Relationship between the blood glucagon, growth hormone and glucose levels in myocardial infarction

Intravenous regional anaesthesia in the reduction of Colles' fracture was compared in 70 patients with 55 others who were treated with general anaesthetics. It was found to be easier and to involve a shorter waiting time, not to require patients to be supervised so long during recovery, and after this method it was less frequently necessary for patients to be taken home by ambulance. Its disadvantages were that it took longer, and could not be used for psychiatric patients or children.     

Comparison of pre- versus post-incision administration of intrathecal bupivacaine and intrathecal morphine in a rat model of postoperative pain

BACKGROUND: Preclinical studies in experimental animals suggest that preemptive analgesia may improve postoperative pain management. The beneficial effects of preemptive analgesia appear less remarkable clinically. The purpose of this study is to examine the effect of pre- and post-incision administration of intrathecal bupivacaine and intrathecal morphine in a rat model for postoperative pain. METHODS: Rats with intrathecal catheters were anesthetized with halothane, and the surgical field was prepared. A saline vehicle or the test drug was administered 15 min before an incision was made in the plantar aspect of the hindpaw or after the incision was completed. After recovery, mechanical hyperalgesia to punctate and nonpunctate stimuli was measured. Rats were tested on the day of surgery for the first 5 h and each day for 6 days. RESULTS: In saline vehicle-treated rats, the median withdrawal threshold decreased from 522 mN to 54 mN or less, and the response frequency to pressure from application of the plastic disc increased from 0 +/- 0% to 96 +/- 12% or greater after incision. Hyperalgesia was persistent through 2 days after surgery and then gradually returned toward preincision values over the next 4 days. Pre- or postincision administration of either intrathecal morphine or intrathecal bupivacaine reduced hyperalgesia on the day of surgery; at all subsequent times, there were no differences between the saline vehicle groups and the drug treatment groups. There were never any significant differences between pre- and postincision treatments. CONCLUSIONS: Early reduction in pain behaviors either by pre- or postincision management had no impact on subsequent measures of hyperalgesia in this model. These results agree with a number of clinical studies and suggest that incisional pain may be initiated and maintained differently than pain in other models.     

Contribution of glycogen and exogenous glucose to glucose metabolism during ischemia in the hypertrophied rat heart

Although hypertrophied hearts have increased rates of glycolysis under aerobic conditions, it is controversial as to whether glucose metabolism during ischemia is altered in the hypertrophied heart. Because endogenous glycogen stores are a key source of glucose during ischemia, we developed a protocol to label the glycogen pool in hearts with either [3H]glucose or [14C]glucose, allowing for direct measurement of both glycogen and exogenous glucose metabolism during ischemia. Cardiac hypertrophy was produced in rats by banding the abdominal aorta for an 8-week period. Isolated hearts from aortic-banded and sham-operated rats were initially perfused under substrate-free conditions to decrease glycogen content to 40% of the initial pool size. Resynthesis and radiolabeling of the glycogen pool with [3H]glucose or [14C]glucose were accomplished in working hearts by perfusion for a 60-minute period with 11 mmol/L [3H]glucose or [14C]glucose, 0.5 mmol/L lactate, 1.2 mmol/L palmitate, and 100 mumol/mL insulin. Although glycolytic rates during the aerobic perfusion were significantly greater in hypertrophied hearts compared with control hearts, glycolytic rates from exogenous glucose were not different during low-flow ischemia. The contribution of glucose from glycogen was also not different in hypertrophied hearts compared with control hearts during ischemia (1314 +/- 665 versus 776 +/- 310 nmol.min-1.g dry wt-1, respectively). Glucose oxidation rates decreased during ischemia but were not different between the two groups. However, in both hypertrophied and control hearts, the ratio of glucose oxidation to glycolysis was greater for glucose originating from glycogen than from exogenous glucose. Our data demonstrate that glycogen is a significant source of glucose during low-flow ischemia, but the data do not differ between hypertrophied and control hearts.     

Changes in plasma glucose, insulin, glucagon, catecholamine, and glycogen contents in tissues during development of alloxan diabetes mellitus in rats

Leishmanial antigens (LAg) were used as a vaccine against Leishmania donovani, the causative agent of visceral leishmaniasis. BALB/c mice, immunized intraperitoneally with 20 micrograms of the antigen in phosphate-buffered saline (PBS) or entrapped in liposomes, were infected intravenously with 2 x 10(7) L. donovani promastigotes. Mice immunized with PBS and empty liposomes showed similar levels of parasite burdens in the liver and spleen. Injection of the antigen alone or entrapped in liposomes, followed with infection, induced significant levels of protection against the disease. After 2 and 4 mo of infection, mice immunized with free antigen induced 7.4% and 50.7% reduction in the liver parasite burden, respectively, compared to control (PBS) mice. With antigen encapsulated in liposome, the liver parasite burden was further reduced by 30.4% and 73% at 2 and 4 mo by infection, respectively. Splenic parasite burden was very low at 2 mo of infection. At 4 mo, the parasite level was reduced by 54.2% with free antigen and 69.3% with antigen entrapped in liposomes. Whereas the protection induced by the free antigen is mainly cell mediated, stimulation of an antibody response together with a strong delayed-type hypersensitivity may be responsible for the better protection with liposomal antigen.     

Protein: metabolism and effect on blood glucose levels

Insulin is required for carbohydrate, fat, and protein to be metabolized. With respect to carbohydrate from a clinical standpoint, the major determinate of the glycemic response is the total amount of carbohydrate ingested rather than the source of the carbohydrate. This fact is the basic principle of carbohydrate counting for meal planning. Fat has little, if any, effect on blood glucose levels, although a high fat intake does appear to contribute to insulin resistance. Protein has a minimal effect on blood glucose levels with adequate insulin. However, with insulin deficiency, gluconeogenesis proceeds rapidly and contributes to an elevated blood glucose level. With adequate insulin, the blood glucose response in persons with diabetes would be expected to be similar to the blood glucose response in persons without diabetes. The reason why protein does not increase blood glucose levels is unclear. Several possibilities might explain the response: a slow conversion of protein to glucose, less protein being converted to glucose and released than previously thought, glucose from protein being incorporated into hepatic glycogen stores but not increasing the rate of hepatic glucose release, or because the process of gluconeogenesis from protein occurs over a period of hours and glucose can be disposed of if presented for utilization slowly and evenly over a long time period.     

Effect of caloric restriction on basal insulin levels and the in vivo lipogenesis and glycogen synthesis from glucose in the Koletsky obese rat

Fasting plasma immunoreactive insulin levels increased with age in hyperinsulinemic Koletsky obese rats, being almost four times as high as in lean siblings at 3 mo (40 +/- 5 muU/ml) and rising steadily to 82 +/- 4 muU/ml at 6 mo (about seven times higher than lean siblings). Restricting the food intake of the obese rats markedly reduced but did not normalize the hyperinsulinemia, which in these rats was accompanied by normal plasma glucose concentrations. The incorporation in vivo of D-U-14C-glucose into tissue lipids and glycogen was measured 1 hr after the intravenous injection of 1 g glucose (containing 100 muDi D-U-14C-glucose) per kg body weight in obese rats eating ad libitum, obese rats after 3 mo on a restricted food intake, and lean siblings. All tissues (heart, diaphragm, skeletal muscle, and adipose tissues and liver) of obese rats exhibited a significantly greater lipogenesis from glucose than those of lean siblings. Dietary restriction of the obese rats reduced the 14C incorporation into lipid to levels not significantly different from lean controls in all tissues except skeletal muscle and liver, where, although greatly reduced, lipogenesis was still significantly higher than in lean rats. Glycogen synthesis tended to be greater in all tissues of obese rats than in lean animals. Dietary restriction of obese rats did not greatly affect glycogen synthesis.     

Glucose effect on glycogen synthetase and phosphorylase in fetal rat liver

The weight and biochemistry of the skeletal muscles of rats developing under conditions of the action of the skeletomuscular loads (the I group), under conditions of hypodynamia - at the environmental temperature of 20-22 degrees C (the II group) and at the environmental temperature of 28-30 degrees C (the III group) were studied. Rats of the I group displayed an increase of the mass of the skeletal muscles and also an elevation of protein, glycogen, ATP, creatine phosphate and a decrease of lactic acid content in these muscles. Rats of the III group showed a considerable decrease in the content of enumerated indices both in comparison with indices of control animals and of rats of the I group. This decrease was less marked in rats of the II group.     

Decrease in isoflurane requirements and of postoperative pain with preanesthetic intrathecal morphine

OBJECTIVES: 1) To determine whether preanesthetic intrathecal administration of 0.5 mg morphine reduces isoflurane requirements for anesthetic maintenance. 2) To assess the duration of postoperative analgesia and the type and frequency of complications attributable to the procedure. PATIENTS AND METHODS: A series of 45 adults were distributed into 3 groups of 15 patients each based on site of surgery and site of preanesthetic (30 min) injection of 0.5 mg pure morphine. Control group (C0) patients underwent lumbar surgery and received subcutaneous morphine. Group C0.5 patients also underwent lumbar surgery but received intrathecal morphine. Group A0.5 patients underwent long-duration high abdominal surgery and received intrathecal morphine. Anesthesia was maintained with nitrous oxide (60%) in oxygen (40%) and a variable concentration of isoflurane. Isoflurane needs were assessed by averaging six consecutive measurements of end-tidal isoflurane pressure (M30FETiso) taken at intervals of 5 min. Postoperative analgesia was evaluated by means of a visual analog scale that was converted to numerical units (VASn). RESULTS: M30FETiso in group C0 (0.8%) was always higher (p < 0.01) than in the other two groups. M30FETiso in group A0.5 was higher (p < 0.01) than in group C0.5 during the first 150 min of surgery. After 180 min, there were no differences in M30FETiso (0.10-0.16%) between the two groups receiving intrathecal morphine. VASn results (mean +/- SD) in the first 4 hours were higher in group C0 (7.33 +/- 0.6) than in group C0.5 (1.13 +/- 0.35) and group A0.5 (1.07 +/- 0.26). The time of morphine-dependent analgesia was shorter (p < 0.01) in group C0 (0.62 +/- 0.38 hours) than in groups C0.5 (30.4 +/- 5.11 hours) and A0.5 (28 +/- 4.34 hours). There were no significant differences between the two groups receiving intrathecal morphine. CONCLUSIONS: Preanesthetic subarachnoid lumbar injection of 0.5 mg of pure morphine reduced early requirements for isoflurane in lumbar surgery (0.14% after 60 min). This reduction was initially less in patients undergoing abdominal surgery (0.44% at 60 min) but was the same after 150 min. Postoperative analgesia was long-term and independent of type or duration of surgery. There was no respiratory depression after surgery and the incidence of postoperative complications was similar in the two groups that received subarachnoid morphine.     

Inhibitory effect of intraventricular administration of morphine on the hyperviscosity and elevation of blood pressure induced by stress in the rat

Experiments were performed on 99 Wistar rats. It was found that hyperviscosity and elevation of blood pressure (BP) could be induced by hanging and restraining conscious rats with their four limbs tied on a frame. These effects were unaffected by bilateral vagotomy. By intravenous injection of propranolol or phentolamine, elevation of BP could be reduced, while stress-induced hyperviscosity could only be reduced by propranolol (i.v.). Stress-induced hyperviscosity and elevation of BP could be inhibited by electroacupuncture applied to the right hind leg or microinjection of morphine into 4th ventricle of the brain. On the other hand, if opiate receptor antagonist naloxone was given into the 4th-ventricle, the stress-induced hyperviscosity and elevation of BP could no longer be inhibited by electroacupuncture. It is suggested that the hyperviscosity and elevation of BP induced by hanging and restraining are mediated by excitatory cardiovascular sympathetic outflow with the result of activation of adrenoreceptors. Activation of the opiate receptors in the hindbrain may be responsible for decrease in stress-induced hyperviscosity and elevation of BP and for the inhibitory effect of electroacupuncture of the right hind leg on stress-induced hyperviscosity and elevation of BP.     

The effect of glypondin on glycogen and protein accumulation in rat organs

Rats were treated for 21 days with 20, 30 and 40 mg/kg Glypondin dissolved in the drinking water. The weight-increasing effect of Glypondin was studied in rat organs. In the liver a significant rise in the concentration of TCA-soluble glycogen was demonstrated. In the myocardium and m. gastrocnemius the concentration of both the labile and glycogen was unchanged. In the m. gastrocnemius of rats treated with Glypondin a significant rise in the concentration of noncollagenous protein was demonstrated.     

Effect of diabetes, insulin, and glucose load on lipid peroxidation in the rat

Lipid peroxidative activity in rats made diabetic with streptozocin and rats made acutely hyperglycemic by intraperitoneal dextrose administration was determined by measurement of exhaled ethane during exposure in vivo to ethane-free air (EFA). Diabetic rats demonstrated increased ethane in the expired breath while breathing EFA (5.82 +/- 0.56 pmol/min/100 g) compared with control rats (4.02 +/- 0.23 pmol/min/100 g). Insulin treatment of diabetic rats attenuated the ethane produced (4.88 +/- 0.23 pmol/min/100 g). Acute hyperglycemia increased exhaled ethane to levels higher than those seen in diabetic rats (9.87 +/- 0.98 pmol/min/100 g). Saline injected intraperitoneally to control rats produced ethane levels similar to those of untreated nondiabetic controls (4.11 +/- 0.52 pmol/min/100 g). Chronic uncontrolled hyperglycemia and acute hyperglycemia are associated with increased in vivo ethane production.     

The effect on plasma glucose, insulin and glucagon levels of treatment of diabetic rats with the medicinal plant Rhazya stricta and with glibenclamide, alone and in combination

We examined the relationship between the changes of serum soluble CD8 (sCD8) and soluble interleukin-2 receptor (sIL-2R) levels and effectiveness of interferon (IFN) in patients with chronic hepatitis (CH) C. Changes in sCD8 levels were parallel with fluctuations of alanine aminotransferase (ALT) in CH patients during IFN treatment but decreases of sCD8 levels were slower than those of ALT. In IFN effective and ALT decreased patients sCD8 levels is also decreased. sIL-2R levels was increased transiently during administration of IFN in most cases. It was suggested that decrease in sCD8 levels is indicative of the effectiveness of IFN therapy.     

Effect of glucagon on pinocytosis by the yolk sac of the rat

The uptake of macromolecular markers by fluid pinocytosis in the rat yolk sac was inhibited by glucagon, with half-maximal effect at a hormone concentration of approximately 3 X 10(-8) M. Glucagon had no effect on the cellular distribution of the marker subsequent to its uptake. Rates of uptake promptly returned to normal when the yolk sacs were transferred from a glucagon-containing to a glucagon-free medium. Epinephrine also inhibited, but only at much higher concentrations. The effect of the latter was augmented by theophylline. Insulin (10(-6) M) had no effect when added alone or with an inhibitory level of glucagon (10(-7) M). The presumption that the hormone effect was mediated by cyclic AMP was supported by the findings that the cellular levels of cyclic AMP were elevated in the presence of glucagon and that dibutyryl cyclic AMP could replace glucagon as an effective inhibitor. The conclusion that the hormone effect was on uptake rather than on subsequent regurgitation was based on the linearity of accumulation in both the presence and absence of glucagon and the inability of glucagon to stimulate loss of invertase from preloaded cells. Colchicine and vinblastine also inhibited uptake. This finding and those of others which are discussed suggest the possibility that effects of cyclic nucleotides on certain cell functions may involve their regulation of microtubular status.     

Effect of GF120918, a potent P-glycoprotein inhibitor, on morphine pharmacokinetics and pharmacodynamics in the rat

PURPOSE: Studies have shown that 11% to 18% of patients with an abdominal aortic aneurysm (AAA) have a first-degree relative with an AAA. A familial pattern among patients with peripheral arterial aneurysms and arteriomegaly has not been reported. The objective of this study was to examine familial patterns among patients with peripheral arterial aneurysm and arteriomegaly and compare them with patterns among patients with AAA. METHODS: Pedigrees were constructed for first-degree relatives of patients who received the diagnosis of peripheral arterial aneurysm, arteriomegaly, or AAA from 1988 through 1996. The presence of aneurysms and risk factors was confirmed for patients and relatives by means of telephone interviews and review of hospital and physician records. RESULTS: Seven hundred three first-degree relatives older than 50 years were contacted for 140 probands with peripheral arterial aneurysm, AAA, or arteriomegaly. There were differences in risk factors for hernia and diabetes mellitus among the probands with peripheral arterial aneurysm, AAA, or arteriomegaly but none for relatives. Patients with peripheral arterial aneurysm (n = 40) had a 10% (4/40) familial incidence rate of an aneurysm, patients with AAA (n = 86) had a 22% (19/86) familial incidence rate, and patients with arteriomegaly (n = 14) had a 36% (5/14) familial incidence rate. AAA (24/28, or 86%) was the aneurysm diagnosed most commonly among first-degree relatives. Most aneurysms (85%) occurred among men. CONCLUSION: There appears to be a gradation of familial patterns from peripheral arterial aneurysm to AAA to arteriomegaly among patients with degenerative aneurysmal disease, and there appears to be a predominance among men. Relatives of patients with any of the 3 lesions-peripheral arterial aneurysm, AAA, arteriomegaly--most frequently have AAA. Relatives of patients with AAA, peripheral arterial aneurysm, or arteriomegaly may be screened by means of a physical examination for peripheral aneurysmal disease. Screening by means of ultrasound examination of the aorta should be limited to first-degree relatives of patients with aortic aneurysms or arteriomegaly.     

Distribution, tolerability and tissue compatibility of intrathecal tizanidine in the sheep

Allelic variants for the HIV-1 co-receptors chemokine receptor 5 (CCR5) and CCR2, as well as the ligand for the co-receptor CXCR4, stromal-derived factor (SDF-1), have been associated with a delay in disease progression. We began this study to test whether polymorphisms in the CCR5 regulatory regions influence the course of HIV-1 disease, as well as to examine the role of the previously identified allelic variants in 1,090 HIV-1 infected individuals. Here we describe the evolutionary relationships between the phenotypically important CCR5 alleles, define precisely the CCR5 regulatory sequences that are linked to the CCR5-delta32 and CCR2-641 polymorphisms, and identify genotypes associated with altered rates of HIV-1 disease progression. The disease-retarding effects of the CCR2-641 allele were found in African Americans but not in Caucasians, and the SDF1-3'A/3'A genotype was associated with an accelerated progression to death. In contrast, the CCR5-delta32 allele and a CCR5 promoter mutation with which it is tightly linked were associated with limited disease-retarding effects. Collectively, these findings draw attention to a complex array of genetic determinants in the HIV-host interplay.     

Effects of branched-chain-enriched amino acid solution on insulin and glucagon secretion and blood glucose level in liver cirrhosis

BACKGROUND: The aim of this study was to determine whether therapeutically used branched-chain amino acids (BCAAs) solution influences glucose metabolism in liver cirrhosis (LC). METHODS: BCAAs solution (200 ml) was infused in LC patients at different stages, and plasma concentrations of glucose and pancreatic hormones were determined. RESULTS: In patients with mild LC, BCAAs caused a significant increase in glucose level (maximal increment, 12.5+/-2.5 mg/dl) with a great increase in insulin (maximal increment, 39.5+/-8.3 microU/ml) and a small increase in glucagon secretion (maximal increment, 101.0+/-16.0 pg/ml). In patients with advanced LC, BCAAs caused a great increase in glucagon secretion (220.5+/-19.4 pg/ml) with only a slight increase in glucose levels (5.8+/-2.2 mg/dl). CONCLUSION: BCAAs solution causes hyperglycemia in mild LC due to insulin resistance, whereas it causes only a slight increase in severe LC due to hepatic glucagon resistance. Thus, there is a possibility that BCAAs solution may lead to hypoglycemia in advanced LC with hepatic glycogen depletion.     

The effect of stevioside on glucose metabolism in rat

This study was conducted to determine the effect of stevioside (SVS) on glucose metabolism. The experiments were performed in male Wistar rats treated with SVS either by intravenous infusion or feeding. SVS infusion (150 mg/mL) was carried out in doses of 0.67, 1.00, and 1.33 mL.kg-1 body weight.h-1. The plasma glucose level significantly increased both during and after SVS infusion, whereas it was not affected by SVS feeding (13.3 mL.kg-1 body weight). The glucose turnover rate (GTR) of [14C(U)]glucose and [3(-3)H]glucose was not significantly different between control and SVS infusion animals. Percent glucose carbon recycling and glucose clearance were reduced from 28.7 +/- 1.3 to 23.0 +/- 1.6% (p < 0.05) and from 6.46 +/- 0.34 to 4.99 +/- 0.20 mL.min-1.kg-1 body weight (p < 0.01), respectively. The plasma insulin level did not change, whereas the plasma glucose level significantly increased from 120.3 +/- 5.9 to 176.8 +/- 10.8 mg% (p < 0.01) during SVS infusion. Animals pretreated with angiotensin II and arginine vasopressin showed no significant effect, while animals pretreated with prazosin had an attenuated hyperglycemic effect of SVS infusion. Pretreatment with indomethacin or N omega-nitro-L-arginine methyl ester (L-NAME) alleviated the plasma glucose level during the second period of SVS infusion. Pretreatment with the combination infusion of indomethacin and L-NAME reduced the plasma glucose level from 117.0 +/- 1.8 to 109.0 +/- 1.7 mg% (p < 0.001), and normalized the plasma glucose level in the second period of SVS infusion. Insulin infusion inhibited the hyperglycemic effect of SVS infusion. The present results show that the elevation of the plasma glucose level during SVS infusion is not due to the reduction of the insulin level. It is probably the effect of SVS on glucose transport across the cell. Insulin response to a high plasma glucose level is suppressed during SVS infusion. Several interactions among norepinephrine, prostaglandin, and nitric oxide are involved in modulating the hyperglycemia during SVS infusion.     

Effect of morphine and stadol on lipid content in liver of rat

The effects of repeated accumulative increasing doses (5, 10, 20 and 40 mg/kg body weight) of morphine and stadol on lipid content have been studied in liver of rat. The results obtained indicate that significant increases were recorded in hepatic triglycerides (TG) content after 1 and 12 hrs of morphine treatment while non-significant increases were recorded after stadol administration. After 36 hrs of treatment with either of the two drugs, the liver TG content was decreased which may indicate that drug tolerance might have developed. The phospholipids content showed increases especially after 12 hrs of morphine or stadol administration. The results obtained suggest enhanced phospholipid synthesis under the action of both drugs. Highly significant increases occurred in cholesterol content after 1, 12 and 24 hrs of treatment of both drugs. This might reflect the occurrence of decreased catabolism and turnover of cholesterol during the experiment. Total lipids content of liver showed marked and highly significant increases after 12 hrs of morphine and after 12 and 24 hrs of stadol administration respectively. The data obtained suggest that morphine and stadol may be hepatotoxic to rats.     

Effect of the sulfonylurea glyburide on glycogen synthesis in alloxan-induced diabetic rat hepatocytes

1. The effect of glyburide (glibenclamide) treatment on the liver glycogen levels of diabetic rats have been studied. 2. 3 weeks treatment with glyburide (5 mg/kg, orally) increased liver glycogen and decreased blood glucose levels. 3. The results of this study demonstrated that the sulfonylurea, glyburide is capable of exerting direct insulin-like effects on liver glycogen values in vivo.