Effect of Chronic Caffeine Consumption on Cardiac Tissue Metabolism in the Rabbit.

Previous studies on the ability of caffeine to enhance endurance and boost performance have focused on theenergy substrates that are utilized by the skeletal muscle and the brain but nothing of such has been reported on cardiactissue. This study was designed to investigate the effect of caffeine on cardiac tissue metabolism in the rabbit. The study wascarried out on adult male New Zealand rabbits divided into 3 groups (n=5). Group I rabbits served as control and were given0.5ml/Kg of normal saline while group II and III rabbits were administered with 2mg/Kg and 6mg/kg of caffeine respectivelyfor 28 days. Blood samples were collected by retro orbital puncture for biochemical analysis. Animals were sacrificed bycervical dislocation and cardiac tissue biopsies were collected for biochemical and immunohistochemical analysis. Cardiactissue glycogen concentration was determined by anthrone reagent method. Cardiac tissue CPT 1 activity and cAMPconcentration were determined by immunohistochemistry and colorimetry techniques respectively, with assay kits obtainedfrom Biovision Inc. The results showed that Caffeine at 2 and 6 mg/kg significantly inhibited MPO activity from 0.72±0.05to 0.164±0.045 and 0.46±0.12 U/L respectively (p<0.05). Caffeine at 2mg/kg had no effect on serum nitric oxide but at6mg/Kg, it significantly increased serum nitric oxide form 28.01±6.53 to 45.25±3.88µM of nitrite (p<0.05). Also, Caffeineat 2 and 6mg/kg increased cardiac tissue glycogen from 15.62±0.73 to 40.69±6.35 and 38.82±6.91mg/100g respectively andcarnitine palmytol transferase 1 activity from 18.3 to 20 and 25.2% respectively. In conclusion, the study showed that caffeineconsumption increased CPT 1 activity suggesting increased utilization of free fatty acids for energy metabolism and sparingof cardiac tissue glycogen by mechanism(s) which probably involved blockade of A1 adenosine receptors and cAMPsignaling pathway.

Metabolic Fate of the Glucose Taken up by the Intestine During Induced Hyperglycaemia in Dogs.

Available data showed that the intestine increases it glucose uptake in response to hyperglycemia induced by anycause. However, what the intestine does with the glucose is not known. This study investigated the metabolic fate of theglucose taken up by the intestine during hyperglycaemia in dogs. Experiments were carried out on fasted, male, anaesthetizedmongrel dogs divided into 4 groups. The control (group 1, n=5) received normal saline (0.2 ml/kg) while groups 2-4(subdivided into two as low or high dose, n=5 each) received adrenaline (1 µg/kg or 5 µg/kg), glucagon (3 ng/kg or 8 ng/kg)and glucose (10 mg/kg/min or 20 mg/kg/min). Through a midline laparatomy, the upper jejunum was cannulated for IntestinalBlood Flow (IBF) measurement. Blood glucose and lactate levels were determined using glucose oxidase and lactatedehydrogenase methods, respectively. Intestinal Glucose/Lactate Uptake (IGU/ILU) was calculated as the product of IBFand arterio-venous glucose /lactate difference [(A-V) glucose/lactate]. Jejunal tissue samples were obtained for the determinationof Glycogen Content (GC) and activities of Glycogen Synthase (GS), Glycogen Phosphorylase 'a' (GPa), hexokinase andglucose-6-phosphatase. Anthrone method was used to determine GC while activities of GS, GPa, hexokinase and glucose-6-phosphatase were determined spectrophotometrically. Data were subjected to descriptive statistics and analyzed usingstudent's t-test and ANOVA at α0.05. Arterial and venous blood glucose and lactate were increased by adrenaline, glucagonand glucose. Venous lactate was higher than arterial lactate in all groups. Intestinal blood flow, (A-V) glucose and (A-V)lactate were increased in all the experimental groups. Intestinal glucose uptake increased by 624% (adrenaline), 705%(glucagon) and 589% (glucose) while intestinal lactate release increased by 422%, 459% and 272% respectively. IntestinalGC increased from 138.72 ± 4.58 mg/100 g to 167.17 ± 4.20 mg/100 g (adrenaline), 229.21 ± 6.25 mg/100 g (glucagon) and165.17 ± 4.20 mg/100 g (glucose). Adrenaline and glucose had no effect on GS activity but it was increased by glucagon;GPa was decreased while hexokinase activity was increased by adrenaline, glucagon, and glucose. Glucose-6-phosphataseactivity was not affected by adrenaline and glucagon but decreased by glucose. The intestine modulates blood glucose levelsthrough lactate formation, glycogen formation and most probably conversion of lactate to glucose through gluconeogenesis.

Effects of Telfairia Occidentalis Leaf Extract on Plasma Lactate and Liver Glycogen in Rats.

Telfairia occidentalis is a green vegetable popularly consumed among the native of Africa and it is generallybelieved to be of medicinal and nutritional value. Studies have reported its hypoglycaemic and hyperglycaemic effects inrats. In addition to these conflicting reports, the mechanisms for its effects on blood glucose remain inconclusive. Theobjective of this study was to investigate the mechanism involved in the increased blood glucose following treatment withT. occidentalis. Twenty five (25) male albino rats (200-250g) were randomly divided into 5 groups (n=5/group). Rats in thecontrol group received normal saline while rats in other groups were orally treated with 100 or 200 mg/kg body weight ofthe extract for either 1 or 2 weeks. At the end of the treatment, the rats were anaesthetized and blood samples were collectedfor the estimation of some biochemical parameters. The results showed significant decreases in plasma glucose after 1 weekof treatment with 100 mg/kg and 200 mg/kg. However, after 2 weeks of treatment with both doses, plasma glucose levelsincreased significantly and were higher than those of the control and the rats treated for 1 week with both doses. There werealso dose- and duration-dependent decreases in glycogen concentration in the treated rats, especially those treated for twoweeks. Glucose-6-phosphatase activity and liver glycogen concentration were lower in rats treated for 2 weeks whencompared with those treated for 1 week with both doses. Moreover, plasma lactate concentration was lower in the treatedgroups when compared with control. The results suggest that Telfairia occidentalis-induced lowering of plasma glucose afterone week of treatment probably favoured lactate oxidation/gluconeogenesis and elicited breakdown of liver glycogen whichresulted in increased plasma glucose after two weeks of treatment.

Effect of Cortisol on Plasma Lactate Levels following Cortisolinduced Hyperglycaemia in Common African Toad, Bufo regularis.

Previous studies in man have shown that cortisol induces hyperglycemia through gluconeogenesis. However,the metabolic substrates involved in cortisol-induced hyperglycemia and the role of adrenergic receptors in lactate productionin toads have not been well studied. This study investigated the effects of adrenergic receptor blockers in cortisol-inducedhyperglycemia and blood lactate levels in the common African toad (Bufo regularis). Each toad was fasted and anaesthetizedwith sodium thiopentone given intraperitoneally (50mg/kg/i.p). The animals (control) received 0.7% amphibian saline whileanimals (untreated) received cortisol intravenously (50µg/kg/i.v). In pre-treatment groups, animals received propanolol (0.5mg/kg/i.v), prazosin (0.2 mg/kg/i.v) and combination of propanolol (0.5mg/kg/i.v) and prazosin (0.2 mg/kg/i.v) respectivelyfollowed by administration of cortisol 50µg/kg/i.v. Thereafter, blood samples were collected for estimation of glucose andlactate using the modified glucose oxidase method and colorimetric method respectively. Cortisol caused significant increase in blood glucose level ((p<0.05) and reduction in blood lactate levels. Pre-treatment with Prazosin (0.2 mg/kg/i.v) causedsignificant (p<0.05) increase in blood glucose level and significant reduction in blood lactate levels while pre-treatment withPropanolol (0.5mg/kg/i.v) abolished cortisol-induced hyperglycemia and caused increase in blood lactate levels comparedwith the untreated group. The combination of both blockers abolished the hyperglycemic effect of cortisol and causedincrease in the blood lactate levels. The results of this study show that cortisol-induced hyperglycemia is a consequent ofgluconeogenesis and mediated through the beta-adrenergic receptors. The results also show that lactate is produced andused as a gluconeogenic substrate to induce cortisol hyperglycemia in the Common African toad bufo regularis. The betaadrenergic receptors are involved in the use of lactate to induce cortisol hyperglycemia in the Common African toad Buforegularis.

Potassium channels and prostacyclin contribute to vasorelaxant activities of Tridax procumbens crude aqueous leaf extract in rat superior mesenteric arteries.

BACKGROUND: Previous studies have shown that aqueous extract of the leaf of Tridax procuinbens is capable of lowering blood pressure through its vasodilatory effects. In the present study attempt was made to examine the biological active components of T procuinbens leaf using GC-MS methods. We further investigated the role of K+ channels in the vasorelaxation effects of Tridax procumbens using rat isolated mesenteric artery. METHODS: The superior mesenteric artery isolated from healthy, young adult Wistar rats (250-300 g) were precontracted with phenylephrine (PE) (10(-7) M) and potassium chloride (KCl) (60 mM) and were treated with Various concentrations of aqueous extract ofT procumbens (0.9.0 mg/ml). The changes in arterial tension were recorded using a force-displacement transducer (Model 7004; Ugo Basil Varese, Italy) coupled to data capsule acquisition system. RESULTS: The results of GG-MS revealed the presence of linoleic acid. The T. procumbens extract (TPE) ranging from 0.5-9.0 mg/mI significantly (p<0.05) reduced the, contraction induced by (PE) and (KCl) in a concentration-dependent manner. The extract also antagonised the calcium-induced vasoconstriction (1(-9) - 10(-5)) in calcium-free with high concentration of potassium as well as. in calcium- and potassium free physiological solutions. The vasorelaxing effect caused by TPE was significantly (p<0.05) attenuated with preincubation of potassium channels blockers (Barium chloride and apamin), NO synthaseinhibitor (L-NAME), prostacyclin inhibitor (indomethacin), atropine; propranolol, and methylene blue while it was not affected by preincubation with glibenclamide and tetra ethyl ammonium, 4-aminopyridine (4-AP) and oxadiazolo quinoxalin (ODQ). CONCLUSION: The results of this study demonstrate that T procumbens extract causes vasodilatory effects by blocking calcium channels and the vasodilatory effect of the extract may also be due to stimulation of prostacyclin production and opening of small-conductance Ga2+ activated potassium channels. The observed effect of this extract may be probably due to the presence of linoleic acid in this extract.

Effects of induced-kwashiorkor on salivary parameters in Wistar rats.

BACKGROUND: This study was undertaken to determine changes induced by protein malnutrition (kwashiorkor). in the secretory functions of salivary glands and biochemical parameters of salivary fluid using rats. METHODS: Eighteen male Wistar rats were randomly divided into two groups (control and kwarshiorkor) of 9 rats each. The rats were fed with normal diet and low protein diet (2% protein) respectively for a period of 6 weeks. Stimulated saliva samples using pilocarpine (10 mg/kg body weight i.p.) were collected and salivary glands (parotid and submandibular) were surgically removed. Biochemical analysis of salivary secretion using salivary lag time, flow rate, pH, total protein and concentrations of electrolytes (Na+, K+, Ca++, Cl-, HCO(2-)3 PO4) were conducted and compared. Morphological assessment of the salivary glands was done using heamatoxyline-eosin and Alcian blue stains. RESULTS: Body weights decreased in the kwashiorkor group. Weights of submandibular and parotid glands (right and left) were lower in the kwashiorkor group compared to the normal diet group. The mean salivary lag time was increased while the salivary flow rate was reduced in the kwashiorkor group compared to normal diet group. Salivary electrolytes and total protein analysis showed reduced concentration of sodium while potassium and bicarbonate concentrations were increased in the kwashiorkor group compared to the normal diet group. Histological analysis of the H-E and alcian blue stained salivary glands in the kwashiorkor group exhibited moderate to severe acinar cell atrophy, periductal fibrosis and reduced mucin content. CONCLUSION: These findings suggest the role of functional and biochemical changes in salivary secretion in the pathophysiology of oral diseases associated with protein malnutrition.

Effects of chronic administration of ethanolic extract of kolanut (Cola nitida) and caffeine on vascular function.

BACKGROUND: Kolanut (Cola nitida) is consumed in virtually every part of the world. The caffeine content of kolanut is scarce and the number of investigations studying the health benefits of kolanut is negligible compared to coffee. OBJECTIVE: The present study was designed to identify the caffeine content of kolanut and evaluate the effect of its chronic consumption on cardiovascular functions in rats. METHODS: The caffeine content of kolanut was determined by Gas chromatography-mass spectrometry (GC-MS). Wistar albino rats were divided into four groups (10 Rats/group). Kolanut extract (11.9 mg/kg), caffeine extracted from kolanut (7.5 mg/kg), decaffeinated of kolanut extract (6 mg/kg) and distilled water (control) was administered orally to each group for six-weeks. Effect of treatment on body weight, blood pressure and relaxation response to acetylcholine (ACh) and sodium nitroprusside (SNP) of the aortic rings was assessed. RESULTS: The total caffeine content of kolanut extract was found to be 51% and it was 96% pure from GC-MS analysis. Chronic consumption of kolanut and caffeine significantly (p < 0.05) decreased body weight. Similarly, kolanut extract decaffeinated kolanut and caffeine significantly (p < 0.05) reduced the contractile response to noradrenaline and higher potassium solution. Kolanut extract and caffeine also significantly (p < 0.05) increased the mean arterial blood pressure. Caffeine and kolanut consumption reduced the relaxation response to both acetylcholine and sodium nitroprusside. Atropine and L-NAME considerably inhibit the ACh-induced relaxation of the rat aortic ring suggesting the involvement of cholinergic mechanism. However, indomethacin (10(-4)M) also attenuated the ACh response indicating involvement of protanoids. CONCLUSION: The results suggest that treatment with both kolanut extract and caffeine had similar characteristics between the two groups with no significant differences in the ACh-induced relaxation of thering suggesting that the action of kolanut extract is due to its caffeine content.

Intestinal glucose uptake responses to infusion of glucose, fructose and galactose in dogs Intestinal glucose uptake responses to infusion of glucose, fructose and galactose in dogs.

The present study was designed to investigate the effects of intravanous (i.v) infusion of fructose, galactose and glucose on canine IGU during postprandial state. Experiments were carried out on fasted, male, anaesthethized adult mongrel dogs divided into four groups with 5 dogs per group. Each of the groups was given i.v infusion of normal saline, fructose (0.15, 0.55 and 1.1mg/dl/min), galactose (0.15, 0.55 and 1.1mg/dl/min) and glucose (0.15, 0.55 and 1.1mg/dl/min) respectively. Through a midline laparatomy, the upper jejunum was secured and cannulated for blood flow measurement. Blood samples were obtained for measurement of glucose content of arterial and venous blood from the upper jejunal segment. The blood glucose was determined by glucose oxidase method and intestinal glucose uptake was calculated as the product of jejunal blood flow and arterio-venous glucose difference. Values are means ± S.E.M, compared by ANOVA and Student t-test. Fructose, galactose and glucose significantly increased arterial blood glucose from 97.60 ± 1.78 mg/dl to 114.20 ± 1.88, 109.80 ± 1.43, and 141.20 ± 5.65 mg/dl, respectively. Glucose also significantly increased jejunal blood flow from 10.0 ± 0.32 ml/min to 14.40 ± 0.93 ml/min, however, fructose and galactose did not produce any significant effect on intestinal blood flow. IGU increased by 600%, 350%, and 700% in response to fructose, galactose and glucose respectively. There is no correlation between the increase in blood glucose levels induced by each of the sugars and its corresponding rise in IGU. The data suggest that the intestine responds to fructose and galactose in a similar manner as glucose probably through similar mechanism.

Role of Adrenergic Receptors in Glucose, Fructose and Galactose-Induced Increases in Intestinal Glucose Uptake in Dogs.

The study investigated the role of adrenergic receptors in glucose, fructose-, and galactose- induced increases in intestinal glucose uptake. Experiments were carried out on fasted male anaesthetized Nigerian local dogs divided into seven groups (with five dogs per group). Group I dogs were administered normal saline and served as control. Dogs in groups II, III and IV were intravenously infused with glucose (1.1 mg/kg/min), fructose (1.1 mg/kg/min) and galactose (1.1 mg/kg/min) respectively. Another three groups, V, VI and VII were pretreated with prazosin (0.2mg/kg), propranolol (0.5mg/kg) or a combination of prazosin (0.2mg/kg) and propranolol (0.5mg/kg) followed by glucose infusion, frutose infusion or galactose infusion respectively. Through a midline laparatomy, the upper jejunum was cannulated for blood flow measurement and blood samples were obtained for measurement of glucose content of the arterial blood and venous blood from the upper jejunal segment. Glucose uptake was calculated as the product of jejunal blood flow and the difference between arterial and venous glucose levels (A-V glucose). The results showed that pretreatment of the animal with prazosin had no effect on glucose and galactose induced increases in glucose uptake. However, pretreatment with propranolol completely abolished glucose, fructose and galactose-induced increases in intestinal glucose uptake. Prazosin also significantly reduced galactose-induced increase in intestinal glucose uptake. The results suggest that the increases in intestinal glucose uptake induced by glucose and fructose are mediated mostly by beta adrenergic receptors while that of galactose is mediated by both alpha and beta adrenergic receptors.

The Aqueous Calyx Extract of Hibiscus sabdariffa Lowers Blood Pressure and Heart Rate via Sympathetic Nervous System Dependent Mechanisms.

The antihypertensive effect of Hibiscus sabdariffa (HS) has been validated in animals and man. This study tested the hypothesis that its hypotensive effect may be sympathetically mediated. The cold pressor test (CPT) and handgrip exercise (HGE) were performed in 20 healthy subjects before and after the oral administration of 15mg/Kg HS. The blood pressure (BP) and heart rate (HR) responses were measured digitally. Mean arterial pressure (MAP; taken as representative BP) was calculated. Results are expressed as mean ±SEM. P<0.05 was considered significant. CPT without HS resulted in a significant rise in MAP and HR (111.1±2.1mmHg and 100.8±2.0/min) from the basal values (97.9±1.9mmHg and 87.8±2.1/min; P<0.0001 respectively). In the presence of HS, CPT-induced changes (ΔMAP=10.1±1.7mmHg; ΔHR= 8.4±1.0/min) were significantly reduced compared to its absence (ΔMAP= 13.2±1.2mmHg; ΔHR= 13.8±1.6/min; P<0.0001 respectively). The HGE done without HS also resulted in an increase in MAP and HR (116.3±2.1mmHg and 78.4±1.2/min) from the basal values (94.8±1.6mmHg and 76.1±1.0/min; p<0.0001 respectively). In the presence of HS the HGE-induced changes (ΔMAP= 11.5±1.0mmHg; ΔHR= 3.3±1.0/min) were significantly decreased compared to its absence (ΔMAP=21.4±1.2mmHg; ΔHR= 12.8±2.0/min; P<0.0001 respectively). The CPT and HGE -induced increases in BP and HR suggest Sympathetic nervous system activation. These increases were significantly dampened by HS suggesting, indirectly, that its hypotensive effect may be due to an attenuation of the discharge of the sympathetic nervous system.

Effect of adrenaline on glucose uptake in the rabbit small intestine.

OBJECTIVES: Previous study had shown that nicotine acts on blood glucose through release of adrenaline. While there are reports on the hyperglyceic effect of adrenaline in rabbits, there is no information on the effect of adrenaline on intestinal glucose uptake of rabbits. The present study was carried out to find out if adrenaline has any effect on glucose uptake in the rabbit small intestine. MATERIALS AND METHODS: Experiments were carried out on fasted anaesthetized male rabbits. Five groups of rabbits (6 rabbits per group) were studied. A vein draining a segment of the upper jejunum was cannulated for blood flow and venous glucose measurements. The left femoral artery and vein were cannulated for arterial blood sampling and drug infusion respectively. Glucose uptake was calculated as a product of jejunal blood flow and the glucose difference between arterial (A) and venous (V) blood. RESULTS: The fasting venous blood glucose levels were 151.8 +/- 4.4mg/dl and 164.0 + 2.3mg/dl in Groups I and V that were not given adrenoceptor blockers. The upper jejunum had a resting (or basal) glucose uptake of 38.3 +/- 1.6mg/min in the control group. When adrenaline (2ug/kg) was injected intravenously, arterial blood glucose rose from a basal value of 245.5 +/- 4.6mg/dl to 307.5+4.7mg/dl at the peak of response while venous glucose rose from 151.8+4.4mg/dl to 275.8 +/- 4.2mg/dl at the peak of response. Glucose uptake increased to 107.4 +/- 2.5mg/ min at the peak of response. The hyperglycaemic response to adrenaline injection was abolished by propranolol but not by prazosin indicating that this effect of adrenaline is mediated through beta adrenoceptor. Both prazosin and propranolol reduced considerably adrenaline-induced increase in blood flow and glucose uptake, prazosin being more potent in flow reduction. CONCLUSION: This study showed that the resting small intestine of rabbits took up large amounts of glucose. The intestinal glucose uptake was markedly increased by adrenaline injection. The response to adrenaline was mediated through alpha and beta adrenoceptors. The responses to adrenaline are different in many respects from those induced by nicotine in rabbits in our earlier study. The reason for the differences is obscure.

Effect of caffeine and ethanolic extract of kolanut on glucose uptake in the canine hindlimb at rest and during contraction.

The study investigated the effects of caffeine and ethanolic extract of kolanut (EEK) on glucose uptake in the canine hindlimb at rest and during contraction. Thirty male anaesthetized mongrel dogs [11-13 kg] were divided into six groups [5 dogs/group] Caffeine [6 mg/kg], EEK [5 mg/kg], or normal saline [control] was administered intravenously to each group at rest. Arterial and venous blood samples were collected at 0, 5, 10, 15, 20, 25, 30, 45, 60, 75 and 90 minutes after drug administration. Blood glucose was measured by glucose oxidase method. Arteriovenous [A-V] glucose difference was calculated and venous blood flow [VBF] was measured during the sampling period. Hindlimb glucose uptake [HGU] was calculated as the product of [A-V] glucose and blood flow. After sampling at rest, the experiments were repeated with the right femoral nerve stimulated using electrical stimulator at 5 Hz. At rest, A-V glucose increased significantly [P<0.05] from 4.2+/-0.2 mg/dl to 29.8+/-8.6, and 24.4+/-2.6 for caffeine and EEK respectively. VBF decreased to 2.0+/-0.9 and 6.0+/-0.6 ml/min for caffeine and EEK respectively. However, HGU significantly increased from 34.8+/-0.1 mg/min to 74.5+/-3.2 mg/min and 175.8+/-3.4 mg/min for caffeine and EEK, respectively. Contraction of the hindlimb muscle alone significantly increased the [A-V] glucose [68%], VBF [26%] and HGU [120%] when compared with the control. During contraction, [A-V] glucose increased from 4.3 +/-1.5 mg/dl to 35.6+/-3.0 mg/dl, and 27.0+/-2.2 mg/dl for caffeine and EEK respectively. VBF also increased from 8.4+/-0.3 ml/min to 12.8+/-0.3 ml/min for EEK. Although, contraction improves VBF [7.3+/-0.5 ml/min] to the hindlimb in response to caffeine, the value was significantly [P<0.05] lower than that of control [8.4+/-0.5 ml/min]. Contraction also significantly increased HGU from 35.8+/-3.6 mg/min to 249.0+/-3.3 and 286.72+/-2.0 mg/min for caffeine and EEK, respectively. The results showed that caffeine and EEK significantly increased HGU and that these effects are due to the increases in glucose extraction [A-V glucose] caused by caffeine and EEK.

Effect of nicotine on glucose uptake in the rabbit small intestine.

A technique for measuring glucose uptake in the small intestine of rabbits was developed. Using this technique, the glucose uptake in the resting jejunum of rabbits and the effect of nicotine infusion on glucose uptake were studied. Experiments were carried out on fasted anaesthetized male rabbits. Four groups of rabbits (6 per group) were studied. A vein draining segment of the upper jejunum was cannulated for blood flow and venous glucose measurements. The left femoral artery and vein were cannulated for arterial blood sampling and drug infusion respectively. Glucose uptake was calculated as a product of jejunal blood flow and the (A-V) glucose difference. The fasting blood glucose levels were 101.0 +/- 8.4 mg/dl and 127.0 +/- 11.3 mg/dl before and after anaesthesia respectively. Basal blood glucose was much higher than this following surgery. The upper jejunum had a resting glucose uptake of 24.1 +/- 7.0 mg/min. When nicotine (50 ug/kg) was infused intravenously, blood glucose rose from a basal value of 253.8 +/- 9.5 mg/dl to 379.8 +/- 20.3 mg/dl at the peak of response. Glucose uptake increased to 73.1 +/- 11.3 mg/min at the peak of response. These effects of nicotine are mediated through both beta and alpha adrenoceptors. Comparison with previous studies in dogs and rats showed that different adrenoceptors are involved in nicotine hyperglycaemia in fasted dogs, rats and rabbits.

Role of adrenergic receptors in the caffeine-induced increase in glucose uptake by the canine hindlimb.

The present study was designed to investigate the effects of alpha and beta adrenergic receptor blockers on caffeine-induced increase in canine hindlimb glucose uptake. The study was carried out on fasted male anaesthetized dogs divided into five groups [5 dogs per group]. Each dog was given a bolus injection of normal saline, caffeine [6 mg/kg] caffeine after pretreatment with prazosin [0.2 mg/kg], caffeine after pretreatment with propranolol [0.5 mg/kg] or caffeine after pretreatment with a combination of prazosin [0.2 mg/kg] and propranolol [0.5 mg/kg]. The experiments were carried out under resting and exercising conditions of the hindlimb. Hindlimb glucose uptake [HGU] was calculated as the product of blood flow and arterio-venous glucose difference. Blood glucose was determined by the glucose oxidase method and blood flow to the hindlimb was determined by time-collection method. The results showed that pretreatment of the animal with either prazosin or propranolol significantly reduced caffeine-induced hyperglycemia, glucose extraction and hindlimb glucose uptake at rest. The two blockers also separately reduced caffeine-induced hyperglycemia during contraction of the hindlimb. Prazosin or propranolol did not however influence the effect of caffeine on glucose extraction and hindlimb glucose uptake during contraction of the hindlimb. It was therefore concluded that alpha and beta adrenergic receptors are involved in caffeine induced responses at rest and not during hindlimb contraction.

Intestinal glucose uptake in normal, untreated and insulin-treated diabetic dogs.

The study was carried out on fasted, anaesthetized diabetic and non-diabetic dogs. Diabetes was induced by i.v injection of alloxan (60 mg/kg). A vein draining a segment of the upper jejunum was cannulated for blood flow measurements, and blood samples were obtained for determination of glucose content of arterial and venous blood. Glucose uptake was calculated as the product of jejunal blood flow and arterio-venous glucose difference ((A-V) glucose. The results showed that following induction of diabetes, there were significant increases in jejunal blood flow, (A-V) glucose and jejunal glucose uptake when compared with non-diabetic dogs. For instance, the glucose uptake increased from 23.10+/-2.34 to 178.40+/-6.93 mg/min. When the diabetic dog was challenged with different doses of insulin (2.5, 5.0, 7.5, 10.0 iu/kg), the blood glucose levels and the intestinal glucose uptake decreased in a dose-dependent manner. In normal dogs, insulin administration caused negative glucose uptake at the lower dose (5.0 iu/ kg) while at the higher dose, 8.0 iu/kg, insulin caused just a transient negative glucose uptake. From the results, it was concluded that the small intestine increased its glucose uptake in response to the hyperglycemia in alloxan-induced diabetes and when the blood glucose was reduced with insulin the intestine also reduced its glucose uptake accordingly. The result of insulin administration in normal dogs suggests that glucose uptake by the gut cannot be explained on the basis of blood glucose concentration alone.

Influence of nitric oxide on histamine and carbachol-induced gastric Acid secretion in the common african toad - bufo regularis.

The study aimed to determine the influence of nitric oxide (NO) on the action of histamine and carbachol on acid secretion in the common African toad - Bufo regularis. Gastric acidity was determined by titration method. The acid secretion was determined when nitric oxide was absent following administration of NO synthase inhibitor; N-nitro-L-arginine methyl ester (L-NAME) and when nitric oxide was in excess by administration of exogenous NO donor, sodium nitroprusside (SNP). Histamine or carbachol increased acid secretion in the toad. Acid output increased from 0.32 +/- 0.04 mEq/15min to 0.56 +/- 0.08 and 0.61 +/- 0.05 mEq/15min for histamine and carbachol respectively [P < 0.05]. Pretreatment of the toad with L-NAME produced further increases in histamine (0.62 +/- 0.06 mEq/15min) or carbachol (0.74 +/- 0.06 mEq/15min) induced acid secretion respectively. SNP however, completely abolished the acid secretion stimulated by either histamine or carbachol. It was therefore concluded that nitric oxide has a negative influence on the histamine or carbachol-stimulated acid secretion in the toad - Bufo regularis.

Effects of different brands of fluoride dentifrices on dental caries incidence in the rat.

The effectiveness of 3 different brands of fluoride-containing dentifrices on the prevention of dental caries was investigated in molars of young rats. Forty albino Wistar rats weighing 50-80g, 28 males and 12 females were inoculated in the mouth with streptococcus viridans daily from day 1 to day 5 of the experiment. The animals were then divided into four groups and fed with rat pellets containing 60% sucrose added as granulated sugar. All the groups were given water ad libitum. Group I had daily tooth brushing with water and served as the control while groups II, III and IV received daily brushing of their molar teeth with different fluoride--containing dentifrices: (Maxam, Florish and Close-Up respectively. All topical treatments were given for one minute daily per rat from day 6 to day 56 of the experiment. At the end of the experiment the animals were sacrificed, the jaws removed and the teeth were scored for occlusal caries. All fluoride--containing dentifrices tested reduced caries in the following order: Maxam 37.86%, Florish 59.22% and Close-Up 57.28%. This study confirmed that fluoride incorporated in Florish and Close-Up showed significant levels of caries reduction (P <0.01) and (P <0.05) respectively in the rat. It also adds credence to Dental Health Education in the application of various tooth pastes in oral hygiene measures.

Effect of adrenaline on the glucose uptake by the canine hindlimb.

The effect of adrenaline on the glucose uptake by a non-exercising hindlimb was studied in fasted anaesthetized dog. Glucose uptake (mg/min) was calculated as the product of the venous blood flow and anterio-venous glucose difference (A - V). Although, adrenaline caused significant increase in venous blood flow, it however, reduced significantly the (A - V) glucose level and the glucose uptake by the hindlimb. The adrenaline effects were however, abolished by pretreating the animal with propranolol, a beta-adrenergic blocker. It was therefore concluded that the skeletal muscle of the canine hindlimb is not involved in glucose homeostasis during adrenaline hyperglycemia.

Studies on the anti-inflammatory properties of Entada abyssinica.

The defatted methanolic extract of Entada abyssinica was evaluated for anti-inflammatory activity in acute and chronic models of inflammation. The extract (50--200 mg/kg, p.o.) exhibited dose-dependent and significant inhibition of both the carrageenan-induced rat paw oedema and granuloma tissue formation in rats. The extract (50--200 mg/kg, p.o.) was also found to inhibit the acetic acid-induced vascular permeability in a dose-dependent fashion in mice. This study demonstrated the anti-inflammatory activity of Entada abyssinica.