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PubMed1986

Route of administration of pentobarbital affects activity of liver glycogen phosphorylase.

Liver phosphorylase a activity in intact animals is mostly determined during anesthesia. The aim of this study was to investigate the effect of administering pentobarbital by different routes on activity of liver phosphorylase a. Rats had chronically implanted venous catheters and received pentobarbital (5 mg/100 g body wt) either intraperitoneally, as a slow intravenous infusion, or as an intravenous or intracardial bolus. Times from administration of barbiturate to sampling of the liver were 10 min, 10 min, 85 +/- 32 s (mean +/- SE), and 53 +/- 10 s, respectively. Phosphorylase a activity in % of total phosphorylase activity was 40 +/- 2, 56 +/- 4, 82 +/- 3, and 92 +/- 2, respectively, all significantly different. Thus the route of administration of pentobarbital affects the phosphorylase a activity and should be considered when evaluating this activity. This fact can only be partially explained by differences in duration before the drug takes effect. It is proposed that intraperitoneal injection of pentobarbital may anesthetize hepatic sympathetic nerves or have a direct inhibiting effect on phosphorylase a activity.

Animals↗

PubMed2001

Glucose and insulin increase the transport of leptin through the blood-brain barrier in normal mice but not in streptozotocin-diabetic mice.

Since fasting is one of the few factors found to change the rate of entry of leptin into brain, we used multiple-time regression analysis to study the effects of pretreatment with glucose or insulin on leptin transport across the blood-brain barrier (BBB). Two hours after intraperitoneal injection of glucose (3 g/kg), there was a statistically significant increase in the entry rate (K(i)) of leptin in fasted (from 4.91 +/- 0.70 x 10(-4) ml/g x min to 9.03 +/- 1.00 x 10(-4) ml/g x min) but not (p = 0.15) in nonfasted normal (from 4.90 +/- 1.21 x 10(-4) ml/g x min to 6.42 +/- 1.79 x 10(-4) ml/g x min) or fasted streptozotocin (STZ)-treated diabetic mice (from 4.043 +/- 0.959 x 10(-4) ml/g min to 5.395 +/- 1.355 x 10(-4) ml/g min). Insulin (10 U/kg) increased leptin influx in fasted (from 4.77 +/- 0.26 x 10(-4) ml/g x min to 10.6 +/- 0.15 x 10(-4) ml/g x min at 0.5 h) and nonfasted (from 4.64 +/- 0.75 x 10(-4) ml/g x min to 7.46 +/- 1.48 x 10(-4) ml/g x min at 0.5 h) normal mice, but not in STZ-diabetic mice deficient in insulin (and leptin), even though basal concentrations of glucose were similarly increased in the nonfasted normal and STZ-treated mice. Moreover, the basal rate of leptin influx was the same in overnight fasted normal mice, nonfasted normal mice and STZ-diabetic mice. The results indicate that glucose and insulin can increase leptin transport, but they probably are not the principal factors responsible for the regulatory effect of the BBB on leptin entry into the brain.

Animals↗

PubMed1979

Accumulation of substances with melanin affinity to the internal ear. Therapeutic or ototoxic mechanism?

The capacity of the melanin in the internal ear to accumulate and retain labelled lidocaine, bupivacaine and chlorpromazine after intravenous and intraperitoneal injection was examined by whole-body autoradiography. Both young pigmented hooded rats and albino rats were studied. In the pigmented rats chlorpromazine showed the greatest accumulation, which was more pronounced in the cochlea than in the vestibular portion. The other two substances were evenly distributed in the internal ear. After a single injection of chlorpromazine and of bupivacaine these substances were still bound to the melanin of the internal ear after 14 days, which was the longest survival time. Lidocaine, on the other hand, had disappeared after only 4 days. In albino animals there was very weak, transient uptake of chlorpromazine and bupivacaine, but not of lidocaine, in the internal ear. In studies in vitro on isolated bovine eye melanin there was considerably greater adsorption of chlorpromazine than of lidocaine and bupivacaine.

Animals↗

PubMed1997

Involvement of a peripheral mechanism in the emesis induced by cardiac glycosides in Suncus murinus.

The ability of three cardiac glycosides, ouabain, digitonin and digitoxin, to induce emesis and their mechanism(s) of action were investigated in Suncus murinus. The intraperitoneal injection of ouabain but not digitonin nor digitoxin caused vomiting in a dose-dependent manner. However, the administration of ouabain into the cerebroventricle did not cause emesis. Ouabain-induced emesis was partly prevented by surgical abdominal vagotomy. Pretreatment with tropisetron, a selective 5-HT3 (5-hydroxytriptamine) receptor antagonist, did not affect the emetic response evoked by ouabain. These results suggest that ouabain exerts emetic effects via peripheral mechanism(s), but 5-HT3 receptors are not involved in the pathway.

Animals↗

PubMed2003

Multiple cedar pollen challenge diminishes involvement of histamine in allergic conjunctivitis of Guinea pigs.

It has been reported that antihistamines do not fully modify symptoms of allergic conjunctivitis in clinical settings, suggesting that histamine is not the only contributor to symptom generation in the disease. However, in the majority of experimental allergic conjunctivitis models, antihistamines are very effective in the reduction of symptoms. In the present study, we used our recently developed guinea pig model of allergic conjunctivitis and evaluated whether involvement of histamine in the induction of symptoms of allergic conjunctivitis is altered by multiple antigen challenges. Guinea pigs were sensitized by intraperitoneal injection of Japanese cedar pollen extracts adsorbed on aluminum hydroxide gel, and then challenged by dropping a pollen suspension without the adjuvant on each eye once a week until the 15th challenge. The magnitude of the conjunctivitis intensity score (CIS), itch-associated scratching response and albumin leakage were found to increase with repeated challenges. At the 1st-3rd challenges, histamine H(1) receptor antagonist, mepyramine (10 mg/kg, p.o.), strongly reduced all these symptoms. However, symptoms at the 5th-15th challenges were not inhibited by mepyramine. On the other hand, a nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (10 mg/kg, i.v.), potently inhibited the increase of CIS and albumin leakage at the 15th challenge. In conclusion, histamine involvement in the induction of conjunctivitis symptoms in our model was diminished by multiple antigen challenges. The allergic conjunctivitis at the chronic stage is partly mediated by nitric oxide (NO) derived from NOSs that may be activated by mediators other than histamine. The histamine-independent allergic conjunctivitis may be useful for analyzing mechanisms underlying chronic conjunctivitis.

Administration, Oral↗

PubMed1992

Distribution of quinidine in rats with carbon tetrachloride-intoxicated hepatic disease.

The disposition of quinidine was investigated in rats with experimental hepatic disease caused by an intraperitoneal injection of CCl4. The plasma disappearance of quinidine after a 12.5 mg/kg i.v. bolus injection was analyzed by a two-compartment open model in both control and CCl4-intoxicated rats. In the CCl4-intoxicated rats, plasma total body clearance (CLtot), elimination rate constant of the central compartment (kel) and the volume of distribution (Vdss) of quinidine were decreased by 73, 51 and 36%, respectively, compared to those in the control rats. At a steady state of quinidine plasma concentration of 1 micrograms/ml, tissue-to-plasma partition coefficient (Kp,vivo) of the drug in the lung, spleen, heart, kidney and liver in the CCl4-intoxicated rats were decreased ranging from 32 to 42% compared to those in the control rats. The plasma free fraction of quinidine in the intoxicated rats was decreased by 34% of that in the control rats. Neither tissue binding of quinidien in vitro, nor plasma pH was altered in the intoxicated rats. Thus, the decrease in Vdss and Kp,vivo for quinidine in the intoxicated rats seems likely to be due to an increase in plasma protein binding of the drug. Metabolic activity in the liver, the hepatic extraction ratio for quinidine, and the hepatic blood flow in the CCl4-intoxicated rats were decreased by 84, 57 and 47%, respectively, compared to those in the control rats. The decrease in CLtot and kel in the intoxicated rats is considered to be attributed to both the reduction of liver functions and the increase in the plasma protein binding of the drug.

Animals↗

PubMed2003

Hypoglycemic effect of Hypoxis hemerocallidea corm (African potato) aqueous extract in rats.

Diabetes mellitus has been recognized as a clinical syndrome since ancient times, and remains a crippling global health problem today. It is a group of heterogeneous, autoimmune, hormonal and metabolic disorders, often accompanied by hypertension, hyperlipidemia and obesity. Current estimates suggest that approximately 150 million people worldwide suffer from diabetes mellitus. The present study was undertaken to examine the hypoglycemic effect of aqueous extract of Hypoxis hemerocallidea (family: Hypoxidaceae) corm (locally known as "African Potato") in normal (normoglycemic) and in streptozotocin (STZ)-treated, diabetic rats. Young adult, male Wistar rats weighing 250-300 g were used. Diabetes mellitus was induced in the group of diabetic test rats by intraperitoneal injections of STZ (90 mg/kg). In one set of experiments, graded doses of the aqueous extract of African Potato (100-800 mg/kg p.o.) were administered to 12-h fasted normal and diabetic rats. In another set of experiments, 800 mg/kg of African potato extract, a dose of the plant extract that produced maximal hypoglycemic effects in fasted normal and diabetic rats in our pilot experiments, was used. The hypoglycemic effect of this single dose was compared with those of insulin (5 micro U/kg s.c.) and glibenclamide (5 mg/kg p.o.) in 12-h fasted normal and diabetic rats. Following acute treatment, relatively moderate to high doses of African potato extract (100-800 mg/kg p.o.) produced dose-dependent, significant reductions (p < 0.05-0.001) in the blood glucose concentrations of fasted normal and diabetic rats. Similarly, insulin (5 micro U/kg s. c.) and glibenclamide (5 mg/kg p.o.) produced significant reductions (p < 0.01-0.001) in the blood glucose concentrations of the fasted normal and diabetic rats. At a dose of 800 mg/kg, the plant extract caused 30.20% and 48.54% reductions in the blood glucose concentrations of fasted normal and STZ-treated diabetic rats, respectively. While it is likely that the hypoglycemic effect of the plant extract is largely due to its phytosterols and/or sterolin content, the exact mechanism of its hypoglycemic action is still obscure and will have to await further studies. However, the results of this experimental animal study indicate that African potato possesses hypoglycemic activity; and thus lends credence to the suggested folkloric use of the herb in the control and/or management of adult-onset, type 2 diabetes mellitus in some communities of South Africa.

Administration, Oral↗

PubMed1979

Suppressive effect of pentagastrin on pituitary-adrenocortical secretion.

The effect of pentagastrin on the pituitary-adrenocortical secretion was examined in male rats. In the morning the intraperitoneal injection of this peptide produced a slight, but significant, decrease in the plasma corticosterone levels, but it had no effect on the evening rise due to circadian periodicity and the stress-induced elevation of the plasma corticosterone level. Following intracerebroventricular administration of pentagastrin, plasma corticosterone tended to decrease and in in vitro incubation of rat pituitary tissue the addition of pentagastrin elicited a suppressive effect on the ACTH release from the tissue into the medium. It was suggested that gastrin-like peptide might control the secretion of ACTH.

Adrenocorticotropic Hormone↗

PubMed1975

Conditions influencing the dose-response effect of growth hormone on longitudinal bone growth in the hypophysectomized rat.

Various factors that might influence the dose-response effect of growth hormone on the longitudinal bone growth were investigated with tetracycline as intravital marker of the bone growth in hypophysectomized rats. These are of practical importance for the bioassay of growth hormone. The growth response was found to be almost the same for subcutaneous and intraperitoneal injection, whereas the intravenous route resulted in significantly lower growth response. The administration of growth hormone in various volumes subcutaneously did not significantly influence the dose-dependent growth response. Freezing of the dissolved growth hormone or addition of NaOH to the solution had no significant effect on growth response. Cortisone acetate 0.5 mg/kg given at hypophysectomy increased the post-operative survival somewhat, without having any post-operative depressing influence on the growth hormone-induced longitudinal bone growth. The present investigation showed that in standardized conditions the dose-dependent growth response is constant.

Animals↗

PubMed1986

Effects of thyrotropin-releasing hormone and cyclo-histidine-proline on the homeothermic development of neonatal rats.

The effects of thyrotropin-releasing hormone (TRH) and its putative metabolite, cyclo-histidine-proline (cHP), on the homeothermic development of neonatal rats were studied. The daily intrathecal administration of 10(-11)-10(-9) moles of TRH during the second week of age produced a significant rise in body temperature by 3 weeks of age and was followed by a transient period of hypothermia. This effect, which could not be produced by an intraperitoneal injection of 10(-7) moles of TRH, was abolished by the simultaneous administration of 6-hydroxydopamine (6OHD). In contrast, intrathecally administered cHP decreased thermogenesis. During TRH treatment, brain norepinephrine (NE) and dopamine (DA) release was accelerated 2- to 4-fold. Two weeks after either TRH or cHP treatment, brain NE and DA were significantly reduced; adrenal NE in cHP-treated rats increased. The weight of the interscapular brown adipose tissue (BAT) was decreased by both cHP and 6OHD. At 3 weeks of age, [3H]guanosine diphosphate binding capacity in BAT mitochondria was reduced by 60% in TRH-treated rats and was associated with reduced mitochondrial levels of alpha-glycerophosphate dehydrogenase and liver cytochrome C reductase. These results indicate that TRH stimulates central NE release thereby enhancing thermogenesis, cHP decreases heat production, and TRH-induced hyperthermia is associated with changes in mitochondrial exothermic processes. The central TRH-cHP system may modulate the maturation of homeothermic mechanism in neonatal rats.

Adipose Tissue, Brown↗

PubMed1979

Plasma aspartate levels in rats following administration of monopotassium aspartate via three routes.

Plasma aspartate levels were measured after potassium aspartate administration through different routes to rats of various ages. The changes in plasma levels were most significant with intraperitoneal injection. Dose- and age-related responses to aspartate load were obtained. The present data suggest that a marked elevation of plasma aspartate levels may result in neuronal necrosis. By comparing the plasma aspartate levels with the results on hypothalamic lesion (Okaniwa et al., 1979), plasma peak value associated with the lesion was estimated in each case of various administration routes and rat ages.

Administration, Oral↗

PubMed1997

Leptin increases hypothalamic pro-opiomelanocortin mRNA expression in the rostral arcuate nucleus.

Melanocortins are peptides, cleaved from the pro-opiomelanocortin (POMC) precursor, that act in the brain to reduce food intake and are potential mediators of leptin action. In the forebrain, melanocortins are derived from POMC-containing neurons of the hypothalamic arcuate nucleus. To test the hypothesis that these POMC neurons are regulated by leptin, we used in situ hybridization to determine whether reduced leptin signaling (as occurs in fasting), genetic leptin deficiency (in obese ob/ob mice), or genetic leptin resistance (in obese db/db mice) lower expression of POMC mRNA. We further hypothesized that leptin administration would raise hypothalamic POMC mRNA levels in leptin-deficient animals, but not in mice with defective leptin receptors. In wild-type mice (n = 12), fasting for 48 h lowered POMC mRNA levels in the rostral arcuate nucleus by 53%, relative to values in fed controls (n = 8; P < 0.001). Similarly, arcuate nucleus POMC mRNA levels were reduced by 46 and 70% in genetically obese ob/ob (n = 6) and db/db mice (n = 6), respectively, as compared with wild-type mice (n = 5) (P < 0.01 for both comparisons). Five daily intraperitoneal injections of recombinant murine leptin (150 microg) raised levels of POMC mRNA in the rostral arcuate nucleus of ob/ob mice (n = 8) by 73% over saline-treated ob/ob control values (n = 8; P < 0.01), but was without effect in db/db mice (n = 6). In normal rats, two injections of a low dose of leptin (3.5 microg) into the third cerebral ventricle (n = 15) during a 40-h period of fasting also increased POMC mRNA levels in the rostral arcuate nucleus to values 39% greater than those in vehicle-treated controls (n = 14; P = 0.02). We conclude that reduced central nervous system leptin signaling owing to fasting or to genetic defects in leptin or its receptor lower POMC mRNA levels in the rostral arcuate nucleus. The finding that leptin reverses this effect in ob/ob, but not db/db, mice suggests that leptin stimulates arcuate nucleus POMC gene expression via a pathway involving leptin receptors. These findings support the hypothesis that leptin signaling in the brain involves activation of the hypothalamic melanocortin system.

Animals↗

PubMed2002

Effects of acute and chronic administration of the melanocortin agonist MTII in mice with diet-induced obesity.

High-fat diet-induced obesity (DIO) in rodents is associated with hyperleptinemia and resistance to leptin, but the response to agents acting downstream of leptin receptors remains unknown. We assessed the response of mice with DIO to treatment with MTII, an alpha-melanocyte-stimulating hormone analog. MTII delivered four times daily by intraperitoneal injection to C57BL/6J mice produced a dose-responsive effect on food intake, body weight, leptin, corticosterone, insulin, and free fatty acids. In DIO mice, administration of MTII 100 microg q.i.d. i.p. markedly suppressed feeding during the first 4 days of treatment, with food intake returning to control levels at day 5. Progressive weight loss also occurred over the first 4 days, after which weight plateaued at a level below control. After 8 days of treatment, MTII-treated DIO mice had major suppression of both leptin and insulin levels. Central administration of MTII for 4 days (10 nmol/day) in DIO mice significantly suppressed food intake, induced weight loss, and increased energy expenditure. These results indicate that 1) MTII administration to DIO mice causes suppression of food intake and body weight loss, and decreased food intake is primarily responsible for weight loss; 2) peripheral MTII improves insulin resistance in DIO mice; 3) "tachyphylaxis" to the effect of chronic MTII treatment on food intake occurs; and 4) at least some of the effects of MTII are exerted centrally. In conclusion, treatment with a melanocortin agonist is a promising therapeutic approach to DIO and associated insulin resistance.

Animals↗

PubMed1979

Melanin capacity to accumulate drugs in the internal ear. A study on lidocaine, bupivacaine and chlorpromazine.

The distribution and retention of labelled lidocaine, bupivacaine, and chlorpromazine to melanin in the internal ear after intravenous and intraperitoneal injection were examined by whole-body autoradiography. Both young pigmented hooded rats and albino rats were studied. In the pigmented rats chlorpromazine showed the greatest accumulation, which was more pronounced in the cochlea than in the vestibular portion. The other two substances were evenly distributed in the internal ear. After a single injection of chlorpromazine and of bupivacaine these substances were still bound to the melanin of the internal ear after 14 days, which was the longest survival time. Lidocaine, on the other hand, had disappeared after only 4 days. Strong uptake and retention of the three substances were observed in the eyes of pigmented animals. In albino animals there was very weak, transient uptake in the internal ear of chlorpromazine and bupivacaine, but not of lidocaine. In studies in vitro on isolated bovine eye melanin there was considerably greater adsorption of chlorpromazine than of lidocaine and bupivacaine. An uptake was noted in the human eye in experiments in vitro. Clinical tests revealed no acute or late damage to hearing or sight after large doses of lidocaine. The participation of melanin in different basal labyrinthine functions such as the energy transfer mechanism and the sound protective mechanism is discussed in the light of the results obtained. Further, the theory is put forward that the melanin affinity of certain substances can be of both therapeutic and ototoxic importance.

Animals↗

PubMed1975

Neuraminidase treated homologous IgG and immune deposit rental disease in inbred rats.

Immune deposit renal disease followed intravenous or intraperitoneal injections of neuraminidase treated homologous IgG or neuraminidase alone. No alterations were associated with several groups of controls. This preliminary study suggests that one mechanism by which microogranisms may be involved in the development of immune renal disease is by chemical alteration of immunoglobulin.

Animals↗

PubMed1999

Comparative study of viral encephalopathy and retinopathy in juvenile sea bass Dicentrarchus labrax infected in different ways.

The transmission of viral encephalopathy and retinopathy (VER) was investigated in juvenile sea bass (3 g) Dicentrarchus labrax by using cell culture supernatant (SSN-1 cell line) containing nodavirus. Five methods of infection were tested: intramuscular injection (IM), intraperitoneal injection (IP), oral infection, bath exposure and cohabitation of healthy fish with infected fish. Some differences were observed in time of disease onset and severity of symptoms depending on the mode of infection used. Clinical symptoms such as whirling swimming and lethargic or hyperactive behaviour were generally reproduced, except for fish infected via oral and IP infection. First mortalities occurred 3 d after IM and IP infection and 6 d after for the other modes of infection. Cumulative mortalities were also variable: 100% after IM infection, 10% after IP infection, 32% for bath exposure, 43% after cohabitation and 24% via oral infection. Histopathologically, vacuolation was observed in the central nervous tissues and in the retina. The observed lesions were more or less severe depending on the mode of infection, the sampling time and the organs: lesions on the surviving fish (42 days post infection, d p.i.) seemed to be generally more conspicuous in the retina than in the brain of the same fish. In most cases, the presence of nodavirus was confirmed in the same samples of brain and retina by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR). The virus was not detected in other organs examined. The present results suggest that 2 forms of VER can be induced: IM injection leads to an acute form (severe nervous disorders with high and fast mortality) whereas oral infection, bath exposure and cohabitation induce a subacute form (less severe disorders and weak daily mortality). This experiment demonstrates experimentally induced horizontal transmission of VER in sea bass for the first time.

Administration, Oral↗

PubMed1999

Routes of entry of Piscirickettsia salmonis in rainbow trout Oncorhynchus mykiss.

Since 1989, Piscirickettsia salmonis, the causal agent of piscirickettsiosis, has killed millions of farmed salmonids each year in southern Chile. The portal of entry for the pathogen was investigated by use of selected experimental infections in juvenile rainbow trout (12 g). The methods used were intraperitoneal injection, subcutaneous injection, patch contact on skin, patch contact on gills, intestinal intubation and gastric intubation. Cumulative mortalities at Day 33 post-inoculation were 98, 100, 52, 24, 24, and 2%, respectively. It was shown that intact skin and gills could be penetrated by P. salmonis. The high mortality obtained in subcutaneously injected fish indicated that skin injuries could facilitate the invasion of this pathogen. Results suggested that the main entry sites are through the skin and gills and that the oral route may not be the normal method by which P. salmonis initiates infection of salmonids.

Administration, Topical↗

PubMed2000

[The effect of oxytocin on Langerhans beta-islet cell function and on carbohydrate metabolic indices in intact rats and in rats with diabetes].

The experiments were carried out on male Wistar rats. Synthetic oxytocin was administrated to intact and streptozotocin-diabetic animals during 10 days by intracerebroventricular and intraperitoneal injections. The state of pancreatic b-cells was studied by a method of indirect immunofluorescence with the following results computing on VIDAS-386 image analyzing system. The measurement of the area of immunofluorescence and Langerhans islets and determination of insulin concentration and its contents in islets was provided automatically. Insulin and glucose concentration in blood was determined with standard techniques. Oxytocin central injections to intact animals stimulated insulin synthesis and secretion without changing of islets area. Peptide administration to diabetic animals resulted in braking of islets destruction, increasing of its area and contents of insulin. These changes were accompanied with the reducing of glycemia level. Thus, oxytocin administration stimulates insulin synthesis and secretion in intact and diabetic animals and this effect is more expressed with central injections. Besides it is necessary to note the oxytocin braking effect on beta-cells destruction in diabetic animals.

Animals↗