bluuebunny/crossref_metadata_2025 huggingface dataset:
Phase-linked variations in the amplitude of the digastric nerve jaw-opening reflex response during fictive mastication in the rabbit
Authors: Lund J. P. , Enomoto S. , Hayashi H. , Hiraba K. , Katoh M. , Nakamura Y. , Sahara Y. , Taira M.
Published: April 2011

The digastric nerve reflex response to stimulation of the upper lip was studied in urethan-anesthetized rabbits paralysed with pancuronium bromide. Rhythmic bursts of masticatory activity were evoked in the nerve by repetitive electrical stimulation of the motor cortex. The amplitude and latency of the reflex responses during fictive mastication were compared with preceding control values. When stimuli close to threshold were given, the largest and earliest responses occurred during the digastric burst. When intense stimuli were employed, the largest responses were out of phase with the burst, although the latency was still shortest when the motoneurons were rhythmically active. Since the pattern is essentially the same as that seen during normal mastication, we conclude that the cyclical modulation of reflex amplitude and latency is not the result of sensory feedback generated by the movements themselves but is instead governed by the central motor program.
Synaptic transmission in the chronically decentralized middle cervical and stellate ganglia of the dog
Authors: Armour J. A.
Published: April 2011

Afferent stimulation of one thoracic cardiopulmonary nerve generated compound action potentials in the efferent axons of other ipsilateral cardiopulmonary nerves in dogs, 14 days after their thoracic autonomic ganglia had been decentralized. The compound action potentials were influenced by the frequency of activation and (in 5 of 12 dogs) by pharmacological autonomic blocking agents (hexamethonium, atropine, phentolamine, and propranolol). Moreover, they were abolished transiently when chymotrypsin was injected locally into the ganglia, and extendedly when manganese was injected. Thus, synapses that can be activated by stimulation of afferent nerves exist in chronically decentralized thoracic autonomic nerves and ganglia. It is proposed that regulation of the heart and lungs occurs in part via thoracic autonomic neural elements independent of the central nervous system.
Modern quantitative acid–base chemistry
Authors: Stewart Peter A.
Published: April 2011

Quantitative analysis of ionic solutions in terms of physical and chemical principles has been effectively prohibited in the past by the overwhelming amount of calculation it required, but computers have suddenly eliminated that prohibition. The result is an approach to acid–base which revolutionizes our ability to understand, predict, and control what happens to hydrogen ions in living systems. This review outlines that approach and suggests some of its most useful implications. Quantitative understanding requires distinctions between independent variables (in body fluids: pCO2, net strong ion charge, and total weak acid, usually protein), and dependent variables ([Formula: see text], [HA], [A−], [Formula: see text], [OH−], and [H+] (or pH)). Dependent variables are determined by independent variables, and can be calculated from the defining equations for the specific system. Hydrogen ion movements between solutions can not affect hydrogen ion concentration; only changes in independent variables can. Many current models for ion movements through membranes will require modification on the basis of this quantitative analysis. Whole body acid–base balance can be understood quantitatively in terms of the three independent variables and their physiological regulation by the lungs, kidneys, gut, and liver. Quantitative analysis also shows that body fluids interact mainly by strong ion movements through the membranes separating them.
Vasopressin and angiotensin in the control of arterial pressure and regional blood flow in anaesthetized, surgically stressed rats
Authors: Pang Catherine Cheuk Ying
Published: April 2011

The effects of vasopressin and angiotensin II in the control of regional blood flow (BF) in halothane-anaesthetized rats were investigated by the administration of specific antagonists of vasopressin and angiotensin II, namely, [1-(β-mercapto-β,β-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine-vasopressin [d(CH2)5Tyr(Me)AVP] and saralasin, respectively. Cardiac output and the distribution of BF was examined by the reference sample microsphere technique. The injection of the vasopressin antagonist into the left ventricle of rats caused reductions of mean arterial pressure (MAP) and total peripheral resistance (TPR), an increase of BF to the stomach and skin and a decrease of BF to the intestine. Intravenous infusion of saralasin caused reductions of MAP and TPR and an increase of BF to the kidneys and skin. The results show that both the vasopressin and the renin–angiotensin systems participate in the control of arterial pressure and peripheral vascular resistance in anaesthetized, surgically stressed rats.
Lactate and pyruvate production in isolated thiamine-deficient rat diaphragm strips
Authors: Lubek B. M. , Mainwood G. W.
Published: April 2011

Rats were maintained on a thiamine-deficient diet to deplete skeletal muscle of thiamine pyrophosphate, and thus decrease the oxidative metabolism of pyruvate. The blood lactate concentration was significantly elevated in thiamine-deficient (TD) animals when compared with pair-fed (TP) controls. Analysis of diaphragm strips from these animals revealed that tissue lactate and pyruvate concentrations were not affected by any of the treatments employed. The rate of lactate efflux from TD tissues was, however, twice that from TP and 4.5 times that from weight-control (WC) tissues. The H+ efflux rate was also much greater in the TD muscle preparation than either of the control groups. Following 3 min of stimulation (150-Hz, 200-ms pulse train every 0.5 s), the degree of fatigue of tissues from each of these three treatment groups was not different. The observation in this study that glycolysis becomes the predominant metabolic pathway in thiamine deficiency without increasing the intracellular level of products, indicates that this treatment also has other effects which increase the effective lactate permeability of the fibre membranes.
Development of isoproterenol-indueed cardiac hypertrophy
Authors: Taylor Paul B. , Tang Qian
Published: April 2011

The development of cardiac hypertrophy was studied in adult female Wistar rats following daily subcutaneous injections of isoproterenol (ISO) (0.3 mg/kg body weight). A time course was established for the change in tissue mass, RNA and DNA content, as well as hydroxyproline content. Heart weight increased 44% after 8 days of treatment with a half time of 3.4 days. Ventricular RNA content was elevated 26% after 24 h of a single injection and reached a maximal level following 8 days of therapy. The half time for RNA accumulation was 2.0 days. The total content of hydroxyproline remained stable during the first 2 days of treatment but increased 46% after 4 days of therapy. Ventricular DNA content was unchanged during the early stage (1–4 days) of hypertrophic growth but increased to a new steady-state level 19% above the controls after 8 days of treatment. Intraventricular pressures and coronary flow measures were similar for control and experimental animals following 4 days of developed hypertrophy. However, dP/dt in the ISO-treated hearts was slightly but significantly (P < 0.05) elevated. These data indicate that the adaptive response to ISO shows an early hypertrophic phase (1–4 days) characterized by a substantial increase in RNA content and cardiac mass in the absence of changes in DNA. However, prolonged stimulation (8–12 days) appears to represent a complex integration of both cellular hypertrophy and hyperplasia within the heart.
Neurotensin inhibition of canine intestinal motility in vivo via α-adrenoceptors
Authors: Sakai Y. , Daniel E. E. , Jury J. , Fox J. E. T.
Published: April 2011

Neurotensin given intra-arterially in bolus doses to the canine small intestine inhibited field-stimulated, atropine-sensitive contractile responses in the duodenum (mean effective dose (ED50) = 3.2 × 10−11 mol) and in the ileum (mean ED50 = 2.1 × 10−11 mol). Norepinephrine (ED50 = 3 × 10−9 mol) also inhibited these contractile responses. Phenylephrine (ED50 = 1.3 × 10−8 mol) was one-fourth as potent as norepinephrine and clonidine (ED50 = 8 × 10−10 mol) was at least as potent as norepinephrine, while isoproterenol (up to 8 × 10−8 mol) failed to show any inhibitory effects. Phentolamine (2 mg/kg) increased significantly the ED50 of neurotensin and norepinephrine. Prazosin (2 mg/kg) increased significantly the ED50 of norepinephrine in the duodenum but had no effect on the ED50 of neurotensin. Yohimbine (2 mg/kg) increased the ED50 values of neurotensin and adrenergic agonists. Both neurotensin and norepinephrine in doses causing maximal inhibition of field-stimulated responses decreased (by 40 to 60%) contractile responses to 9 × 10−10 mol (approximately the intra-arterial ED50 dose) of acetylcholine. Reserpine pretreatment markedly diminished the inhibition of spontaneous or field-stimulated phasic contractions by distention or field stimulation of a distal site. Reserpine also diminished the ED50 for neurotensin from 1 × 10−11 to 2 × 10−11 mol (p < 0.02), but did not abolish neurotensin's inhibitory effect. Tetrodotoxin (10–15 μg, intra-arterially) increased the dose of neurotensin required to inhibit spontaneous activity in the ileum but after this toxin, as after adrenergic antagonists or reserpine, maximal inhibition could still be obtained. These results suggested that neurotensin inhibited contractile activity of canine intestine by acting on neural receptors to release norepinephrine. Norepinephrine activated primarily α2-adrenoceptors and ultimately inhibited acetylcholine release. Neurotensin also inhibited contractions by activating a second, less sensitive receptor on smooth muscle.
Isolation of Ca2+-tolerant myocytes from adult rat heart
Authors: Bihler I. , Ho T. K. , Sawh P. C.
Published: April 2011

A procedure for the isolation of myocytes from adult rat hearts is described. It is based on successive treatments with Ca2+-free medium, disaggregating enzymes (collagenase and hyaluronidase) and mechanical agitation. Several recent isolation methods were compared and their best features were combined, together with some original modifications. A good yield of high purity myocytes with excellent morphological and functional integrity was obtained. The cells are tolerant to physiological concentrations of Ca2+. Cellular levels of ATP, Na+ and K+ are close to those in intact hearts and glucose oxidation rates and succinate exclusion are also close to normal. These characteristics are maintained for periods over 1 h.
Renal brush border membranes from mice with X-linked hypophosphatemia: protein composition, phosphate binding capacity, and protein kinase activity
Authors: Brunette Michèle G. , Allard Serge , Béliveau Richard
Published: April 2011

Phosphate uptake by brush-border membrane (BBM) vesicles prepared from hypophosphatemic mice (Hyp) is reduced by half relative to BBM vesicles from normal mice. To investigate this abnormality, we studied the protein composition of BBM, their capacity to bind inorganic phosphate, and their protein kinase activity with and without the addition of exogenous cAMP, in normal and Hyp mice. Gradient polyacrylamide gel electrophoresis of BBM proteins showed 27 bands which were identical in normal and Hyp mice. Incubation of the membranes with ortho[32P]phosphate at 0 °C revealed a phosphate binding protein with an apparent molecular weight (Mr) of 79 000, which has been previously identified in rats as the monomer of alkaline phosphatase. In normal mice, the Scatchard plot of phosphate binding was not linear, suggesting heterogeneity of the binding sites with two major components. At high substrate concentrations, the affinity (K) was 1.42 rnM and maximal binding (Bmax) was 83 pmol/mg protein. At low substrate concentrations, these values were 0.07 mM and 10.9 pmol/mg, respectively. In Hyp mice BBM, only one binding system was found with K and Bmax values of 0.38 mM and 53.8 pmol/mg. Incubation of the membranes with 25 μM[γ-32P]ATP resulted in the phosphorylation of 11 proteins. The major band (Mr: 79 000) corresponded to the inorganic phosphate binding protein, i.e., to the alkaline-phosphatase monomer. The 11 proteins showed maximal phosphorylation at pH 10. The protein of 79 000 Mr showed a second peak of phosphorylation at pH 7.5. When cAMP was added to the incubation medium, another phosphorylated protein clearly appeared at apparent Mr of 85 000. A dose–response curve demonstrated a maximal phosphorylation with 10 μM cAMP. In Hyp mice, the phosphorylation showed a tendency to be decreased for all 11 proteins. However, cAMP-dependent phosphorylation was preserved, suggesting a normal membrane protein kinase activity.
Skeletal muscle histochemical and biochemical characteristics in sedentary male and female subjects
Authors: Simoneau J. A. , Lortie G. , Boulay M. R. , Thibault M.-C. , Thériault G. , Bouchard C.
Published: April 2011

The purpose of this study was to assess the relationship between muscle fiber type distribution and enzymatic characteristics in sedentary male and female subjects. Muscle biopsy samples from the vastus lateralis muscle of 38 females and 37 males were analyzed to determine the fiber type composition (I, IIa, and IIb), the fiber size, and maximal activities of enzyme markers of energy metabolic pathways. Significant correlations were found (p < 0.05) between percent fiber type I area and hexokinase (r = −0.39), phosphofructokinase (r = −0.39), lactate dehydrogenase (r = −0.41), and oxoglutarate dehydrogenase (r = 0.33) activities, whereas such correlations with total phosphorylase (r = −0.02), malate dehydrogenase (r = 0.12), and 3-hydroxyacyl CoA dehydrogenase (r = 0.12) activities were not significant. The results of the present study also suggest the presence of a significant but low covariation of less than 30% between the fiber type distribution and muscle enzyme activities. They confirm the presence of an important metabolic heterogeneity independent of the muscle fiber type distribution in sedentary male and female subjects. Moreover, these results indicate that sedentary males exhibit a lower mean value of percent fiber type I and higher glycolytic enzyme activities than sedentary females.
Erratum: Modern quantitative acid–base chemistry
Authors: Stewart Peter A.
Published: April 2011

not available
Differential pharmacokinetics for oral and intraperitoneal administration of ethanol to the pregnant guinea pig
Authors: Clarke D. W. , Steenaart N. A. E. , Breedon T. H. , Brien J. F.
Published: April 2011

The disposition of ethanol was studied in third-trimester pregnant guinea pigs (56–59 days gestational age) following maternal administration of ethanol, 0.5 g/kg total body weight, by oral intubation and by intraperitoneal injection. For oral administration, exposure of the fetus to ethanol involved bidirectional placental transfer of ethanol between the maternal and fetal compartments. For ip administration, there was distribution of ethanol from the peritoneal space across the uterus and chorioamniotic membranes into the amniotic fluid in addition to absorption into the maternal blood circulation and subsequent placental transfer into the fetus. This resulted in exposure of the fetus to very high ethanol concentration in the amniotic fluid immediately following ethanol administration. The data indicate that the ip route of ethanol administration does not mimic ingestion of ethanol and should be avoided in future studies of the fetal alcohol syndrome in rodent animal models.
Oxygen radicals in the adult respiratory distress syndrome, in myocardial ischemia and reperfusion injury, and in cerebral vascular damage
Authors: Hammond Billy , Kontos Hermes A. , Hess Michael L.
Published: April 2011

Recent work suggests that oxygen radicals may be important mediators of damage in a wide variety of pathologic conditions. In this review we consider the evidence supporting the participation of oxygen radicals in the adult respiratory distress syndrome, in ischemia reperfusion injury in the myocardium, and in cerebral vascular injury in acute hypertension and traumatic brain injury. In the adult respiratory distress syndrome there is active sequestration of polymorphonuclear neutrophils in the pulmonary vascular system. There is evidence that activation of these neutrophils results in the production of oxygen radicals which injure the capillary membrane and increase permeability, leading to progressive hypoxia and decreased lung compliance which are hallmarks of the syndrome. In acute arterial hypertension or experimental brain injury oxygen radicals are important mediators of vascular damage. The metabolism of arachidonic acid is the source of oxygen free radical production in these conditions, in myocardial ischemia and reperfusion injury, the ischemic myocyte is "primed" for free radical production. With reperfusion and reintroduction of molecular oxygen there is a burst of oxygen radical production resulting in extensive tissue destruction. Myocardial ischemia–reperfusion injury shares in common with the other two syndromes activation of the arachidonic acid cascade and acute inflammation. Thus it would appear that the generation of toxic oxyoen species may represent a final common pathway of tissue destruction in several pathophysiologic states.
Symposium: Recent advances in the understanding of luteal function
Authors: Manns J. G. , Murphy B. D.
Published: April 2011

not available
Effects of coronary sinus pressure elevation on coronary blood flow distribution in dogs with normal preload
Authors: Rouleau Jacques R. , White Michel
Published: April 2011

Coronary sinus pressure (Pcs) elevation shifts the diastolic coronary pressure–flow relation (PFR) of the entire left ventricular myocardium to a higher pressure intercept. This finding suggests that Pcs is one determinant of zero-flow pressure (Fzf) and challenges the existence of a vascular waterfall mechanism in the coronary circulation. To determine whether coronary sinus or tissue pressure is the effective coronary back pressure in different layers of the left ventricular myocardium, the effect of increasing Pcs was studied while left ventricular preload was low. PFRs were determined experimentally by graded constriction of the circumflex coronary artery while measuring flow using a flowmeter. Transmural myocardial blood flow distribution was studied (15-μm radioactive spheres) at steady state, during maximal coronary artery vasodilatation at three points on the linear portion of the circumflex PFR both at low and high diastolic Pcs (7 ± 3 vs. 22 ± 5 mmHg; p < 0.0001) (1 mmHg = 133.322 Pa). In the uninstrumented anterior wall the blood flow measurements were obtained in triplicate at the two Pcs levels. From low to high Pcs, mean aortic (98 ± 23 mmHg) and left atrial (5 ± 3 mmHg) pressure, percent diastolic time (49 ± 7%), percent left ventricular wall thickening (32 ± 4%), and percent myocardial lactate extraction (15 ± 12%) were not significantly changed. Increasing Pcs did not alter the slope of the PFR; however, the Pzf, increased in the subepicardial layer (p < 0.0001), whereas in the subendocardial layer Pzf did not change significantly. Similar slopes and Pzf were observed for the PFR of both total myocardial mass and subepicardial region at low and high Pcs. Subendocardial: subepicardial blood flow ratios increased for each set of measurements when Pcs was elevated (p < 0.0001), owing to a reduction of subepicardial blood flow; however, subendocardial blood flow remained unchanged, while starting in the subepicardium toward mid-myocardium blood flow decreased at high Pcs. This pattern was similar for the uninstrumented anterior wall as well as in the posterior wall. Thus as Pcs increases it becomes the effective coronary back pressure with decreasing magnitude from the subepicardium toward the subendocardium of the left ventricle. Assuming that elevating Pcs results in transmural elevation in coronary venous pressure, these findings support the hypothesis of a differential intramyocardial waterfall mechanism with greater subendo- than subepi- cardial tissue pressure.
Effects of hypo- and hyper-capnia on myocardial blood flow and metabolism during epinephrine infusion in the dog
Authors: Wexels Jan C. , Myhre Eivind S. P. , Mjøs Ole D.
Published: April 2011

We have previously demonstrated a 40% increase in myocardial blood flow (MBF) during hypercapnia but no significant decrease of MBF during hypocapnia. The present study was undertaken to evaluate if epinephrine infusion, which increases both myocardial oxygen consumption [Formula: see text] and myocardial performance, might influence the effects of hypocapnia and hypercapnia on MBF. Induction of hypocapnia was performed by hyperventilation in closed-chest dogs anesthetized with pentobarbital. By adding carbon dioxide to the inspiratory gas, normocapnia and hypercapnia were created. Epinephrine infusion (0.8 μg∙kg−1∙min−1) increased MBF and cardiac output (CO) by 90 and 140%, respectively, while [Formula: see text] was increased by 45%. Epinephrine had a direct coronary vasodilating effect in excess of myocardial needs evidenced by increased oxygen content of the coronary sinus blood. During epinephrine infusion, induction of hypocapnia effected no change of MBF, while myocardial oxygen extraction increased significantly. Although oxygen saturation [Formula: see text] and [Formula: see text] in the coronary sinus blood decreased, these values remained well above those observed with hypocapnia without epinephrine infusion, thereby excluding impaired oxygen supply to the heart. Hypercapnia induced an increase of MBF by nearly 40% despite the coronary vasodilatation already induced by epinephrine infusion.
Acute effect of salmon calcitonin on renal magnesium transport in the magnesium-loaded rat
Authors: Roy Denis R.
Published: April 2011

The present studies were undertaken to examine whether salmon calcitonin, by increasing magnesium reabsorption in the thick ascending limb, and presumably the tubulointerstitial magnesium concentration gradient, would lead to an increase in fractional magnesium delivery to the end-descending limb (magnesium secretion) in magnesium-loaded rats. Thyroparathyroidectomized, postprandial Munich–Wistar rats were prepared for micropuncture of papillary end-descending limbs and of superficial end-accessible proximal tubules. Group 1 served as clonidine–water diuresis time controls; group 2 was treated as group 1 but also received synthetic salmon calcitonin (10 mU/min); and group 3 was treated as group 2 but also received calcium chloride intravenously. Calcitonin, alone or with calcium, produced a significant fall in fractional magnesium excretion. A significant relationship was also observed between fractional magnesium excretion and urine flow rate (r = 0.56, p < 0.01). Calcitonin did not modify fractional magnesium delivery to the end-descending limb. A highly significant relationship was observed between tubule fluid-to-ultrafiltrate magnesium ratio and tubule fluid-to-plasma inulin ratio (r = 0.88, p < 0.001). Within each group, fractional magnesium delivery to the end-descending limb was similar to the corresponding value in the superficial end-accessible proximal tubule. Our results suggest that despite intense magnesium reabsorption, presumably in the thick ascending limb, magnesium secretion does not occur in the juxtameduilary pars recta and (or) thin descending limb.
Distal pressure–flow relations during in vivo distal microperfusion in the rat
Authors: Levine David Z. , Gutsche Hans-Ulrich
Published: April 2011

Distal convoluted tubule reabsorptive fluxes for various substances have been measured using the technique of in vivo microperfusion with quantitative sampling of the perfusate after it traverses a known length of tubule. It is unclear, a priori, whether physiologic pressures can be maintained under these sampling conditions. The present experiments were designed to monitor these pressure changes continuously by means of a microtransducer. We have found that over the range of 10–20 nL/min, during repeat sampling, the rise in pressure is 0.11 mmHg∙nL−1∙min−1 (1 mmHg = 133.322 Pa) a value which is similar to 0.15 mmHg∙nL−1∙min−1 obtained without sampling. This small rise in pressure over the microperfusion range supports the view that this technique does not introduce unphysiologic pressure effects. The present study also provides for the first time directly measured in vivo distal tubule pressure values over a wide flow range without changing whole kidney urine flow.
Ca2+-dependent depolarization and burst firing of rat CA1 pyramidal neurones induced by N-methyl-D-aspartic acid and quinolinic acid: antagonism by 2-amino-5-phosphonovaleric and kynurenic acids
Authors: Peet M. J. , Curry K. , Magnuson D. S. , McLennan H.
Published: April 2011

The excitatory effects of microiontophoretically applied quisqualic (QUIS), N-methyl-D-aspartic (NMDA), and quinolinic (QUIN) acids were investigated using intracellular recording from CA1 pyramidal neurones in slices of rat hippocampus. QUIS evoked only simple action potentials superimposed upon a depolarization which attained a clear plateau. When this level had been reached, increased ejecting currents did not produce further depolarization. By contrast, with low currents NMD A and QUIN elicited small membrane depolarizations which triggered bursts of action potentials superimposed upon rhythmically occurring depolarizing shifts. Larger currents caused depolarization which if sufficiently large completely blocked spike activity. Tetrodotoxin (TTX) prevented the spikes evoked by QUIS and the bursts of action potentials seen with NMDA and QUIN, and the rhythmic depolarizing shifts then appeared as broad spikes of up to 50 mV in amplitude. These and the underlying membrane depolarization were blocked by Co2+, by the NMDA antagonist D(−)-2-amino-5-phosphonovaleric acid (DAPV), and by kynurenic acid (KYNU). It thus appears that the depolarization and burst firing of rat CA1 pyramidal neurones elicited by NMDA and QUIN are Ca2+ dependent while the actions of QUIS are not.
Effects of strontium on calcium-dependent hexose transport in muscle
Authors: Bihler I. , Charles P. , Sawh P. C.
Published: April 2011

Hexose transport in isolated perifused rat and guinea pig left atria and in isolated intact rat hemidiaphragms was followed by measuring the tissue/medium distribution of the nonmetabolized glucose analog, 3-O-methyl-D-glucose. Stimulation of 3-methylglucose transport by insulin, hyperosmolar medium, K+-free medium, and ouabain was depressed or absent in Ca2+-free medium. Addition of 2 mM Sr2 to Ca2+-free media restored the response of transport to the stimulatory factors. Sr2+ also increased basal hexose transport. The Ca2+ dependence and the effect of Sr2+ was greatest in guinea pig atria and least in rat hemidiaphragms. It is concluded that Sr2+ plays a Ca2+-like role in the regulation of hexose transport.
Presynaptic inhibitory effects of sotalol, propranolol, and acebutolol on noradrenaline release upon cardiac sympathetic nerve stimulation in anesthetized dogs
Authors: Yamaguchi Nobuharu , Naud Michel , Lamontagne Daniel , Nadeau Reginald , Champlain Jacques de
Published: April 2011

Effect of sotalol (STL) was compared with that of (±)-propranolol, (+)-propranolol (PPL), and acebutolol (ABL) on noradrenaline (NA) release as measured in coronary sinus (CS) blood during postganglionic stimulation (2 Hz, 30 s) of the left cardiac sympathetic nerves in anesthetized dogs. In control dogs receiving saline, increasing responses of CS-NA concentration, mean CS blood flow, and CS-NA output to repetitive stimulation were relatively stable throughout a given experimental period. Both STL (1, 2.5, and 5 mg/kg, i.v.) and (±)-PPL (0.5 and 2.5 mg/kg, i.v.) diminished the increased CS-NA concentration by approximately 35 (P < 0.05) to 60% (P < 0.01) in a dose-dependent fashion. However, (+)-PPL (0.02–2.5 mg/kg, i.v.) and ABL (0.5–5 mg/kg, i.v.) did not significantly alter the increasing response of CS-NA concentration upon stimulation. STL, (±)-PPL, and ABL markedly inhibited the CS blood flow response to stimulation at all doses tested, while (+)-PPL did not significantly diminish the flow response even at the highest dose tested. Consequently, CS-NA output decreased significantly (p < 0.01) in the presence of STL, (±)-PPL, and ABL at all doses tested but not with (+)-PPL at any dose tested. The inhibitory effect of STL and (±)-PPL on the increasing response of CS-NA concentration upon stimulation could be related to their beta-blocking effect, which exerts presumably on postulated presynaptic β-adrenoceptors, as (+)-PPL did not at all diminish the response. On the other hand, ABL does not seem to exert a similar presynaptic inhibitory effect, owing presumably either to its β-1 selectivity or to its intrinsic sympathetic activity. The results support the existence of facilitatory presynaptic β-adrenoceptors in the normal dog heart under in vivo conditions. The findings also suggest that NA release upon cardiac sympathetic nerve stimulation may be reflected more precisely by CS-NA concentration than by NA output.
Comparison of 1-oleoyl-2-acetyl-glycerol and phorbol myristate acetate as secretagogues for human neutrophils
Authors: Wong Kenneth , Chew Christine
Published: April 2011

Cellular responses induced in human neutrophils by the synthetic diacylglycerol, 1-oleoyl-2-acetyl-glycerol (OAG), paralleled those induced by phorbol myristate acetate (PMA). Like PMA, OAG caused the preferential release of enzymes from specific granules and promoted superoxide (O2−) generation. The efficacy of OAG was similar to that for PMA, but its potency was lower by four orders of magnitude. First derivative kinetic analysis showed that rates of O2− generation elicited by PMA decayed exponentially in a first order manner; the half life was found to be 21 ± 6 min. Results obtained in studies carried out with high OAG concentrations were similar except that after 40 min, the rate of decay increased and became complex order. This difference was attributed to the greater susceptibility of OAG to metabolic alteration, and was reflected in the NADPH oxidase activity of granule rich membrane fractions (GRF) of cells stimulated for 90 min with PMA or OAG. It was found that the O2− generating activity of the PMA treated GRF was significantly greater than that for the OAG treated fraction. Current evidence indicates that cellular responses arise from direct activation of protein kinase C by PMA-OAG. The stability of this complex and the bypassing of normal regulatory constraints may account for the relative longevity of the PMA–OAG O2− respiratory burst.
Starvation-induced changes in metabolic rate, blood flow, and regional energy expenditure in rats
Authors: Ma Stephanie W. Y. , Foster David O.
Published: April 2011

Starvation results in an energy-conserving reduction in metabolic rate that has features of an adaptive response. Tissue and organ sites of this response were investigated by examining the effects of starvation for 5 d on tissue blood flow (microsphere method) and regional arteriovenous O2 differences [Formula: see text] in conscious rats resting quietly at 28 °C. Comparison was with fed and overnight-fasted animals. Whole body resting metabolic rates (MR), colonic temperatures (Tc), and tissue weights were also determined. Quantitative changes in energy expenditure (as O2 consumption) were obtained for two regions: the portal-drained viscera (PDV) and the hindquarters (HQ). Fasting overnight resulted in increased blood flow to white adipose tissue (WAT) and decreased flow to the brain, PDV, testes, and skin; however, MR, Tc, the two regional [Formula: see text], and the weights of most tissues were not significantly altered. In comparison with overnight fasting, starvation for 5 d resulted in a 13% reduction in body weight, weight loss in many tissues and organs, a 26% reduction in MR, a decline of 0.5 °C in Tc, decreased [Formula: see text] across both the PDV and HQ, reduced cardiac output, and decreased blood flow to the heart, PDV, skin, WAT, leg muscle, HQ, and the musculoskeletal body as a whole. Utilization of O2 by the PDV and HQ [Formula: see text] declined by amounts that accounted for 22 and 18%, respectively, of the reduction in MR. The reductions in cardiac output (18%) and heart blood flow (36%) indicate that the heart also made a contribution to energy conservation (roughly estimated as 5%). Overall, the data suggest that gut and muscle together accounted for two-thirds to three-quarters of the starvation-induced energy conservation.
Effects of dietary zinc and copper on free radical production in rat lung and liver
Authors: Kubow Stan , Bray Tammy M. , Bettger William J.
Published: April 2011

The effects of dietary copper and zinc on free radical production in lung and liver microsomes were studied in male weanling rats. The rats were fed for 6 weeks on one of seven diets, with different copper and zinc concentrations representing low, adequate, and high dietary levels of copper and low and adequate levels of zinc. Rats were put on diets arranged in a 3 × 2 factorial design with copper and zinc supplementations of 0, 15, and 500 mg/kg and 0.5 or 100 mg/kg, respectively. The low copper diet depressed copper levels in both the lungs and liver, although zinc levels were unchanged in rats on the low zinc diets. Endogenous carbon-centered lipid radical production in microsomes induced by NADPH was measured using spin-trapping techniques. The low zinc diets increased free radical production in lung microsomes but not in liver microsomes. No change in free radical production was obsrved in lung or liver microsomes obtained from rats on low copper diets. The data indicate that endogenous free radical production is increased in lung microsomes as a function of dietary zinc deficiency but is not influenced by copper status.
Autoregulation of superior mesenteric artery is blocked by adenosine antagonism
Authors: Lautt W. Wayne
Published: April 2011

Pressure–flow autoregulation of the intact superior mesenteric artery (SMA) was demonstrated in the fasted, pentobarbital-anesthetized cat by use of a micrometer-controlled screw clamp to produce progressive decreases in vascular pressure. Administration (ia) of bolus doses of 8-phenyltheophylline (8-PT) were followed by infusion of adenosine to verify adenosine antagonism. 8-PT doses were progressively doubled until adenosine responses were blocked. If higher doses of 8-PT were used, SMA flow declined to very low levels and autoregulatory curves could not be obtained. Comparison of vasodilator responses to isoproterenol and adenosine before and after adenosine receptor blockade verified that, whereas adenosine responses were blocked, isoproterenol effects were not altered. The autoregulation was quantitated using three methods (the autoregulatory index, the percent decrease in vascular resistance, and the slope index) as blood pressure was reduced from a standardized control pressure of 110 mmHg (1 mmHg = 133.3 Pa). Maximal vasodilation appeared at a blood pressure of 56 ± 5 mmHg (range 34–70). 8-PT resulted in dose-related antagonism of the dilator response to exogenous adenosine and autoregulation. All indices of autoregulation were significantly reduced by 8-PT. The data are compatible with the hypothesis that pressure–flow autoregulation in the SMA is not myogenic (responding to altered transmural pressure) but is dependent upon local concentrations of adenosine.
Glucose oxidation in white adipose tissue from BIO 14.6 dystrophic hamsters
Authors: Elbrink J. , Hunter E. G.
Published: April 2011

In studies of glucose oxidation in white retroperitoneal adipose tissue of BIO 14.6 dystrophic and FIB normal hamsters aged 55–67 and 368–379 days, no difference was found in the basal state of radiolabelled 14CO2 production using either D-[6-14C]glucose or D-[1-14C]glucose. When C6-labelled glucose was used, insulin induced a slightly greater increase in glucose oxidation in dystrophic adipose tissue at both ages. When C1-labelled glucose was used, insulin enhanced glucose oxidation in dystrophic tissue more than twice normal in tissues from young animals and five times normal in tissues from the old ones. The increase in oxidation with D-[1-14C]glucose likely represents enhanced activity of the pentose phosphate pathway, which has also been observed in certain tissues of other animals with inherited skeletal-muscle degeneration. The change can probably be classified as being compensatory, an attempt by tissues to maintain functional integrity.
Endothelium-dependent relaxation and experimental atherosclerosis in the rabbit aorta
Authors: Sreeharan N. , Jayakody R. L. , Senaratne M. P. J. , Thomson A. B. R. , Kappagoda C. T.
Published: April 2011

This study was undertaken to determine whether the production or release of the endothelium-dependent relaxatory factor is impaired in atherosclerotic New Zealand White rabbits. Atherosclerosis was induced by feeding a diet containing 2% cholesterol for 6 weeks. The production or release of endothelium-dependent relaxatory factor was assayed as follows. A 5-cm length of aorta donor was perfused with Krebs–bicarbonate buffer and the perfusate drained over a deendothelialized ring of recipient aorta set up for recording isometric tension. The recipient was precontracted with norepinephrine (0.2 μmol/L) in the perfusate. When acetylcholine was added to the perfusate, the recipient relaxed in a dose-dependent manner. This assay was used to compare the relaxatory responses produced in recipient rings by adding acetylcholine to donors from atherosclerotic and control rabbits. The relaxation produced by atherosclerotic donors were smaller than those generated by control donors (16.5 ± 4.9 vs. 32.7 ± 5.3%; n = 10, p < 0.05). It is suggested that in atherosclerotic rabbits the ability of aortic endothelium to produce or release endothelium-dependent relaxatory factor is impaired.
Cyclic AMP and the vascular action of parathyroid hormone
Authors: Pang Peter K. T. , Yang May C. M. , Tenner Jr. Thomas E. , Kenny Alexander D. , Cooper Cary W.
Published: April 2011

The involvement of tissue cAMP in the vasodilating action of parathyroid hormone (PTH) was investigated. The bovine active fragment bPTH-(1–34) was used in all studies. In anesthetized dogs, theophylline, a phosphodiesterase inhibitor, potentiated the hypotensive action of bPTH-(1–34) at the dose of 1 μg/kg. The potentiation was related to the dose of theophylline infused. In an in vitro rat tail artery helical strip assay, dibutyryl cAMP produced dose-related relaxation in arginine vasopressin (AVP) constricted blood vessels. bPTH-(1–34) also produced dose-related relaxation in the tail artery constricted by AVP. In the presence of isobutylmethylxanthine, another phosphodiesterase inhibitor, the bPTH-(1–34) dose-response curve was shifted to the left, indicating potentiation. Imidazole, which has phosphodiesterase stimulating activity, significantly decreased the in vitro vasorelaxing effect of bPTH-(1–34). In addition, bPTH-(1–34) increased significantly the rat tail artery cAMP content. b-PTH-(1–34) oxidized with hydrogen peroxide lost its vasorelaxing activity and was also ineffective in increasing the tail artery cAMP content. All these data strongly suggest that cAMP may be involved in eliciting the vasorelaxing action of bPTH-(1–34).
Mechanisms of response to antigen in isolated guinea pig trachea after active sensitization
Authors: Mansour S. , Daniel E. E.
Published: April 2011

A study was made of the responses of guinea pig tracheal muscle in vitro after sensitization by either subcutaneous or intraperitoneal administration of antigens. No difference was observed in the responses of strips from either group to cumulative or single doses of antigen. The responses of the tracheal muscle to antigen were analyzed as to magnitude (relative to maximal carbachol responses), time to peak contraction, and time to half decay. Pyrilamine, an H1-receptor antagonist, slowed the onset of contraction and decay. The latter result suggested a role for histamine in controlling the release of or the response to other mediators and the former was consistent with previous evidence that histamine release augments the initial response. An inhibitor of 5′-lipoxygenase and cyclooxygenase (5,8,11,14-eicosatetraynoic acid), indomethacin, and the slow-reacting substance of anaphylaxis (SRS-A) antagonist FPL-55712 all shortened the time to half decay of the contraction, presumably by different mechanisms. The release and actions of leukotrienes may have been limited by eicosatetraynoic acid and FPL55712, respectively, but the action of indomethacin suggests a modultaing role for prostanoids in leukotriene action or release. Nordihydroguaiaretic acid both reduced the maximum response and accelerated decay of this response, suggesting that the maximum response depends upon leukotriene release. Cromoglycate, methysergide, and an inhibitor of thromboxane synthetase were without effect. Both tetrodotoxin and atropine delayed the time to peak contraction and tetrodotoxin also delayed the decay of the contraction. These results suggest that, in addition to the accepted occurrence of sequential histamine and leukotriene release, there may be a role for nerves and prostanoids in modulating mediator release but no role of thromboxanes or serotonin. Histamine may not only initiate the response but also may modulate the response to released leukotrienes. The lack of effect of cromoglycate is unexplained.
Central 6-hydroxydopamine and renal sodium retention in mineralocorticoid-treated rats
Authors: Hall J. L. , Mecca Thomas E. , Malvin Richard L. , Webb R. Clinton
Published: April 2011

Cerebroventricular administration of 6-hydroxydopamine attenuated the development of deoxycorticosterone hypertension in the rat but did not affect the initial period of renal sodium retention. However, escape from the sodium retention was greater in 6-hydroxydopamine-treated rats. These data support the hypothesis that destruction of central catecholamine-containing neurons influences the renal handling of sodium. The enhanced escape may lead to diminished total body sodium, which attenuates the development of deoxycorticosterone hypertension.
Stress- and cold-induced adrenocortical responses in repetitively immobilized or cold-acclimated rats
Authors: Yahata Takehiro , Murazumi Kazuhiko , Kuroshima Akihiro
Published: April 2011

To evaluate the role of adrenocortical hormones in stress- or cold-induced nonshivering thermogenesis, plasma corticosterone (CS) and deoxycorticosterone (DOCS) were measured with the aid of HPLC under various conditions. Repetitive immobilization stress (3 h/day, for 1 or 4 weeks) elevated the resting level (24 h after the last immobilization) of CS, but not DOCS. Acute stress (immobilization for 30 min) or cold exposure (−5 °C for 15 min) caused marked increases of CS and DOCS in both nonstressed naive controls and repetitively stressed rats. Four weeks, but not 1 week, of repetitive immobilization stress potentiated the responsiveness of CS to both acute stress and cold, and that of DOCS to acute stress, but not to cold. Cold acclimation (5 °C, 4 weeks) significantly elevated both corticosteroids but did not affect the resting levels (18 h after being transferred to 25 °C) or the responsiveness of both CS and DOCS to either acute stress or cold. These results suggest that repetitive immobilization stress, but not cold acclimation, could enhance nonshivering thermogenesis, at least in part, through an improvement in the responsiveness of adrenocortical hormone secretion to acute stress or cold.
Sodium and guanine nucleotide regulation of dopamine receptor agonist and antagonist binding sites in MtTW15 pituitary tumors
Authors: Paolo Thérèse Di , Lévesque Daniel
Published: April 2011

The modulation of the dopamine receptor in MtTW15 tumors was investigated. The antagonist dopaminergic binding site in MtTW15 tumors labelled with [3H]spiperone remains unchanged at 25 °C in the presence or absence of sodium or guanine nucleotides (Gpp(NH)p); by contrast at 37 °C sodium increases the affinity while Gpp(NH)p decreases it slightly. The dopamine receptor in this tumor, such as the intact adenohypophysis, exists in a high and low affinity state for dopamine agonists. These agonist affinity states evaluated with apomorphine competition for [3H]spiperone binding show similar affinities as those of intact tissue but have a lower proportion of the high affinity state. At 25 °C, a partial conversion of the high into the low affinity state is obtained in the presence of both sodium and Gpp(NH)p, while at 37 °C a complete conversion is observed. These data show differences in the modulation of antagonist and agonist dopaminergic binding sites in MtTW15 pituitary tumors compared with the intact pituitary.
3-O-Methyl-D-glucose uptake in cultured bovine adrenal chromaffin cells
Authors: Bigornia Luisa , Bihler Ivan
Published: April 2011

The membrane transport of glucose was studied in bovine adrenal chromaffin cell cultures by following the cell/medium distribution of the nonmetabolizable glucose analog, 3-O-methyl-D-glucose. Uptake of this sugar in day-1 cultures that are undergoing rapid morphological change and differentiation had a Vmax of 138 nmol/(mg protein∙min) and Km of 15 mM, and was only slightly increased by 50 mU/mL insulin. In day-5 cultures where morphological changes were essentially completed, Vmax and Km decreased to 51 nmol/(mg protein∙min) and 9.5 mM, respectively, and the response to insulin was restored to the level found in freshly isolated cells; this effect was abolished in the nominal absence of Ca2+. Thus, saturation kinetics and insulin and Ca2+ sensitivity of 3-methylglucose uptake observed in freshly isolated cells were maintained in culture. However, the insulin response was almost absent during the initial period of rapid morphological change when sugar transport was strongly stimulated. Culture of chromaffin cells in the presence of dexamethasone did not inhibit the formation of processes, but decreased 3-methylglucose uptake in day-5 cultures by an apparently competitive effect.
Somatosensory cortical mechanisms of feature detection in tactile and kinesthetic discrimination
Authors: Gardner Esther P.
Published: April 2011

Neurons in somatosensory cortex of primates process sensory information from the hand by integrating information from large populations of receptors to extract specific features. Tactile neurons in areas 1 and 2 are shown to select features such as contact area, edge orientation, motion across the skin, or direction of movement. Features coded by kinesthetic neurons in areas 3a and 2 relate to joint movement, the joint angle around which the movement occurs, or coordinated postures of the hand and arm. An even higher order cortical cell integrates tactile and kinesthetic information; these "haptic neurons" respond optimally to contact of objects actively grasped in the hand. These global features are coded at the expense of loss of information concerning fine-grained spatial detail.