells IL-1-induced IL-2 secretion was reduced by 90%. These results imply that together with Rho A an additional member of the Rho family G proteins, i.e. Rac-2, is critically involved as an upstream regulator in IL-1-induced activation of different MAPK, stress-activated protein kinases, and in NFkappaB activation controlling IL-2 gene expression in response to IL-1, acting in close proximity to the IL-1-receptor complex.

Animals↗

PubMed2001

Dendritic cells and tumor immunity.

Researchers and clinicians have tried for decades to use the mechanisms of immunity for the fight against cancer. Early attempts aimed at the instrumentation of soluble immune mediators such as antibodies or cytotoxic proteins for the therapy of malignancies. Major improvements in understanding the induction and regulation of cellular immunity have now made it possible to generate effector cells in cancer patients which are specific for the neoplastic disease. At the beginning of every cellular immune reaction against cancers tumor antigens have to be presented to T cells in order to activate them and drive them into clonal expansion. This is done by antigen presenting cells, the most powerful of which is the dendritic cell (DC). While DC were hard to isolate initially, they can be generated in large numbers in vitro today and manipulated in multiple ways before given back to a patient to induce tumor immunity. Thus, a great amount of hope lies in the use of DC as inducers of tumor immunity. However, the first clinical studies, which have now been completed with only limited success make clear, that still a lot of open questions remain to be answered. This review tries to give an overview of this rapidly developing field, mentioning the major conceptual approaches and techniques, but also discussing important caveats. The next years will show whether we can improve our understanding of DC biology and the mechanisms of immune induction strongly enough to effectively employ DC for immunotherapy of cancer.

Animals↗

PubMed2001

Larynx-preserving pharyngo-esophagectomy after chemoradiation in the treatment of cancer of the pharyngo-esophageal junction.

Pharyngo-laryngo-esophagectomy in the treatment of advanced tumors of the pharyngo-esophageal junction is associated with a high morbidity and poor quality of life due to loss of the larynx. Neoadjuvant chemoradiotherapy resulted in a considerable tumor reduction in 6 patients allowing radical tumor resection by larynx-preserving pharyngo-esophagectomy. The operation consisted of total esophagectomy and resection of the posterior pharyngeal wall and reconstruction by a pharyngogastrostomy in 5 patients, and ileocolon interposition in 1 patient.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2001

GRP-receptor-mediated signal transduction, gene expression and DNA synthesis in the human pancreatic adenocarcinoma cell line HPAF.

Bombesin-like peptides have been implicated as growth factors in various human cancers. Human adenocarcinoma cell lines (Capan-1, Capan-2, MiaPaCa-2 and HPAF) were tested to determine whether they express the gastrin-releasing peptide-preferring bombesin receptor (GRPR) and neuromedin B-preferring bombesin receptor (NMBR). Using RT-PCR the highest level of GRP receptor mRNA was found in HPAF cells. NMB receptor mRNA expression moderate in all cell lines investigated. We therefore selected the HPAF cell line to investigate whether bombesin treatment affects intracellular Ca(2+) ([Ca(2+)](i)), cAMP level, DNA synthesis as a measure of cell proliferation, and expression of three transcription factors: c-fos, c-myc and high mobility group protein IY (HMG-I(Y)).Bombesin administration led to an immediate increase in free intracellular Ca(2+) concentration ([Ca(2+)](i)) but did not change cAMP levels. The peptide also enhanced [(3)H]thymidine incorporation in HPAF cells (but not in the other cell lines), an effect that was concentration dependent, reaching 36 +/- 5% stimulation over control values at 24 h with an EC(50) of 2.27 x 10(-12) M. Furthermore, bombesin stimulated c-fos, c-myc and HMG-I(Y) expression in a time-dependent manner: the c-fos mRNA level increased dramatically in the first 30 min of exposure, then returned to basal level within 2 h, while the c-myc and HMG-I(Y) mRNA levels peaked at 2 h and 4h, respectively. All actions of bombesin were blocked by BME (D-Phe(6)-bombesin-(6-13)-methylester), a selective GRP receptor antagonist, but not by the NMB receptor antagonist BIM-23127 (D-Nal-cyclo[Cys-Tyr-D-Trp-Orn-Val-Cys]-Nal-NH(2)). We conclude that HPAF cells express mRNA for GRP receptors and that functional receptors are present in the cell membrane. The occupation of these receptors leads to a sequence of intracellular events involving rapid mobilization of intracellular Ca(2+), expression of c-fos, c-myc and HMG-I(Y) mRNA, and stimulation of cell proliferation. Conversely, although NMB receptor mRNA can be detected, its actual translation to functional receptors does not reach a detectable level.

Adenocarcinoma↗

PubMed2001

Induction of potent human immunodeficiency virus type 1-specific T-cell-restricted immunity by genetically modified dendritic cells.

A novel technology combining replication- and integration-defective human immunodeficiency virus type 1 (HIV-1) vectors with genetically modified dendritic cells was developed in order to induce T-cell immunity. We introduced the vector into dendritic cells as a plasmid DNA using polyethylenimine as the gene delivery system, thereby circumventing the problem of obtaining viral vector expression in the absence of integration. Genetically modified dendritic cells (GMDC) presented viral epitopes efficiently, secreted interleukin 12, and primed both CD4(+) and CD8(+) HIV-specific T cells capable of producing gamma interferon and exerting potent HIV-1-specific cytotoxicity in vitro. In nonhuman primates, subcutaneously injected GMDC migrated into the draining lymph node at an unprecedentedly high rate and expressed the plasmid DNA. The animals presented a vigorous HIV-specific effector cytotoxic-T-lymphocyte (CTL) response as early as 3 weeks after a single immunization, which later developed into a memory CTL response. Interestingly, antibodies did not accompany these CTL responses, indicating that GMDC can induce a pure Th1 type of immune response. Successful induction of a broad and long-lasting HIV-specific cellular immunity is expected to control virus replication in infected individuals.

Animals↗

PubMed2001

Different actions of secretin and Gly-extended secretin predict secretin receptor subtypes.

Only one secretin receptor has been cloned and its properties characterized in native and transfected cells. To test the hypothesis that stimulatory and inhibitory effects of secretin are mediated by different secretin receptor subtypes, pancreatic and gastric secretory responses to secretin and secretin-Gly were determined in rats. Pancreatic fluid secretion was increased equipotently by secretin and secretin-Gly, but secretin was markedly more potent for inhibition of basal and gastrin-induced acid secretion. In Chinese hamster ovary cells stably transfected with the rat secretin receptor, secretin and secretin-Gly equipotently displaced (125)I-labeled secretin (IC(50) values 5.3 +/- 0.5 and 6.4 +/- 0.6 nM, respectively). Secretin, but not secretin-Gly, caused release of somatostatin from rat gastric mucosal D cells. Thus the equipotent actions of secretin and secretin-Gly on pancreatic secretion appear to result from equal binding and activation of the pancreatic secretin receptor. Conversely, secretin more potently inhibited gastric acid secretion in vivo, and only secretin released somatostatin from D cells in vitro. These results support the existence of a secretin receptor subtype mediating inhibition of gastric acid secretion that is distinct from the previously characterized pancreatic secretin receptor.

Animals↗

PubMed2001

Identification and localization of aquaporin water channels in human salivary glands.

Aquaporin (AQP) water channels are expressed in a variety of fluid-transporting epithelia and are likely to play a significant role in salivary secretion. Our aim was to identify and localize the aquaporins expressed in human salivary glands. Total RNA was extracted from human parotid, submandibular, sublingual, and labial glands and from human brain. Expression of aquaporin mRNA was assessed by RT-PCR using specific primers for human AQP1, AQP3, AQP4, and AQP5. All four aquaporins were detected by RT-PCR in all of the glands, and the sequences were confirmed after further amplification with nested primers. Cleaned PCR products were then used as (32)P-labeled cDNA probes in a semiquantitative Northern blot analysis using glyceraldehyde-3-phosphate dehydrogenase as reference. Only AQP1, AQP3, and AQP5 mRNAs were present at significant levels. AQP localization was determined by immunohistochemistry on paraffin sections using affinity-purified primary antibodies and peroxidase-linked secondary antibodies. Each salivary gland type showed a broadly similar staining pattern: AQP1 was localized to the capillary endothelium and myoepithelial cells; AQP3 was present in the basolateral membranes of both mucous and serous acinar cells; AQP4 was not detected; and AQP5 was expressed in the luminal and canalicular membranes of both types of acinar cell. We conclude that AQP3 and AQP5 together may provide a pathway for transcellular osmotic water flow in the formation of the primary saliva.

Antibodies↗

PubMed2000

Control of SIV rebound through structured treatment interruptions during early infection.

In a randomized controlled trial with acute simian immunodeficiency virus (SIV)-infected macaques, both highly active antiretroviral therapy (HAART) and HAART with fixed-schedule structured treatment interruption (STI-HAART; alternating 3 weeks on and 3 weeks off therapy) suppressed viral load. In the STI-HAART group, T cell virus-specific immune response (VIR) and control of viral rebound increased concurrently during subsequent interruptions. In contrast, VIR did not increase and SIV rebounded after permanent treatment withdrawal in all animals on continuous HAART. Fixed-schedule STI-HAART appears to be an effective alternative to continuous HAART for the early treatment of retroviral infection.

Adenine↗

PubMed2000

[Detection of minimal residual diseases in B-cell tumors using PCR specific for the immunoglobulin heavy chain gene].

In B-cell non-Hodgkin's lymphomas (NHL), clonal rearrangement of the immunoglobulin heavy chain (IgH) gene provides a useful marker for the detection of minimal residual disease (MRD) after treatment. To explore clinical usefulness of polymerase chain reaction (PCR) analysis of clonal IgH gene rearrangement in the detection of MRD a follow up study of 10 patients with B-cell NHL have been performed. At the time of diagnosis, tumor DNAs were PCR-amplified using sense primer specific for the heavy chain variable region (VH) and antisense primer specific for the heavy chain joining region (JH) of the IgH gene. The clonal rearrangement of IgH gene detected by PCR was used as clonal marker to determine MRD after treatment. In three cases, where clinical remission was not achieved, clonal IgH gene rearrangement was detected after the treatment. In seven cases, clinical remission was achieved after induction therapy but the PCR analysis revealed clonal IgH gene rearrangement in three of the cases. In all of the three cases, where MRD was detected by PCR, clinical relapse developed after 7-28 months of the therapy. In all cases that have relapsed, the IgH gene rearrangement was identical at the time of initial diagnosis and at the relapse. This study demonstrates that PCR analysis of clonal IgH gene rearrangement is a useful method to monitor and detect MRD before clinical relapse.

Biomarkers, Tumor↗

PubMed2000

[Recent advances in the classification and treatment of myelodysplastic syndrome].

The French-American-British (FAB) classification for myelodysplastic syndromes (MDS) is widely accepted in the clinical practice. However, advances in medical science in recent years have prompted some alterations to this purely morphological classification. In the comprehensive new classification four categories are distinguished, such as I. Primary MDS, II. MDS with myeloproliferative features, III. Mutagen induced (secondary) MDS and IV. MDS with hereditary predisposition. Treatment of MDS patients is nowadays stratified according to age of patient, availability of an HLA-identical sibling donor and risk assignment. Therapeutic strategies have been inspired by either missionary approaches converting premalignant cells into normal behaviour or by crusader tactics destroying non-compliant elements at the expense of innocent bystanders. Since apoptosis appears to be final pathway by which the hematopoietic cells undergo premature cell death, reversal of apoptosis would be the principal goal in the missionary treatment. The rational approach to suppress apoptosis would either aim at eliminating inducers of apoptosis or at preventing apoptosis by the administration of factors that can shift the balance to cell survival. Intensive acute leukemia-type treatment studies showed complete remission rates varying from 15% to 64%. The prolonged cytopenia leads to high early death rate. Transplantation of allogeneic stem cells has proven to be the only curative treatment option, but the expense of considerable transplant related mortality. The elaboration of risk adapted treatment algorithms has been much facilitated by the publication of the International Prognostic Scoring System (IPSS), which uses marrow blast percentage, cytogenetic data and number of cytopenias to delineate low, intermediate (1 and 2) and high risk categories.

Animals↗

PubMed2000

[Psychosomatic dermatologic symptoms].

The explanations of the psychosomatic dermatological symptoms are based on the dysfunction of the emotional and autonomic nervous system. In the first instance the dermatological symptoms of psychic origin are examined by the general practitioner, than the dermatologist and finally after negative findings--the psychiatrist. Behind the non-improving, itching and scratched eczema sometimes was found either Ekbom-syndrome (often diagnosed as gerontological delusions of parasitosis) or therapy-resistant allergy (which conceals depression). The authors present condensed case--stories (about delusions of parasitosis and allergic syndromes) proving the excellent results achieved using citalopram and in the case of Ekbom-syndrome--risperidone therapy.

Aged↗

PubMed2000

[Larynx-preserving pharyngoesophagectomy in the treatment of cancer of the pharyngoesophageal junction].

UNLABELLED: Pharyngo-laryngo-esophagectomy has been the sole surgical option in the management of advanced tumors arising from the pharyngoesophageal junction. This operation is associated with high morbidity, mortality and poor quality of life due to loss of larynx. The aim of the author was to achieve a reduction in tumor size by means of neoadjuvant chemoradiotherapy and so to make the tumor amenable to a larynx preserving operation avoiding pharyngo-laryngo-esophagectomy. Between 1. January 1998 and 31. December 1999, 11 consecutive patients with advanced cancer of pharyngo-esophageal junction were treated with neoadjuvant chemoradiotherapy (carboplatin, 5-fluorouracil, 30-35 Gy telecobalt irradiation). The tumor regressed in all cases and moreover, in 6 patients a larynx preserving pharyngo-esophagectomy could be carried out. This operation consists of total esophagectomy, resection of posterior pharynx wall and Akiyama-type gastric pull up with side-to-side pharyngo-gastrostomy. All 6 patients recovered. In 2 cases after neoadjuvant therapy the tumor disappeared from the cervical esophagus and so that a pharyngo-laryngectomy and free jejunum transfer could be performed. 3 other patients remained irresectable due to lymph node metastases. CONCLUSION: Larynx preserving pharyngo-esophagectomy is a safe operation by means of which the larynx can be preserved even in those patients whose tumor is located at the level of pharyngo-esophageal junction, on the posterior wall of the pharynx.

Aged↗

PubMed2000

[Correlation of alcohol consumption and pancreatitis in Hungary].

Alcoholic etiology of acute pancreatitis is outstanding high in Hungary. The aim of this retrospective study was to analyse the etiology of patients of 5 years. Between 1990 and 1994 altogether 374 patients were admitted with acute pancreatitis, which is three and half times higher than between 1970 and 1974. From the 374 cases 220 had alcoholic and only 115 had biliary etiology. Altogether in 127 patients developed necrosis, the rate of alcoholic etiology was 80% in this subgroup. During the last two decades the trend of alcohol consumption became one of the most burning question in Hungary. Based on the Jellinek's formula alcohologists estimate the number of alcoholics more than one million. The number of pancreatitis related death multiplied almost four times between 1970 and 1994. The doubling of alcohol consumption was practically simultaneous with the increase of morbidity and mortality of pancreatitis. Hungary shows the most disfavourable distribution of drink varieties among the high-consuming countries in Europe.

Acute Disease↗

PubMed1999

Effect of deramciclane, a new 5-HT receptor antagonist, on cholecystokinin-induced changes in rat gastrointestinal function.

Recent studies suggested that serotonin receptors may be involved in modulating the actions of cholecystokinin (CCK) in the gastrointestinal tract. The present work was designed to compare the effects of deramciclane, a recently developed serotonin-2 (5-HT2A/2C) receptor antagonist, and lorglumide, a CCK(A) receptor antagonist, on exogenous and endogenous CCK-induced pancreatic enzyme secretion and pancreatic growth, as well as on the emptying of the stomach and the gallbladder. Pancreatic secretory function was tested while CCK release was evoked by diversion of bile-pancreatic juice in rats. Adaptive growth of the pancreas was induced by chronic intragastric administration of camostate, a potent synthetic trypsin inhibitor in rats. Gastric emptying of a noncaloric test meal was investigated in response to intraduodenal intralipid infusion, also in rats. In fasted mice, gallbladder emptying was examined in response to intragastric egg yolk administration. In rats, diversion of bile-pancreatic juice from the duodenum stimulated pancreatic amylase secretion. This action was blocked by deramciclane and by lorglumide. Pancreatic hypertrophy and hyperplasia induced by chronic camostate administration was also suppressed by both the serotonin- and the CCK-receptor antagonists. Intraduodenal administration of intralipid induced a significant delay in gastric emptying. This effect was inhibited by both deramciclane and lorglumide in rats. In mice, intragastric administration of egg yolk elicited an accelerated release of bile from the gallbladder. Prior treatment with either deramciclane or lorglumide abolished this response. Lorglumide was able to inhibit the functional responses elicited by exogenous CCK administration in both pancreas, stomach and gallbladder, while deramciclane was not effective under such circumstances. Our data show that deramciclane inhibited the effects of CCK on pancreatic, gastric and gallbladder function when its endogenous release was stimulated, but did not alter the effects of exogenously administered peptide. These results suggest that serotonin, primarily via 5-HT2A receptors, may modulate CCK-mediated gastrointestinal functions in rats.

Animals↗

PubMed1999

Secretion from minor salivary glands following ablation of the major salivary glands in rats.

Since minor salivary glands are tiny and dispersed, ductal cannulation cannot be used when studying their function. The present study was devised to develop a method of measuring minor salivary gland function by excision of the major glands. Female rats (230-280 g) were anaesthetized with sodium pentobarbital. Ablation of the submandibular, sublingual and parotid glands was performed through a sagittal neck incision. Sham-operated rats served as controls. Groups of sialadenectomized animals were investigated immediately and after 1 week, 2 weeks and 3 months. To study secretory function, the mouth was rinsed with 250 microl water in every 5 min and protein and amylase concentrations were measured. After an initial 50 min of basal secretion pilocarpine (1 mg/kg, i.p.) was given. Bilateral ablation of both submandibular, sublingual and parotid glands led to a moderate loss of body weight and a considerable increase in water intake. No other obvious abnormality was observed for periods up to 90 days following surgery. We deduce that the minor glands secrete approximately 14 % of protein and 1% of amylase in whole saliva Secretion is maintained even after 90 days following removal of the major glands. Surgical removal of the major salivary glands allows the secretory function of the minor glands in rats to be studied in vivo.

Amylases↗