bluuebunny/crossref_metadata_2025 huggingface dataset:
Cerebrospinal fluid transients induced by hypercapnia
Authors: Fisher M. J. , Heisey S. R. , Adams T. , Traxinger D. L.
Published: December 2017

Ventriculocisternal perfusion studies using tracers have shown that hypercapnia causes a transient increase in cerebrospinal fluid (CSF) outflow rate (displaced CSF volume, Vd) and a decrease in CSF effluent tracer concentration (tracer-free CSF, CSFtf). This dilution could be due to an increase in CSF formation rate (Vf) and/or to displacement of unequilibrated CSFtf sequestered in poorly mixed compartments. To facilitate convection in the subarachnoid spaces, we used a “stop-flow” procedure (by clamping the cisternal outflow tube while infusion was constant) in anesthetized cats during ventriculocisternal perfusion with mock CSF containing [14C]dextran. Each animal spontaneously breathed air, then 5% CO2 both before and after stopflow. Although Vd and the times over which Vd and CSFtf were defined were unaffected, CSFtf was decreased by 50% after stop-flow. We conclude that during ventriculocisternal perfusion, mixing is incomplete in CSF spaces, and that unequilibrated CSF contributes significantly to the reduced tracer concentration in Vd during acute hypercapnia. To determine whether Vf transiently increases in response to CO2 breathing, or to any perturbation causing craniospinal fluid redistribution, homogeneity in CSF spaces must be verified.
Maternal blood volume and cardiac output during pregnancy: a hypothesis of endocrinologic control
Authors: Longo L. D.
Published: December 2017

During the course of gestation the increase of maternal total blood volume and cardiac output may result from two mechanisms acting in concert: 1) the production of several hormones by the fetus and the placenta, and 2) the uteroplacental circulation acting as an arteriovenous shunt. Plasma volume appears to increase as a consequence of renal Na+ reabsorption and water retention, which result from increased aldosterone production via the renin-angiotensin system, as a consequence of placental estrogen production. This estrogen production in turn results from increasing availability of the estrogen substrate dehydroepiandrosterone (chiefly from the fetal adrenal gland). Erythrocyte volume increases as a consequence of the erythropoietic effect of placental chorionic somatomammotropin, progesterone, and perhaps prolactin. In addition, maternal blood volume increases in response to the uteroplacental circulation functioning as a low-resistance circuit. In turn, this increases cardiac output and nutrient delivery for further growth of the products of gestation. Thus there may exist a feedback mechanism whereby fetal growth and, in particular, increasing steroidogenesis by the developing fetal adrenal gland result in the maternal cardiovascular adaptations to pregnancy that optimize further fetal development. In certain complications of pregnancy the less-than-normal maternal blood volume increase may result from failure of these mechanisms, while in turn contributing to the further genesis of these disorders.
Uterine blood flow: periodic fluctuations of its rate during pregnancy
Authors: Caton D. , Pendergast J. F. , Bazer F. W.
Published: December 2017

Daily measurements of the rate of uterine blood flow (ml/min) during the last half of pregnancy of four normal sheep reflected a 17-day cyclic fluctuation (range, 9.5–42 days) superimposed on a linear increase over time. The cyclic increase was not detected in two (of 7) intact ewes or in four pregnant ewes that had been ovariectomized. The cyclic pattern of increase may be related to ovarian activity.
Role of calcium in cAMP-mediated effects in the elasmobranch rectal gland
Authors: Shuttleworth T. J.
Published: December 2017

The effects of A23187 and verapamil on the vasomotor and secretory effects of adenosine 3',5'-cyclic monophosphate (cAMP) in the rectal gland were investigated in Scyliorhinus canicula and Squalus acanthias. A23187 was a potent vasoconstrictor in the gland and reversed the vasodilatory action of cAMP in glands constricted with norepinephrine. Verapamil, like cAMP, prevented the vasoconstriction induced in the gland by norepinephrine. A23187 had no effect on the secretory activity (measured as ouabain binding and ouabain-sensitive oxygen consumption) of the glands. Verapamil inhibited the stimulation of ouabain binding, ouabain-sensitive oxygen consumption, and sodium secretion rate induced by cAMP plus theophylline, but did not affect the stimulation of ouabain binding and ouabain-sensitive oxygen consumption induced by amphotericin B. These data indicate that it is the cAMP-induced stimulation of the sodium-chloride cotransport system that is verapamil sensitive, and it is suggested that this stimulation is a calcium-dependent process. This emphasizes the independent nature of the secretory and vasomotor effects of the nucleotide in the gland.
Mechanisms of the central pressor action of angiotensin II in conscious rats
Authors: Lappe R. W. , Brody M. J.
Published: December 2017

Previous studies have demonstrated that, due to a central action, angiotensin II (ANG II) infused via the carotid artery of the rat elicited a greater pressor response than ANG II infused via the abdominal aorta. In the present study, regional vascular resistance responses to carotid and abdominal aortic infusions of ANG II and angiotensin I (ANG I) were compared in conscious unrestrained rats. Miniaturized pulsed Doppler flow probes were used to record regional blood flows. Carotid and aortic infusions caused vasoconstriction in the hindquarters, renal, and mesenteric vascular beds; the carotid route resulted in greater increases in arterial pressure and regional vascular resistances. The enhanced vasoconstrictor responses to carotid infusions of ANG II were significantly attenuated by systemic hexamethonium or central saralasin. Unlike ANG II, carotid and aortic infusions of ANG I produced equivalent regional vasoconstrictor responses not affected by central saralasin. It is concluded that in addition to its peripheral effects, central actions of ANG II induce neurally mediated vasoconstriction of the hindquarters, renal, and mesenteric vascular beds. Central effects of ANG II do not appear to result from conversion in the brain of blood-borne ANG I.
In vivo effect of volume expansion on rectal gland function. I. Humoral factors
Authors: Solomon R. , Taylor M. , Stoff J. S. , Silva P. , Epstein F. H.
Published: December 2017

The spiny dogfish Squalus acanthias responds to volume expansion by increasing the rate of chloride secretion by its rectal gland. The response is elicited by intravascular infusion of either isotonic shark Ringer solution, a 1 M hypertonic sodium chloride solution, or an isotonic hyponatremic solution containing equal volumes of shark Ringer solution and 10% mannitol. The effect of volume expansion was evoked in explanted glands connected to a host fish only by the arterial supply, indicating that the response is mediated by a humoral factor. The explanted gland responded to theophylline (2.5 X 10(-3) M) and adenosine 3',5'-cyclic monophosphate (5 X 10(-4) M) by increasing the rate of secretion of chloride by an amount similar to that induced by volume expansion of the perfusing fish. Theophylline at concentrations (10(-6) to 5 X 10(-5) M) that are known to inhibit the effect of adenosine in isolated perfused glands failed to inhibit the effect of volume expansion on explanted glands. Somatostatin (4.5 X 10(-6) M), which inhibits the effect of vasoactive intestinal peptide (VIP) in the isolated perfused gland, completely prevented the secretory response to volume expansion in explanted glands. Volume expansion is a major stimulus for chloride secretion by the rectal gland. The effect is mediated by a humoral factor that appears to be VIP.
Prostacyclin release following endoperoxide analogue infusion in the intact dog
Authors: Mehta J. , Nichols W. W. , Goldman R.
Published: December 2017

We examined the systemic and coronary hemodynamic responses after infusion of an endoperoxide analogue U 46,619 in anesthetized dogs and related the hemodynamic effects to the release of thromboxane A2 (TXA2) and prostacyclin (PGI2). Immediately after U 46,619 infusion, increases in mean arterial and left ventricular end-diastolic pressures (LVEDP) occurred, whereas coronary and aortic blood flows were unchanged. Calculated vascular resistances in the systemic and coronary vascular beds increased significantly. At 3-5 min after infusion, mean arterial pressure and LVEDP spontaneously decreased and vascular resistances also declined, whereas coronary and aortic blood flows were unchanged. Simultaneously measured plasma TXB2 and 6-keto-PGF1 alpha (stable hydrolysis metabolites of TXA2 and PGI2, respectively) increased in the femoral and coronary arterial blood samples in conjunction with the vasoconstrictor effects. At 3-5 min, plasma 6-keto-PGF1 alpha concentrations showed a further increase, whereas TXB2 concentrations slightly decreased, suggesting release of PGI2 as a possible mechanism of vasodilation. To examine this possibility, nine dogs were treated with cyclooxygenase inhibitors (aspirin or indomethacin) and given U 46,619. In these animals neither vasoconstrictor nor vasodilator effects were observed. Plasma TXB2 and 6-keto-PGF1 alpha concentrations also did not increase after U 46,619. These data show that the vasoconstrictor and platelet aggregatory agent U 46,619 results in PGI2 release in the dog. Release of PGI2 may be a protective and autoregulatory mechanism in the canine systemic and coronary vascular beds.
PAH excretion in two species of cancroid crab Cancer irroratus and C. borealis
Authors: Holliday C. W. , Miller D. S.
Published: December 2017

To determine the characteristics of p-aminohippuric acid (PAH) excretion in Cancer irroratus and C. borealis, crabs were given a single injection of radiolabeled PAH and polyethylene glycol (PEG), and serum, urine, tissue, and seawater concentrations of each were measured over the next 6 days. In both species, PEG clearances averaged 5-10 ml serum/day; serum PAH concentrations fell exponentially after a 1-day equilibration period. In C. irroratus, urine PAH rose over the first 2 days and then fell; during days 2-6, mean urine PAH averaged two to four times mean serum PAH. In C. borealis, urine-to-serum ratios for PAH were 20-40 during days 2-6. PAH-to-PEG clearance ratios exceeded unity in both species, with ratios in C. borealis about three to six times those in C. irroratus. Tissue distribution data showed that C. irroratus midgut gland accumulated up to 50% of injected PAH, with gland-to-serum concentration ratios of 15-45; in this species, stomach fluid-to-serum PAH concentration ratios averaged 87, and nonurinary routes accounted for more than half of excreted PAH. In C. borealis, midgut gland-to-serum ratios never exceeded 2, and the urinary routes accounted for all excreted PAH. Thus, in C. irroratus, injected PAH accumulated in the midgut gland, with slow excretion through renal and nonrenal routes; in C. borealis, PAH remained in hemolymph, and only the renal route of excretion was utilized.
Metabolic regulation via intracellular pH
Authors: Busa W. B. , Nuccitelli R.
Published: December 2017

Despite earlier notions that intracellular pH (pHi) was invariant with time, recent studies have documented pHi changes of from 0.1 to 1.6 U during metabolic and developmental transitions in a variety of cells. Here we review the evidence for pHi-mediated regulation of gamete activation, cellular dormancy, the cell cycle, and stimulus-response coupling. Intracellular Ca2+ level changes also accompany many of these same transitions, and mounting evidence suggests that pHi and Ca2+ changes can be interdependent, both in their mechanisms and their effects. Although the significance of such interactions is still largely unclear, one example--the pronounced pH dependence of Ca2+ binding by calmodulin--suggests their potential importance in metabolic regulation. Similar evidence suggests that pHi changes also influence intracellular adenosine 3',5'-cyclic monophosphate levels, and vice versa. Finally we show that changes in adenylate energy charge can significantly alter pHi. In light of these interactions--and because pHi, unlike most other effectors, does not require specialized receptors--we suggest that pHi functions as a synergistic messenger, providing a metabolic context within and through which the actions of other effectors are integrated.
Body composition in the rat: interactions of exercise, age, sex, and diet
Authors: Pitts G. C.
Published: December 2017

Changes in rat body composition (15 components) associated with changes in level of physical activity (cage restraint, ad libitum activity in living cages, and ad libitum wheel running), age at initiation of regimen (22 days-16 wk), sex, and diet (chow and 60% fat) are evaluated. Running regimen initiation at 7 wk of age or younger is associated with a decrease in the fat-free body mass (FFBM) in males and an increase in females. Initiation at 11 wk or older does not change FFBM. Both reduce body fatness in either sex. Age altered the mass of 11 components, diet altered the mass of 10 components, and activity altered the mass of 8 components, and there were 6 interactions between the experimental variables. The significance of interactions in general is discussed. Our data together with those of other investigators indicate that the responses to volitional wheel running and forced treadmill running are similar, but data from swimming rats may not be comparable in some cases.
Modulation of feeding by endogenous sugar acids acting as hunger or satiety factors
Authors: Shimizu N. , Oomura Y. , Sakata T.
Published: December 2017

Endogenous sugar acids, 3,4-dihydroxybutanoic acid (2-deoxytetronic acid, 2-DTA) and 2,4,5-trihydroxypentanoic acid (3-deoxypentonic acid, 3-DPA), have been identified in the serum of fasted rats. Effects of these sugar acids on rat feeding behavior and neuron activity were investigated. Injections of 2-DTA (2.5 mumol) into the third cerebral ventricle of chronic rats suppressed food intake and single-neuron activity in the lateral hypothalamic area (LHA). Food consumption was reduced for 24 h, even in 72-h food-deprived rats. The same amounts of 3-DPA elicited feeding and increased LHA single-neuron activity with latencies of 6-8 min. Electrophoretically applied 2-DTA significantly and specifically suppressed activity of glucose-sensitive neurons in the LHA, whereas 3-DPA facilitated the activity. Nonglucose-sensitive LHA neurons were not affected by these sugar acids. The high correlation between modulation of feeding behavior and changes in LHA neuron activity after injection of these sugar acids suggested that 2-DTA may act as an endogenous satiety substance and 3-DPA as a hunger substance. The effects may be mediated through glucose-sensitive neurons in the LHA.
High-altitude adaptation and maximum work performance
Authors: Johnson E. S. , Finch C. A.
Published: December 2017

The treadmill work performance of rats at sea level with normal or elevated hematocrits was compared with that of rats conditioned in a hypobaric chamber at 450 Torr for 3 wk with similar hematocrit adjustments. A mean increase in hematocrit to 62 significantly improved the work performance of rats at sea level and at ambient O2 tensions of 100, 75, and 35 Torr. By contrast, rats conditioned in a hypobaric chamber with mean hematocrits of 40 and 58 performed similarly at all O2 tensions compared with sea-level rats with hematocrits of 43. Thus, although an increase in O2-carrying capacity of the blood of sea-level animals increased work capacity, altitude adaptation did not appear to result in any positive effect on work capacity, and indeed, seemed to interfere with the beneficial effect of polycythemia on maximum work performance.
Mechanisms of CO2 transport in rectal salt gland of aedes. I. Ionic requirements of CO2 secretion
Authors: Strange K. , Phillips J. E.
Published: December 2017

Rectal salt glands of Aedes dorsalis can be successfully isolated and microperfused in vitro. Microperfused salt glands maintain a large, stable transepithelial potential (-40 to -50 mV, lumen negative) and secrete total CO2 at high and stable rates [CO2 net flux ( JCO2net ) = 799 +/- 57 pmol . min-1 . mm-1]. Bilateral Na+ and K+ or serosal Cl- substitutions and serosal addition of 1.0 mM ouabain, 2.0 mM amiloride, or 0.5 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid had no effect on JCO2net . Removal of luminal Cl- inhibited JCO2net by 80%, whereas serosal addition of 1.0 mM acetazolamide or 0.5 mM 4,4'-diisothiocyano-2,2'-disulfonic acid inhibited JCO2net by 80 and 40%, respectively. Net Cl- reabsorption ( JClnet = -888 +/- 57 pmol . min-1 . mm-1) was equivalent to total CO2 secretion, suggesting that CO2 transport was mediated by a 1:1 exchange of luminal Cl- for serosal HCO-3.
Isoproterenol-induced blood flow in rats acclimated to room temperature and cold
Authors: Wickler S. J. , Horwitz B. A. , Flaim S. F. , LaNoue K. F.
Published: December 2017

Blood flow was measured with labeled microspheres in cold (6 degrees C)- and room-temperature-acclimated rats at rest and during infusion of the beta-agonist, isoproterenol. Isoproterenol elicited decreased mass-specific blood flows (ml . g-1 . min-1) to liver (55% of control), kidney (48%), and white fat (64%) in room-temperature-acclimated (RT) rats. Blood flow was similarly decreased in liver (51%), kidney (37%), and white fat (70%) in cold-acclimated (CA) rats. In contrast, isoproterenol increased blood flows to brown fat and cardiac and skeletal muscles. The blood flows to cardiac muscle during isoproterenol infusion were comparable in both RT (12.7 ml . g-1 . min-1) and CA (11.7 ml . g-1 . min-1) animals, representing increases of 2.9- and 2.6-fold above control values, respectively. Blood flow to skeletal muscle was also similarly elevated in RT and CA animals, representing increases 5.9 and 5.6 times those of their respective control values. In contrast, although isoproterenol greatly stimulated (ca. 8-fold) blood flow to brown fat (interscapular plus cervical depots) in RT animals, it had a greater effect on these two depots in the CA rats (18-fold increase). These data emphasize the importance of brown fat as a major effector of nonshivering thermogenesis as well as the importance of beta-adrenergic receptors in mediating the metabolic response of nonshivering thermogenesis.
Cholecystokinin persistently suppresses meal size but not food intake in free-feeding rats
Authors: West D. B. , Fey D. , Woods S. C.
Published: December 2017

Food and water intake of free-feeding rats with indwelling intraperitoneal catheters connected to infusion pumps was continuously monitored and recorded by a microcomputer-based data acquisition system. Initially, at the start of every spontaneous meal for 4 days, each rat was infused with 0.27 ml of physiological saline. Saline infusion did not affect any feeding or drinking patterns, and the rate of weight gain remained unchanged. For 6 subsequent days, the octapeptide of cholecystokinin (CCK-8, 1.1 micrograms/meal) dissolved in physiological saline was infused at the onset of each meal. CCK-8 infusion caused a dramatic shift of patterns of food intake. Average meal size was reduced by at least 44%, whereas daily meal number increased by 162% or more for all 6 days of CCK-8 infusion. Total daily food intake recovered to predrug levels by the 4th day of CCK-8 infusion, primarily due to increased feeding frequency. Average body weight dropped by 12.4 g on the 1st day of CCK infusion, but over the following 5 days the growth rate was not different from the base-line predrug rate. With discontinuation of CCK-8 infusion all meal patterns returned rapidly to normal and body weight immediately recovered.
Hepatic ammonia metabolism in a uricotelic treefrog Phyllomedusa sauvagei
Authors: Campbell J. W. , Vorhaben J. E. , Smith D. D.
Published: December 2017

Glutamine synthetase, a mitochondrial enzyme in liver of uricotelic reptiles and birds, is present in the cytosolic compartment of Phyllomedusa sauvagei liver. The average level is sufficient to account for the rate of uric acid excretion by adult frogs but is far lower than that present in birds and reptiles. Except for lower carbamoylphosphate synthetase activity, the activities of the urea cycle enzymes in P. sauvagei liver are comparable with those in adult ureotelic amphibians. The subcellular distribution of the urea cycle enzymes is much the same as in ureotelic amphibians and mammals with the possible exception of the occurrence of a small percentage of the carbamoylphosphate synthetase and ornithine transacarbamylase activities in the cytosol. In keeping with the subcellular localization of the enzymes, citrulline, and not glutamine, is formed by isolated liver mitochondria. The rapid degradation of glutamine by these mitochondria suggests a high degree of compartmentation of glutamine in the cytosol of P. sauvagei if it is to function as a precursor of uric acid in this compartment.
Common cortical and thalamic mechanisms for language and motor functions
Authors: Ojemann G. A.
Published: December 2017

Evidence for common mechanisms in the human brain for motor and language functions is reviewed, particularly evidence derived from electrical-stimulation mapping during cortical and thalamic operations in awake patients. Several systems in the dominant hemisphere are identified where language and motor function share common mechanisms, including a lateral thalamic attentional system and a lateral perisylvian cortical system common to sequential movement and speech sound identification, where precise timing may be a common mechanism.
Functional precursors to language and its lateralization
Authors: MacNeilage P. F. , Studdert-Kennedy M. G. , Lindblom B.
Published: December 2017

An adequate account of language evolution must reconcile the propositions that language is unique but has precursors. The paper of Bellman and Goldberg and that of Tzeng and Wang each neglects one of these propositions. We suggest that the uniqueness of language lies primarily in its dualistic structure which has a frame-content mode of organization: at the phonological level, consonant and vowel elements are inserted into syllabic frames; and at the morphological level, stem forms of content words are inserted into syntactic frames. We suggest that the morphological level evolved from the phonological level and that the frame-content mode of organization in phonology had a precursor in the form of bimanual coordination in which the nonpreferred (frame) hand holds an object operated on by the preferred hand (content). It is argued that lateralization of cortical function evolved first for bimanual coordination, then for language. Old World monkey hand preferences may be consistent with both the putative left-hemisphere specialization for bimanual coordination and the human right-hemisphere specialization for spatial functions.
Reflex and local thermal control of rabbit ear blood flow
Authors: Roberts M. F. , Zygmunt A. C.
Published: December 2017

We measured thermal conductance (K) of the ears of 12 New Zealand White rabbits during periods of core heating in which mean skin temperature and ear temperatures (Te) were controlled. Right Te was always held at 28 degrees C; left Te was 15, 20, 24, 28, 31, 33 degrees C in separate core heating periods. Core heating was obtained by perfusing a previously implanted intravascular heat exchanger with hot water. Blood temperature (Tbl) was measured with a thermocouple that had been previously placed in contact with the common carotid artery. During heating, K rose with rising Tbl, but the relation between K and Tbl depended on Te. At high Te, K rose rapidly in the initial stages of core heating and soon reached its maximal value. At cool Te, K rose slowly with rising Tbl until high Tbl was reached; then K rose rapidly to maximal values. The maximal value of K reached at high Tbl was independent of Te. The results suggest that local temperature affects ear blood flow by affecting the way that ear blood vessels react to sympathetic reflex signals.
Glucose responsiveness and acetylcholine sensitivity of pancreatic beta-cells after vagotomy
Authors: Campfield L. A. , Smith F. J. , Eskinazi R. E.
Published: December 2017

The chronic effects of removal of parasympathetic neural input to the pancreas on in vitro insulin secretion were assessed. Groups of Wistar and Long-Evans rats received total subdiaphragmatic vagotomy or sham operation. Four to ten weeks later, after the return of food intake and body weight in the vagotomized groups to values similar to the sham-operated groups, pancreatic islets were isolated and statically incubated with selected concentrations of glucose and acetylcholine. Two experimental protocols were used. In the first experiment, insulin secretion in response to basal (5 mM) glucose was 59 +/- 15 (SE) and 65 +/- 13% greater in islets from the vagotomized Wistar and Long-Evans groups, respectively, than in the corresponding sham groups. The enhancement of insulin secretion by several doses of acetylcholine observed in islets from sham-operated groups was totally absent in islets from both vagotomized strains. In the second experiment, insulin secretion was determined in response to selected glucose concentrations by using islets from Wistar rats. An upward and leftward shift of the dose-response curve was observed in the vagotomized group causing 5 mM to become a stimulatory glucose concentration and increasing the stimulatory potency of 10 mM glucose. These results suggest that interruption of vagal input to pancreatic beta-cells may induce a compensatory increase in responsiveness to glucose and a functional suppression of acetylcholine receptors. These data provide further support for the hypothesis that vagal input plays a functionally important role in the control of insulin secretion and maintenance of acetylcholine sensitivity.
Cardiac output of dogs exercising in the heat
Authors: Chapman L. W. , Baker M. A.
Published: December 2017

We measured cardiac output and central blood temperature in five large dogs (27 kg mean body wt) running at 7.5 km/h for 30 min at two work loads and at low and high ambient temperature (Ta). Each animal ran on a level treadmill (O2 cost about 4 times that of resting) at 25 and 35 degrees C Ta and at a 20% slope (O2 cost about 10 times that of resting) at 25 and 35 degrees C Ta. Cardiac output (CO) was the same at 15 and 30 min of exercise at both work loads and both TaS. CO was higher at 35 degrees C Ta at both work loads. Blood temperature rose 0.6 degrees C during exercise on the level treadmill at 25 degrees C and stabilized after the 15th min of exercise. On the level treadmill at 35 degrees C, blood temperature increased by 1.9 degrees C after 30 min. During 30 min of running at 20% slope, blood temperature increased by 3.2 degrees C at 25 degrees C and by 4.6 degrees C at 35 degrees C. At these work loads the dog is able to increase CO during exercise in the heat. This response is similar to that of humans doing moderate exercise in the heat but is in contrast to that of humans doing heavy exercise in the heat, in whom CO shows a drop or no change compared with cool conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
Brain stem tonic inhibition of thermoregulation in the rat
Authors: Amini-Sereshki L. , Zarrindast M. R.
Published: December 2017

It was shown, by selective levels of decerebration, that a drop in body temperature occurred in a midpontine rat due to impairment in thermoregulatory responses. Lowering the level of decerebration to the lower pons restored a coordinated thermoregulatory response. The response was inadequate to raise the core temperature to normal level, but it was nevertheless an integrated response of vasoconstriction, piloerection, and shivering and was appropriately turned off by warming the skin or core. In intact unanesthetized rats, microinjection of a local anesthetic in the pontine tegmentum resulted in thermoregulatory responses, such as curling of the body, piloerection, tremor in facial muscles, and shivering. Similar injections in the pontine tegmentum of the midpontine decerebrate rat also restored some heat gain responses, including shivering. These experiments suggest that in rats the heat gain responses are powerfully regulated by a tonic inhibitory mechanism located in the midbrain and upper pons that exerts a complete inhibitory effect on the thermoregulatory areas caudal to the midbrain in decerebrate rats and a partial inhibitory effect in intact animals. These experiments also confirm the previous observation in the cat of the presence of a facilitatory area(s) in lower levels of the central nervous system which is responsible for coordinated heat gain responses observed in low-level decerebrate animals. In addition, these experiments suggest that the brain stem thermoregulatory mechanisms are in fact functioning in intact unanesthetized animals.
Area postrema and adjacent nucleus of the solitary tract in water and sodium balance
Authors: Hyde T. M. , Miselis R. R.
Published: December 2017

Lesions of the area postrema (AP) and adjacent caudal medial nucleus of the solitary tract (cmNTS) cause significant changes in water and sodium balance. Lesioned rats display a permanent polydipsia, which in part is due to a primary polyuria. Water-to-food ratios are elevated chronically. Lesioned rats are unable to concentrate their urine as well as controls. In addition, lesioned rats overdrink in response to 24-h water deprivation. This lesion also causes a natriuresis and an overconsumption of 3% NaCl solution. These findings establish the AP-cmNTS as an important part of the neurocircuitry underlying water and sodium balance.
Dopaminergic efferent inhibition of carotid body chemoreceptors in chronically hypoxic cats
Authors: Lahiri S. , Smatresk N. , Pokorski M. , Barnard P. , Mokashi A. , McGregor K. H.
Published: December 2017

The observations that the dopamine concentration of the carotid body and efferent inhibition of carotid chemoreceptors are increased during chronic hypoxia led to the hypothesis that the inhibition was due to the effect of an increased dopamine release by the activity of carotid sinus nerve (CSN) efferents. The hypothesis was tested by measuring the effect of dopamine receptor blockade on efferent inhibition of carotid chemosensory responses to graded levels of arterial O2 partial pressure in chronically hypoxic and normoxic cats. Chronically hypoxic cats were prepared by exposing the cats to 10% O2 at sea level for 30–34 days. Carotid chemosensory activity was first measured from a slip of an otherwise intact CSN. The measurements were then repeated after sectioning the remaining nerve trunk. The effect of sectioning the CSN provided the measure of efferent inhibition. In each group of cats the effects of sectioning the CSN with and without dopamine receptor blockade by haloperidol were also studied. CSN section augmented the chemosensory responses in the chronically hypoxic cats. Haloperidol, a dopamine antagonist, augmented the responses further, indicating that a part of the endogenous dopamine effect was independent of the CSN efferents. After haloperidol treatment CSN section did not influence the chemosensory responses. This study confirmed that the efferent inhibition significantly increased in the chronically hypoxic cats and demonstrated that haloperidol blocked the efferent inhibition, suggesting that the mechanism of the augmented inhibition is dopaminergic.
Lymphatic, renal, and urinary kallikreins in the rat
Authors: Garcia R. , Thibault G. , Genest J.
Published: December 2017

In pentobarbital-anesthetized rats the lymphatic vessels next to the renal artery and the urinary bladder were cannulated and lymph and urine were collected for 3 h. The kidneys were then washed and removed. Four experimental groups were studied. Kallikrein was measured in lymph, urine, and kidney extracts by a direct radioimmunoassay. Immunoreactive renal and urinary kallikreins were higher in a Na-deficient group. No changes were brought about by furosemide administration or Na supplementation. A very low concentration of immunoreactive kallikrein was found in lymph, with no differences between the groups. In the same urine and kidney extract samples, both total (trypsin-activated) kallikrein and naturally active kallikrein were determined as kininogenase activity in the rat uterus bioassay. Both active and inactive kallikreins were found in kidney and urine, but most of the changes induced by a Na-deficient diet or furosemide administration were restricted to the active form. It is suggested that the lymphatic route in the kidney is probably not an important source of circulating immunoreactive glandular kallikrein.
Cardiovascular shunts and oxygen transport in lower vertebrates
Authors: Wood S. C.
Published: December 2017

O2 transport in animals with normal or abnormal cardiovascular shunts is analyzed using a two-compartment model. This analysis reveals that the O2 affinity of blood is a key factor determining the arterial, venous, and tissue O2 partial pressure (PO2) levels. Depending on the value of “critical” PO2, factors that decrease O2 affinity (e.g., increased temperature and reduced pH) should increase tissue PO2 and favor increased tissue oxygenation. Species comparisons suggest that O2 affinity is closely linked to critical PO2. In contrast to the model for environmental hypoxia, hypoxia due to shunting a right-shifted O2 dissociation curve is, at sea level, always adaptive. When hypoxia due to shunting is combined with external hypoxia, a decreasing O2 affinity causes increased blood and tissue PO2 values up to a “breaking point,” which varies with shunt fraction, inspired PO2, lung PCO2, and respiratory properties of the blood. External hypoxia would cause ectotherms with high preferred body temperatures (e.g., lizards) to have blood and tissue PO2 values beyond the breaking point. This led to the hypothesis, now confirmed in several species, that external hypoxia would result in a reduction of preferred body temperature.
Physiological regulations and compartments in cells
Authors: Adolph E. F.
Published: December 2017

Quantitative short-term regulation of a chemical component (glucose) in a single cell (hepatocyte of rat) is represented by an "equilibration diagram," which relates concentration of the regulated component or substrate (glucose) to loss and to gain of the same substrate (glucose). Loss and gain are separately active through specific enzymatic processes. Evidence indicates that some of these processes require the presence of subcellular compartments for their participation.
Effects of osmotic pressure, glucose, and temperature on neurons in preoptic tissue slices
Authors: Silva N. L. , Boulant J. A.
Published: December 2017

The preoptic area contains thermosensitive, osmosensitive, and glucosensitive neurons, which have been implicated in thermal, osmotic, and metabolite regulations, respectively. In this study, rat preoptic tissue slices are used to examine the specificity of these neurons by determining their individual firing rate responses to thermal, osmotic, and glucose stimuli. Of the neurons classified according to thermosensitivity, 35% were warm sensitive, 10% were cold sensitive, and 55% were temperature insensitive. Of these, 107 neurons were also tested for their responses to tissue slice perfusions of low-glucose and/or hyperosmotic media. These experimental perfusions affected one-third of the temperature-insensitive neurons and nearly half of the thermosensitive neurons and generally excited warm-sensitive neurons and inhibited cold-sensitive neurons. A lack of specificity was also observed between the groups of osmosensitive and glucosensitive neurons, since most of the responsive neurons were affected by both hyperosmotic and low-glucose media. Although these findings do not suggest a strong functional specificity for preoptic neurons, they do support previous studies that emphasize interactions between regulatory systems.
Sodium appetite during captopril blockade of endogenous angiotensin II formation
Authors: Moe K. E. , Weiss M. L. , Epstein A. N.
Published: December 2017

Angiotensin II and aldosterone increase in response to sodium deficiency to promote sodium and water conservation. In addition, they may act synergistically to arouse a sodium appetite. If so, then blockade of endogenous angiotensin should decrease the appetite. In experiments reported here, captopril (SQ 14,225) was given peripherally to rats to block conversion of angiotensin I to angiotensin II. It both enhanced and suppressed sodium depletion-induced sodium appetite. The appetite was suppressed when captopril was given in high doses, which block conversion centrally as well as peripherally. The same doses of captopril had no effect on urinary sodium excretion or on sodium appetite aroused by mineralocorticoid treatment. Low doses, which block conversion only in the periphery, enhanced salt intake elicited by depletion, and the enhancement was abolished by captopril given directly into the brain. Therefore the enhancement was probably due to a captopril-induced increase of peripheral angiotensin I, which gained access to the brain and was converted there to angiotensin II.
Effects of repeated isocaloric macronutrient loads on daily food intake of rats
Authors: Geliebter A. , Liang J. T. , Van Itallie T. B.
Published: December 2017

The effects of repeated administration of different macronutrient loads on spontaneous food intake and body weight of male Sprague-Dawley rats were studied. For 6 wk, eight groups of five rats each received two daily intragastric loads, 3.5 h apart, consisting of isocaloric amounts of one of the following: albumin, sucrose, cornstarch, corn oil, a mixture of the preceding four loads, butter, medium-chain triglyceride, or a noncaloric load of water. Spontaneous intakes of rat chow were measured 3.5 and 24 h after the first daily load. All the macronutrient loads depressed subsequent 3.5-h intakes more than the water load (P less than 0.01), and protein loads depressed 3.5-h intakes the most (P less than 0.01). The macronutrient loads also depressed 24-h intakes more than water loads (P less than 0.01) but did not differ among themselves. The mixture load depressed 3.5- and 24-h food intakes by an amount comparable with the average effects of its component loads. Neither body weight nor body fat as measured by the Lee index differed among the groups after 6 wk. The results indicate that fairly accurate long-term regulation of spontaneous energy intake occurs regardless of the type of macronutrient in the load.
Renin and ACTH responses to hypercapnia and hypoxia after chronic carotid chemodenervation
Authors: Raff H. , Shinsako J. , Dallman M. F.
Published: December 2017

We studied the effect of chronic carotid body denervation on renin (plasma renin activity, PRA), adrenocorticotropin (ACTH), blood pressure, and hematocrit responses to acute normocapnic (arterial CO2 partial pressure, PaCO2, 35 Torr) and hypercapnic (PaCO2, 65 Torr) hypoxia (arterial O2 partial pressure, PaO2, 31 Torr) in five anesthetized, artificially ventilated dogs. Animals were studied at least 3 days before and again at least 10 days after carotid body denervation (bilateral carotid sinus nerve resection). Increases in PRA during hypercapnic normoxia [21.8 +/- 6.4 ng angiotensin I (ANG I) X ml-1 X 3 h-1] and normocapnic hypoxia (13.3 +/- 4.2 ng ANG I X ml-1 X 3 h-1) were not attenuated by carotid body denervation. Increases in ACTH during normocapnic hypoxia (117 +/- 34 pg/ml) were attenuated but not eliminated by carotid body denervation; the increase in ACTH during hypercapnic hypoxia (295 +/- 93 pg/ml) was not attenuated by carotid body denervation. Both the blood pressure and hematocrit responses to normocapnic and hypercapnic hypoxia were attenuated by carotid body denervation. We concluded that 1) the renin response to hypercapnia and hypoxia is not a carotid chemoreflex, 2) the ACTH response to hypoxia is partially a carotid chemoreflex, and 3) blood pressure and hematocrit responses to hypoxia are primarily carotid chemoreflexes.
Effects of meclofenamate on the renin response to aortic constriction in the rat
Authors: Villarreal D. , Davis J. O. , Freeman R. H. , Sweet W. D. , Dietz J. R.
Published: December 2017

This study examines the role of the renal prostaglandin system in stimulus-secretion coupling for renal baroreceptor-dependent renin release in the anesthetized rat. Changes in plasma renin activity (PRA) secondary to suprarenal aortic constriction were evaluated in groups of rats with a single denervated nonfiltering kidney (DNFK) with and without pretreatment with meclofenamate. Suprarenal aortic constriction was adjusted to reduce renal perfusion pressure to either 100 or 50 mmHg. In addition, similar experiments were performed in rats with a single intact filtering kidney. Inhibition of prostaglandin synthesis with meclofenamate failed to block or attenuate the increase in PRA in response to the decrement in renal perfusion pressure after both severe and mild aortic constriction for both the DNFK and the intact-kidney groups. The adequacy of prostaglandin inhibition was demonstrated by complete blockade with meclofenamate of the marked hypotensive and hyperreninemic responses to sodium arachidonate. The results in the DNFK indicate that in the rat, renal prostaglandins do not function as obligatory mediators of the isolated renal baroreceptor mechanism for the control of renin release. Also the findings in the intact filtering kidney suggest that prostaglandins are not essential in the renin response of other intrarenal receptor mechanisms that also are stimulated by a reduction in renal perfusion pressure.
Mechanism of pressor effects by angiotensin in the nucleus tractus solitarius of rats
Authors: Casto R. , Phillips M. I.
Published: December 2017

We recently reported that microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius (NTS) results in an increase in mean arterial pressure (MAP) in urethan-anesthetized rats in a dose range of 50-500 ng. To investigate the mechanism of this response, hexamethonium (20 mg/kg iv) was used to inhibit sympathetic activation. There was a highly significant (P less than 0.001) reduction in the magnitude of the pressor response (4.7 +/- 1.1 mmHg) compared with preblockade ANG II (500 ng) responses (15.5 +/- 1.6 mmHg). A vasopressin antagonist and hypophysectomized rats were used to study the contribution of pituitary vasopressin. Injection of 500 ng ANG II in hypophysectomized rats produced a pressor response (14.8 +/- 3.2 mmHg) indistinguishable from that in intact controls (15.5 +/- 1.6 mmHg). Pretreatment with the vasopressin antagonist d(CH2)5Tyr(Me)AVP (1 microgram iv) in intact rats also had no effect on the magnitude of the pressor response (15.7 +/- 1.7 mmHg). Microinjection of ANG I and II produces an increase in arterial pressure. It is concluded that the angiotensin pressor response in the NTS is mediated by activation of descending sympathetic fibers and is not dependent on release of blood-borne pressor agents from the pituitary.
Sleep changes in long-term fasting geese in relation to lipid and protein metabolism
Authors: Dewasmes G. , Cohen-Adad F. , Koubi H. , Le Maho Y.
Published: December 2017

The proportion and the distribution over 24 h of the different arousal stages characterized in geese--wakefulness (W), drowsiness (D), and slow-wave (SWS) and paradoxical sleep (PS)--were studied in caged birds when fed and then fasted during about 40 days. In both the fed and fasted state, each arousal stage was distributed through numerous episodes of a short duration. The geese slept a little more during the night than during the day, a difference that was moderately emphasized during the fast. Fasting induced only a slight decrease in W. There were important changes in SWS and D in relation to the periods of fasting that were previously found to correspond to changes in lipid and protein utilization. When proteins were spared and lipids accounted for most of the energy expenditure, the fasted geese went more and more rapidly from W to SWS (proportion of D decreased from 33 to 13%/day) and slept for progressively longer periods (SWS increased from 23 to 49%/day). By contrast, when protein utilization rose, the general trend in sleep was a decrease in SWS and an increase in D. During the fast, changes in PS were in the same proportion as those in SWS. These reactions are examined for their implications in energy-saving and sleep mechanisms.
Vagal inhibition of respiratory-linked efferent activity in the carotid sinus nerve
Authors: Kostreva D. R. , Palotas G. L. , Kampine J. P.
Published: December 2017

The hypothesis tested in this study was that glossopharyngeal efferent nerve activity coursing through the carotid sinus nerve has a central origin. Efferent activity in the carotid sinus nerve exhibited a respiratory rhythm in spontaneously breathing, closed-chest, mongrel dogs anesthetized with pentobarbital sodium (30 mg/kg iv). Carotid sinus nerve activity was recorded from the intact or cut central end of the carotid sinus nerve. Diaphragm electromyogram (D-EMG), carotid sinus pressure, systemic blood pressure, and electrocardiogram were also recorded. Before vagotomy, small increases in carotid sinus efferent nerve activity (CSENA) synchronous with increases in the D-EMG were observed during spontaneous inspiration. Section of the contralateral cervical vagosympathetic trunk markedly potentiated the increases in CSENA. Bilateral superior cervical ganglionectomy or nodose ganglionectomy failed to alter the increases in CSENA. Section of the ipsilateral glossopharyngeal nerve near the skull abolished the CSENA. This study demonstrates that respiratory-modulated glossopharyngeal efferents course through the carotid sinus nerve to the carotid sinus or carotid body. These efferents may be part of a central respiratory regulatory mechanism that may rapidly alter the sensitivity of the carotid sinus baroreceptors and/or carotid body receptors on a breath-to-breath basis.
Effects of vasoactive intestinal peptide on canine prostatic contraction and secretion
Authors: Smith E. R. , Miller T. B. , Wilson M. M. , Appel M. C.
Published: December 2017

Vasoactive intestinal peptide (VIP)-like immunoreactivity was found in intrinsic autonomic ganglion cells and nerve fibers located at the surface and within the canine prostate. In anesthetized dogs, porcine VIP (100–3,000 ng/kg iv) decreased arterial pressure and increased heart rate but did not result in the release of fluid from the prostate, indicating that VIP neither contracted glandular smooth muscle to expel fluid nor provoked secretion. Intravenous infusions of VIP at 10, 50, 100, and/or 200 ng X kg-1 X min-1 produced dose-related decreases in arterial pressure, increases in heart rate, and potentiation of the secretory response to the intravenous administration of pilocarpine and to electrical stimulation of the hypogastric nerves at 2 but not at 20 Hz. VIP at 1 microgram/ml neither contracted isolated strips of prostate nor modified their contraction by norepinephrine. It is unlikely that VIP mediates hypogastric nerve-induced prostatic contraction or secretion in the dog, but VIP may serve as a neuromodulator of nerve-induced secretion.