Inhibition of gastric secretion in the dog by 16,16-dimethyl prostaglandin E2.

The synthetic prostaglandin 16,16-dimethyl E2 (PGE2) given by intravenous infusion at 0.4 mug/kg-h inhibited gastric secretion of H+, K+, Cl-, and pepsin in four fistula dogs stimulated by histamine (H), pentagastrin (P), urecholine (U), and 2-deoxy-D-glucose (2-DG). When given for 90 min during steady infusions of near-maximal doses of H, P, and U, PG-E2 caused 75% inhibition of H+ maximally at 90 min and over 85% inhibition of pepsin secretion maximally at 45 min. Recovery of secretion took 1-2 h after infusion of PGE2 was stopped. Injection of KCl, 1 meq/kg, during inhibition of histamine by PGE2 gave only a 15-min transient reversal in inhibition. When PGE2 was given as background to 45-min step-dose responses, 0.1 mug/kg competitively inhibited histamine stimulation and 0.4 mug/kg-h gave 100% inhibition. Against pentagastrin, 0.1 mug PGE2/kg-h had no effect and 0.4 mug caused uncompetitive inhibition; against urecholine, 0.4 mug PGE2/kg-h caused competitive inhibition of H+ secretion. Pepsin was more markedly inhibited in each case. There were no side effects at either dose of PGE2, which is a potent inhibitor of gastric secretion with all forms of stimuli.     

Comparison of remifentanil and fentanyl for postoperative pain control after abdominal hysterectomy

PURPOSE: In this randomized, double-blind study, we investigated the analgesic efficacy and side effects of continuous constant-dose infusions of remifentanil after total abdominal hysterectomy and compared it to fentanyl. MATERIALS AND METHODS: Fifty-six adult female patients scheduled for elective total abdominal hysterectomy were enrolled in this study. Patients were randomly assigned to two groups according to fentanyl (group F, n=28) or remifentanil (group R, n=28) for postoperative analgesia. Patients in group F were given fentanyl intravenously with an infusion rate of fentanyl 0.5 microg/kg/hr; group R was given remifentanil with an infusion rate of remifentanil 0.05 microg/kg/min for 2 days. Pain intensity at rest, occurrence of postoperative nausea and vomiting (PONV), dizziness, pruritus, and respiratory depression were assessed 1 hr after arrival at the post-anesthesia care unit, at 6; 12; 24; and 48 hr post-operation and 6 hr post-infusion of the study drug. Pain was evaluated by using visual analogue scale (VAS; 0-10). The time that patients first requested analgesics was recorded as well as additional analgesics and antiemetics. RESULTS: There were no significant differences in VAS, time to first postoperative analgesics, and additional analgesics between the 2 groups. The incidences and severities of PONV and opioid related side effects were not different between the groups; however, there were 3 episodes (10.7%) of serious respiratory depression in group R. CONCLUSION: Continuous infusion technique of remifentanil did not reveal any benefits compared to fentanyl. Furthermore, it is not safe for postoperative analgesia in the general ward.     

Cerebrospinal fluid pressure of anaesthetized rats during intracerebroventricular infusion

Increases in cerebrospinal fluid pressure (CSFP) were measured in the lateral ventricle in barbiturate anaesthetized male Sprague Dawley rats during intracerebroventricular (IVT) infusions into the contralateral ventricle. IVT infusions of isotonic artificial CSF (art-CSF) solutions at 10 and 38 microliters/hr increased mean CSFP from control preinfusion level of 3.6 cm H2O to 4.6 cm H20 (n.s.) and 5.2 cm H2O (p less than 0.01) respectively with CSFP appearing to attain equilibrium after 30-60 min of infusion. IVT infusion of hyperosmolar art CSF solutions (saccharide and salt solutions of approximate 1000 mOsm/kg) at 38 microliters/hr resulted in a larger increase of CSFP which equilibrated at 8.5 cm H2O (p less than 0.001) after 90 min of infusion. It is suggested that on the basis of CSFP measurements in these and other experiments cited that IVT infusions be run at infusion rates of less than 40 microliters/hr to ensure minimal physiological change.     

The contribution of the arterial chemoreceptors to the stimulation of respiration by adrenaline and noradrenaline in the cat

1. Intravenous infusions of adrenaline and noradrenaline in doses averaging 0.8 mug/kg.min increased the respiratory minute volume of anaesthetized cats breathing room air. The mean increase in respiratory minute volume was 14% during adrenaline infusion and 8% during noradrenaline infusion.2. In a small group of decerebrate cats infusions of adrenaline and noradrenaline increased ventilation by 19 and 27% respectively.3. Intravenous catecholamine infusions also increased the respiratory responses of anaesthetized animals to the inhalation of 5% or 10% O(2) in N(2) and to the inhalation of 5% CO(2) in air.4. Adrenaline and noradrenaline infusions had no significant effect on the ventilation of animals breathing 100% O(2), nor did they significantly alter the respiratory response to the inhalation of 5% CO(2) in O(2).5. After section of the carotid sinus and aortic nerves, a blood-pressure compensator being used to minimize changes in arterial pressure, catecholamines had no effect on the respiration of cats breathing air.6. An increase in carotid body chemoreceptor discharge accompanied the increase in ventilation during catecholamine infusion.7. Intravenous catecholamine infusions still produced an increase in ventilation and carotid body chemoreceptor discharge after both aortic nerves and both cervical sympathetic nerves had been cut.8. Intra-arterial infusions into one carotid artery of 0.2 mug/kg.min of adrenaline or 0.1 mug/kg.min of noradrenaline led to mean increases in respiratory minute volume of 9.9 and 11.5% respectively. No increase occurred after section of the corresponding carotid sinus nerve. Such infusions also evoked an increase in carotid body chemoreceptor discharge.9. It is concluded that the hyperpnoea produced by adrenaline and noradrenaline infusions in the cat is predominantly reflex in origin and is mediated by the arterial chemoreceptors.10. The increase in ventilation produced by adrenaline appears to have a component additional to its effect upon the chemoreceptors though the nature of this action has not been identified.     

Safety and Tolerability of Increased Rate of Infusion of Intravenous Immunoglobulin G, 10% in Antibody-Deficient Patients

The incidence and severity of infusion-related adverse events (AEs) after infusions of IGIV-C, 10%, (Gamunex^®) at 0.14 mL/kg/min versus 0.08 mL/kg/min (standard rate) were compared. Patients with confirmed PID received two infusions 3–4 weeks apart with IGIV-C, 10% 400–600 mg/kg. Patients received their first infusion at 0.08 or 0.14 mL/kg/min and their second infusion 3–4 weeks later at the alternate rate, at an established step-wise rate increase. Ninety-seven of 100 patients remained valid for safety assessment. There were three infusion-related reactions at the standard rate and five at the increased rate. The incidence of all reported AEs was similar for both rates. Despite the time required for step-wise increases in infusion rate, the increased rate resulted in a shortened overall infusion time. Increasing the rate of infusion of IGIV-C, 10% by 75% up to 0.14 mL/kg/min (840 mg/kg/h) was well tolerated, suggesting safe administration of IGIV-C, 10% at this rate.Declaration: Dr. Gelfand is a consultant to Talecris Biotherapeutics     

Androgen dependence in hamsters: overdose, tolerance, and potential opioidergic mechanisms

Anabolic steroids are drugs of abuse. However, the potential for steroid reward and addiction remains largely unexplored. This study used i.c.v. testosterone self-administration and controlled infusions of testosterone or vehicle in hamsters to explore central mechanisms of androgen overdose. Forty-two hamsters used nose-pokes to self-administer 1 μg/μl testosterone i.c.v. 4 h/day in an operant chamber. During 1–56 days of androgen self-administration, 10 (24%) hamsters died. Deaths correlated with peak daily intake of testosterone. Of the hamsters that self-administered a peak intake of <20 μg/day, there was 100% survival (10/10). Survival decreased to 86% (19/22) when daily testosterone intake peaked at 20–60 μg/day. Only 30% (three of 10) survived when daily testosterone intake exceeded 60 μg/day. Deaths are not due to volume or vehicle because i.c.v. infusions of 80 μl vehicle had no effect. Testosterone overdose resembles opiate intoxication. When male hamsters received infusions of 40 μg testosterone, locomotion (25.1±18.8 grid-crossings/10 min), respiration (72.7±5.4 breaths/min) and body temperature (33.5±0.4 °C) were significantly reduced, compared with males receiving vehicle infusions (186.1±8.1 crossings/10 min, 117.6±1.0 breaths/min, 35.9±0.1 °C, P<0.05). However, males developed tolerance to continued daily testosterone infusion. After 15 days, locomotion (170.2±6.3 crossings), respiration (118.4±1.3 breaths/min), and body temperature (35.3±0.3 °C) in testosterone-infused males were equivalent to that in vehicle controls (P>0.05). The depressive effects of testosterone infusion are blocked by the opioid antagonist, naltrexone. With naltrexone pre-treatment (10 mg/kg s.c.), locomotion (183.7±1.8 crossings/10 min), respiration (116.9±0.3 breaths/min), and body temperature (36.1±0.4 °C) during testosterone infusion were equivalent to vehicle controls. Likewise, naltrexone prevents the reinforcing effects of i.c.v. testosterone self-administration. These results indicate that testosterone at high doses causes central autonomic depression, which may be a factor in deaths during self-administration. As well, the depressive effects of large quantities of testosterone may be mediated, at least in part, by an opioidergic mechanism.     

Rapid infusion of Sandoglobulin in patients with primary humoral immunodeficiency

We studied 16 patients with primary disorders of humoral immunity to determine the practicality of infusing intravenous gamma globulin at rates of infusion and concentrations higher than the 4 mg/kg/min and 6% currently recommended. In the first portion of the study, the concentration of Sandoglobulin was increased from 6% to 12%. In the second portion, the flow rate was increased to 5 mg/kg/min, and if no reactions occurred, the time of each successive infusion was decreased by 10 minutes until infusions were completed in 15 to 20 minutes or vasomotor reactions occurred. Thirteen of the 16 patients completed the study; six patients achieved reaction-free rates greater than 15 mg/kg/min, and the other patients achieved rates ranging from 7.1 to 12 mg/kg/min. Seven patients had infusion times less than 30 minutes, with four patients completing infusions in 15 minutes. In the 13 patients who completed the study, there were 14 reactions in 159 infusions, mostly fever and chills, and often at the end or after the infusion. Only one infusion could not be completed because of an adverse reaction. Three patients were not able to complete the study because of adverse reactions; there were seven reactions in 11 infusions in these three patients, although none of the reactions were considered serious. Overall, in this study, most immunodeficient patients (13/16) were able to tolerate infusion rates of Sandoglobulin two to 10 times higher than the standard rates now recommended. The maximal rate of infusion must be individualized, but for carefully selected patients, infusions of 400 mg/kg can be completed in 1 hour or less.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular alterations in the rabbit infused with platelet activating factor (PAF): effect of kadsurenone, a PAF-receptor antagonist

The ECG and haemodynamic alterations caused by the i.v. infusion of platelet-activating factor (PAF) in the rabbit were studied after pretreatment with Kadsurenone, a specific PAF-receptor antagonist. Infusion of PAF at 0.8 microgram/kg in the rabbit caused important ECG changes, such as ST-segment depression and conduction arrhythmias, concomitantly with a marked reduction in left ventricular systolic pressure, mean arterial pressure and cardiac output, with a rise in total peripheral resistances and mean right atrial pressure. These physiological parameters became maximal at 75-120 seconds after PAF challenge, and returned to near prechallenge values within 25-60 minutes. Pretreatment with Kadsurenone, administered either intravenously (0.014 M, 1 ml/kg) or intraperitoneally (0.14 M, 1 ml/kg), exerted a quite complete protective effect in regard to the ECG changes and caused a significant reduction in the magnitude of all the haemodynamic alterations observed after intravenous infusion of PAF (0.8 microgram/kg). These results suggest that Kadsurenone is an effective inhibitor of PAF-induced cardiovascular changes in the rabbit, probably due to its competitive antagonism against PAF binding to specific receptors.     

The effects of histamine on skeletal muscle vasculature in cats.

1. Experiments have been made to determine the vascular effects of histamine and the mechanism of histamine-induced oedema formation in cat skeletal muscle. 2. Histamine caused dose-dependent dilatation of resistance vessels and increased intravascular volume over the dose range 1 X 10(-10)-1 X 10(-8) mol/kg min. The dilatation of resistance vessels resulted in dose-dependent increases in capillary hydrostatic pressure. 3. Histamine increased vascular permeability, as measured by accumulation of [131I]human serum albumin in the tissue, during infusions at 1 X 10(-8) mol/kg min but no albumin accumulation could be detected at lower infusion rates. 4. Oedema formation during histamine infusion of 1 X 10(-10) and 1 X 10(-9) mol/kg min seemed to be due to increases in capillary hydrostatic pressure and independent of increased vascular permeability. During infusions of histamine 1 X 10(-8) mol/kg min oedema was due predominantly to increased vascular permeability and to a lesser extent, the increase in capillary hydrostatic pressure.     

家兔高钾血症心电生理机制的实验研究

目的观察家兔高钾血症心电生理特征,研究家兔高钾血症对心脏的毒性作用机制。方法对照组输注0．9％NaCl,记录家兔正常的心电图特征及血钾浓度,实验组分别输注1％、4％、10％KCl溶液（2mL／kg）复制高钾血症模型,观察家兔心电生理的变化特征,记录输钾前后血钾浓度、吸光度、心率、心电图异常率及各指标之间的变化关系。结果实验组输钾前后血钾浓度、吸光度、心率、心电图异常率、心电图各波形时限及振幅差异有显著变化（P〈0．05）,随着输钾浓度增高发生高血钾时间缩短,差异具有显著性（P〈0．05）,实验家兔血钾浓度与心电图诊断高钾血症的一致性良好（P〈0．01）,在ROC曲线上心电图变异率诊断水平最高（P〈0．01）,其次为血钾浓度（P〈0．05）,而心率诊断水平最差（P〉0．05）,血钾浓度与心电图变异率高度相关（P〈0．05）,血钾浓度与心率相关性较差（P〉0．05）。结论实验家兔高钾血症心电生理机制的研究对临床急性高钾血症的鉴别诊断、及时治疗有重要参考价值。     

Transient vasopressin release and thirst in response to prolonged intracerebroventricular infusions of hypertonic mannitol in saline

In the conscious goat infusions of 0.4 M mannitol in 0.15 M NaCl into the lateral cerebral ventricle (40 or 100 min, 0.02 ml/min) caused slight, transient vasopressin release and temporary thirst, whereas infusions or pure, hypertonic (0.7 M) mannitol did not elicit thirst and inhibited the basic vasopressin release in the nonhydrated animal. In contrast, infusions of equiosmolal (0.35 M) NaCl induced persistent thirst and pronounced elevation of the plasma vasopressin concentration throughout the infusion period. The cerebrospinal fluid (CSF) osmolality was raised by the same order of magnitude (= 13%) after the mannitol/NaCl and the hypertonic NaCl infusions. The CSF Na+ concentration was elevated by greater than 10% at 5 min after hypertonic NaCl infusions, but it was reduced by approximately 10% at 5 min after the mannitol/NaCl infusions. There was no appreciable difference in the CSF K+ concentration after the infusions. The results are discussed with regard to the possible importance of CSF Na+-concentration as opposed to strict osmotic factors for the excitation of receptors involved in the control of water balance.     

The effects of infusions of synthetic adrenocorticotrophin in the conscious calf

1. A technique is described by which the whole of the effluent blood from the right adrenal gland can be collected as required from conscious, unrestrained calves. The technique may be used to measure adrenal blood flow gravimetrically and to compute the output of adrenal hormones under various conditions in the normal calf.2. In a group of seven calves mean cortisol output from the right adrenal gland was found to vary between 20 and 40 ng.kg(-1) min(-1) and corticosterone between 6 and 18 ng.kg(-1) min(-1) during a 2 hr period, 24 hr after surgery.3. Intravenous infusions of synthetic adrenocorticotrophin (5 ng.kg(-1) min(-1)) produced a significant increase in the output of both cortisol and corticosterone within 5 min. The output of both hormones rose to maximal values within 10-20 min and mean values of approximately 300 ng.kg(-1) min(-1) (cortisol) and 120 ng.kg(-1) min(-1) (corticosterone) were maintained thereafter for the duration of the infusion (120 min). The output of both steroids fell to values comparable with those observed initially within 45-60 min after the infusion was discontinued.4. These changes in glucocorticoid output in response to adrenocorticotrophin produced a significant rise in the concentration of both cortisol and corticosterone in peripheral plasma. It is noteworthy that the rise in the mean corticosterone concentration in the peripheral plasma was substantially less than that which might be expected from relating the rise in mean plasma cortisol concentration to cortisol output.5. The results of control experiments have eliminated the possibility that the sampling procedure might itself increase steroid output or peripheral plasma concentration. Comparison of results from calves of widely disparate ages (8-38 days) provided no evidence that either the resting output of cortisol or corticosterone or the response to adrenocorticotrophin changes with age within the range examined.6. Infusion of adrenocorticotrophin (5 ng.kg(-1) min(-1)) also stimulated an abrupt rise in adrenal blood flow; mean resting flow (210 +/- 23 mul.kg(-1)) increased by approximately 30% within 5 min and attained peak values (355-365 mul.kg(-1) min(-1)) between 10 and 30 min. Thereafter, adrenal blood flow steadily decreased and then fell rapidly to within the resting range when the infusion was terminated. No significant changes in heart rate or aortic blood pressure occurred during these infusions.7. The results are discussed in relation to those obtained in other species and under differing conditions by other workers.     

The evaluation of glucagon infusion algorithms for a counterregulatory system in artificial endocrine pancreas

As counterregulatory system of artificial endocrine pancreas, glucagon infusion algorithm has been developed and its usefulness has been examined in pancreatectomized dogs and a pancreatectomized diabetic patient. Glucagon infusion rate (G1nIR(t)) was determined depending on proportional plus derivative action to blood glucose concentration (BG(t] with the time delay (tau) to start infusion as follows. G1nIR(t) = Gp(BGp- BG(t-tau)) + Gd(-dBG(t-tau)) + Gc where BGp is the projected value of blood glucose concentration, Gp, and Gd are the coefficients and Gc is the constant for basal glucagon supplement. Glucagon infusions based only on proportional action (Gp/Gd/Gc/tau) = (0.2/0/0.4/10 or 0.4/0/0.4/10) failed in simulating the pattern of blood glucose or glucagon response seen in normal dogs. Glucagon infusion based on proportional plus derivative action (Gp/Gd/Gc/tau = 0.2/0.4/0.4/10) successfully mimicked the pattern of blood glucose concentration and plasma glucagon profile seen in normal dogs. This glucagon infusion algorithm has been applied to control insulin-induced hypoglycemia in a pancreatectomized patient with the same infusion parameters. Hypoglycemia was recovered to normoglycemia in 80 min and the plasma glucagon patterns showed no significant difference from those in healthy volunteers. These data indicate that glucagon infusion algorithm thus developed is effective to render hypoglycemia to normoglycemia and mimic plasma glucagon response seen in normal subjects.     

Influence of isoproterenol on plasma immunoreactive atrial natriuretic peptide and plasma vasopressin in the anesthetized rabbit

Changes in levels of plasma immunoreactive atrial natriuretic peptide (IR-ANP) were measured in response to administration of isoproterenol in the anesthetized, vagotomized rabbit. A dose-dependent increase in plasma IR-ANP was seen in response to 10 min isoproterenol infusions between 0.1 and 10.0 g/kg/min. The time course of these responses showed the maximum levels of IR-ANP to be attained 10 min after the cessation of infusion. In rabbits in which plasma vasopressin (AVP) levels were also measured, the maximum levels of AVP were attained during the infusion period. There was no correlation between levels of AVP and IR-ANP suggesting that AVP released into the plasma did not affect directly the release of IR-ANP. The changes in IR-ANP in response to isoproterenol were significantly reduced in rabbits which had been administered the beta-1-adrenoceptor blocking agent, atenolol. In six rabbits in which the vagi remained intact, the increases in IR-ANP were reduced and became significant only with 10 g/kg/min isoproterenol infusion. The results demonstrate that isoproterenol infusion increases the level of plasma IR-ANP in the anesthetized rabbit and suggest that this is through an effect on the heart rather than on peripheral vessels.     

Pharmacokinetics of the enantiomers of ibuprofen in the rabbit

The stereoselective disposition of ibuprofen was studied in male New Zealand White (NZW) rabbits (n=4) following an infusion (0.16 mg/kg/min) to steady-state of each of the enantiomers of ibuprofen with one week between treatments. The mean (±SEM) steady-state clearances of (R)-ibuprofen (15.5±1.1 ml/min/kg) and (S)-ibuprofen (13.6±1.9 ml/min/kg) were not significantly different from each other (p>0.05) and exceeded the plasma clearance of indocyanine green (4.3±0.4 ml/min/kg) in a separate group of rabbits (n=6). When the infusion rate of the enantiomers was doubled there was a significant decrease in the mean clearance of both (R)-ibuprofen (28%;p<0.018) and (S)-ibuprofen (24%;p<0.003). There was enantiospecific chiral inversion of (R)-ibuprofen to (S)-ibuprofen (fi=0.30±0.07) as has been observed in all species so far studied for this 2-arylpropionic acid. The metabolic capacity for elimination of ibuprofen enantiomers was much greater than reported for either fenoprofen or ketoprofen and suggests that the clearance of ibuprofen enantiomers may be flow dependent in this species.     

Studies in the rat of antibody-coated and N-ethylmaleimide-treated erythrocyte clearance by the spleen. II. Effects of immune complex infusion.

The effects of immune complex infusion on the clearance of antibody (R3/13)-coated and NEM-treated rat erythrocytes by the splenic component of the rat mononuclear phagocyte system (MPS) were investigated. Equivalence complexes of BSA-anti-BSA produced a significant delay in the clearance of the NEM cells (pre-infusion T1/2 19.7 +/- 3.9 min, post-infusion T1/2 26.5 +/- 3.8 min, mean +/- SE, n = 6, P less than 0.01), but this effect could be abolished by agents that prevented the changes in the splenic blood flow that followed complement activation. The immune complexes formed in 10-fold antigen excess (mean size 15S) did not delay the clearance of the NEM cells. Clearance of R3/13-coated cells was impaired by the infusion of immune complexes prepared at equivalence. 10-fold antigen excess or complexes prepared with F(ab')2 fragments of rabbit anti-BSA antibody. The inhibition of red cell clearance was independent of changes in blood flow, but the degree of inhibition produced did not correlate well with the dose of immune complex injected.     

Stimulation of insulin release and suppression of feeding by hepatic portal glucagon infusion in rats

Plasma insulin and glucose concentrations were measured in rats by remote blood sampling techniques 5 and 25 min after the start of a continuous intraportal glucagon infusion (0.33, 1.0, 3.3, 10 and 33 micrograms/kg/min). Plasma insulin levels were elevated in a dose-related fashion by glucagon, with the highest dose producing a 23-fold increase above control levels. In contrast, the glycemic effect of glucagon was not dose-related. Glucagon-induced hyperglycemia was similar for all glucagon doses, despite the fact that a glucagon dose range spanning two orders of magnitude was used. In a second experiment, plasma glucose and insulin were measured as described above at two glucagon infusion rates (1 and 10 micrograms/kg/min), but the animals were allowed to eat during the infusion. Results showed that the effects of glucagon infusions on plasma insulin and glucose were additive with the normal prandial changes in these substances. Finally, food intake was inversely related to insulin level and dissociated from the hyperglycemia during glucagon infusion. These results show that exogenous glucagon provides a potent stimulus for insulin release in the rat both in the presence and in the absence of food. Furthermore, these results in combination with other data suggest that glucagon-induced hyperinsulinemia merits further investigation as one possible determinant of glucagon satiety in the rat.     

Experimental membrane-destructive model of cardiac arrhythmia

We propose a method for experimental modeling of cardiac arrhythmias. The method consists in intravenous injection of LPO inductors: 5% ascorbic acid (50 mg/kg), 1 min later 1% iron sulfate (10 mg/kg), and after the appearance of giant T waves on ECG infusion of 10% calcium chloride in a nonarrhythmogenic dose 100 mg/kg. Cardiac arrhythmias were induced in 100% animals. A significant relationship between increased permeability of erythrocyte membranes and development of fatal cardiac arrhythmias was detected. We assumed that this methodologically simple membrane-destructive model of cardiac arrhythmia is pathogenetically close to arrhythmogenesis in patients with coronary heart disease.     

Failure of portal glucose and adrenaline infusions or liver denervation to affect food intake in dogs

Total liver denervations were attempted on 5 mongrel dogs. At the same time, the hepatic portal vein was cannulated with a polyethylene cannula which was exteriorized. Five sham operated, cannulated dogs served as controls. Both denervated and sham operated dogs returned to preoperative food intake within 8 days post surgery. After recovery, intraportal infusions of 6 to 25 g of glucose prior to food presentation in 23 hr fasted sham or denervated dogs resulted in no anorexia. The portal vein and jugular vein were cannulated in an additional 4 dogs. Jugular blood samples were taken prior to and after portal infusion of 20 g of glucose in 23 hr fasted dogs. Both jugular blood glucose and insulin concentration increased significantly 1 to 2 min after portal infusion. The dogs were presented with food 3 to 5 min after the cessation of infusion, yet they showed no anorexia. These same 4 dogs were given portal infusions of either 0.5 μg/kg, 1.0 μg/kg or 1.5 μg/kg of adrenaline after a 23 hr fast. When food was presented 10 min after the infusions were stopped, the dogs ate immediately showing no signs of anorexia. These results question the role or the existence of hepatic glucoreceptors in the control of food intake in the dog.     

甘氨酸对心肌缺血-再灌注小鼠一氧化氮系统和Bcl-2 mRNA表达的影响

目的:探讨甘氨酸(Gly)对心肌缺血-再灌注(MI/R)损伤的防治作用及机制,为临床缺血性心脏病的防治提供新的思路与方法。方法: 将小鼠随机分为5组,以Gly等药物定量灌胃处理。1周后,腹腔注射垂体后叶素和硝酸甘油复制MI/R模型,同时记录不同时点的肢体Ⅱ导联心电图。4 h后,分别用比色法和硝酸还原酶法检测小鼠心肌组织中一氧化氮合酶(NOS)、诱导型一氧化氮合酶的活性(iNOS)和一氧化氮(NO)的含量;用逆转录-多聚酶链式反应(RT-PCR)测定各组小鼠心肌组织Bcl-2 mRNA的表达。结果: MI/R组小鼠心电图J点发生明显偏移。 Gly预处理组小鼠心肌组织总NOS活性、NO含量及Bcl-2 mRNA的表达显著升高,而iNOS的活性显著下降。结论: Gly能保护心脏,减轻MI/R引发的损伤。Gly的这一作用可能与其增加缺血再灌注心肌组织中NOS的活性及NO的生成,抑制iNOS的活性,以及促进Bcl-2 mRNA的表达有关。