bluuebunny/crossref_metadata_2025 huggingface dataset:
Ventricular function and morphology in chick embryo from stages 18 to 29
Authors: Clark E. B. , Hu N. , Dummett J. L. , Vandekieft G. K. , Olson C. , Tomanek R.
Published: December 2017

We evaluated wet and dry ventricular and embryo weights, hemodynamic parameters of ventricular function, and myocardial myocyte organelle composition in the developing chick embryo. Phasic and dP/dt ventricular pressure were measured with a servo null pressure system, and phasic, mean, and dV/dt dorsal aortic velocities were measured with a 20-MHz pulsed-Doppler meter. Ventricular and embryo weight increased geometrically with development, but at different rates, so that the ventricle-to-embryo weight ratio decreased from 0.02 to 0.001 just prior to hatching. Ventricular systolic and end-diastolic pressure increased from 1.31 +/- 0.05/0.33 +/- 0.03 mmHg at stage 18 to 3.45 +/- 0.10/0.82 +/- 0.03 mmHg at stage 29, while dP/dt increased from 23.04 +/- 1.32 to 79.55 +/- 3.69 mmHg/s over the same period. Dorsal aortic dV/dt increased from 878 +/- 17 to 2.076 +/- 65 mm/s2 from stage 18 to 29. Myocyte percent volume of myofibrils increased from 16.7 +/- 0.9% at stage 18 to 23.6 +/- 1.1% at stage 27 and diminished to 18.4 +/- 0.8% at stage 29. Mitochondrial percent myocyte volume remained constant at about 11%. These data define the parameters of normal ventricular function and morphology during embryonic development in the chick.
Preload reserve and mechanisms of afterload mismatch in normal conscious dog
Authors: Lee J. D. , Tajimi T. , Patritti J. , Ross J.
Published: December 2017

Preload reserve and mechanisms of afterload mismatch were examined in 10 normal conscious dogs. The left ventricular (LV) pressure, wall thickness, and external major and minor axis diameters (sonomicrometry) were measured during sinus rhythm, and beat-averaged pressure-volume loops were generated. With maximum angiotensin II infusion, LV end-diastolic volume (EDV) increased by 13 +/- 2% (SEM), LV peak pressure (LVSP) increased by 44 +/- 6%, and stroke volume decreased by 12 +/- 3% (P less than 0.01), demonstrating an apparent descending limb of LV performance. With volume load alone, EDV increased by 9 +/- 2% from control (P less than 0.01), and stroke volume increased by 13 +/- 2%; mean wall stress during ejection was not increased, and heart rate and end-systolic pressure-volume relations showed no changes. To test whether the descending limb of function was due to maximum use of preload reserve or to inadequate venous return, angiotensin infusion was repeated during volume load. The descending limb relating LVEDV to stroke volume was always shifted upward and to the right after volume load, and the stroke volume at a comparable wall stress was 12 +/- 3% higher than during control angiotensin infusion (P less than 0.01). During pressure loading plus volume loading, the maximum EDV increase was 16 +/- 2%, and assuming unchanged afterload and end-systolic volume, an average maximum stroke volume reserve of 31 +/- 4% is calculated. 1) We conclude that sizable preload and stroke volume reserves exist in the normal resting dog; and 2) we describe a mechanism for the descending limb of LV performance curves produced by pressure loading in the intact circulation, which is related to inadequate venous return.
Effect of canine cardiac nerves on heart rate, rhythm, and pacemaker location
Authors: Schuessler R. B. , Boineau J. P. , Wylds A. C. , Hill D. A. , Miller C. B. , Roeske W. R.
Published: December 2017

In open-chest dogs, right- and left-sided cardiac nerves were stimulated to determine their effect on heart rate, rhythm, and pacemaker location. The majority of the nerves produced chronotropic changes; 72% of the induced rhythms originated from within the atrial pacemaker complex. Ten percent of the stimulations produced an atrio-ventricular (AV) nodal rhythm; most of the time this was induced by the left posterior and anterior ansae and ventrolateral nerves. The dominance of a lateral right atrial pacemaker was observed in 8% of the stimulations; the dorsal cardiac and innominate nerves induced this rhythm the majority of the time. The general trend was for a cranial shift in the location of the pacemaker within the pacemaker complex with sympathetic stimulation and a caudal shift with parasympathetic stimulation. Exceptions to the pattern may be explained by the preferential effect of the nerves on the pacemakers in the right atrium. The study demonstrates, in the canine model, that in addition to the sinus and AV nodes, there is a system of pacemakers controlled by the cardiac nerves.
Reactive dilation and late-hyperemic constriction of epicardial coronary artery after short coronary occlusion
Authors: Yamamoto H. , Tomoike H. , Hisano K. , Inoue T. , Mohri M. , Nakamura M.
Published: December 2017

Coronary blood flow and epicardial coronary artery diameter were simultaneously measured by an electromagnetic or Doppler flow probe and a pair of ultrasonic crystals, respectively, during reactive hyperemia in conscious dogs. Reactive dilation appeared after the full appearance of reactive hyperemia and lasted for a period of 4-20 times the duration of the coronary occlusion. beta-Receptor blockade (propranolol, 1 mg/kg iv) attenuated both the reactive hyperemia in volume by 21-22% (P less than 0.01) and dilative responses of the epicardial coronary diameter by 27-28% (P less than 0.01), despite a nonsignificant attenuation of the resting or peak hyperemic coronary blood flow. When coronary blood flow was held constant during reperfusion, by an occluder distal to the ultrasonic crystals, the reactive dilation disappeared. A peculiar reactive constriction was noted when coronary occlusion was performed proximal to the site of the ultrasonic crystals. Appearance of this constriction was at 149 and 385 s after the release of 5 and 60 s of coronary occlusion, respectively. This late reactive constriction disappeared after pretreatment with alpha- (phentolamine, 1 mg/kg iv) and/or alpha- + beta-blockade, but not with beta-blockade alone, and it was not observed when the coronary diameter was measured proximal to the occluder. Thus reactive dilation of the epicardial coronary artery derives from an increase in coronary flow and is reduced by propranolol via a reduction in the hyperemic flow, suggesting a flow-dependent change in the diameter of the epicardial coronary artery. Reactive constriction is a local phenomenon following marked reduction in the coronary diameter and is abolished by alpha-adrenergic blockade with phentolamine.
Hydraulic conductivity of venous endothelium as measured with a volume clamp method
Authors: Vargas F. F. , Sanabria P. , Osorio H. , Schulz C.
Published: December 2017

Hydraulic conductivity (Lp) of cava vein endothelium was obtained with a new method that measures fluid flow at constant volume. Dogs were anesthetized with pentobarbital sodium. A vessel segment was removed, cannulated, and hung free from a force transducer calibrated to measure weight. Hydraulic pressure difference drove fluid across the vessel wall. This fluid was washed out from the vessel surface by external perfusion, causing a weight loss that was transmitted to a Grass polygraph through the force transducer. Shifting the polygraph balance caused a voltage output which was used to activate a controller operating a microsyringe pump. By injecting fluid into the vessel lumen, this servomechanism counteracted weight changes and kept volume and pressure at a fixed level. Recording the volume injected allowed continuous monitoring of fluid flow. This avoided the problems caused by frequent pressure and volume resetting in previous methods. Fluid flow was a linear function of the applied pressure (r = 0.87). Lp was 0.91 +/- 0.05 (SD) X 10-7 cm X s-1 X cmH2O-1. This value was very similar to those in continuous capillaries and arterial endothelium.
Zona glomerulosa cell responses to atrial natriuretic factor in genetically hypertensive rats
Authors: Racz K. , Kuchel O. , Buu N. T. , Gutkowska J. , Debinski W. , Cantin M. , Genest J.
Published: December 2017

We examined whether abnormalities in target cell responsiveness to atrial natriuretic factor (ANF), similar to those previously found in the kidney, could also be present in the zona glomerulosa cells of spontaneously hypertensive rats (SHR) and salt-sensitive Dahl rats (S rats). We found an attenuated aldosterone (Aldo) response to angiotensin II (ANG II) in zona glomerulosa cell suspensions isolated from hypertensive SHR compared with those from Wistar-Kyoto (WKY) rats, whereas cells derived from hypertensive S rats showed a significantly higher Aldo response to the maximum stimulatory dose of ANG II than those from salt-resistant Dahl rats (R rats). The maximum observed Aldo responses to ACTH stimulation were not different in SHR or S rats compared with their respective controls. ANF exerted a potent inhibitory action on both ANG II- and ACTH-stimulated secretions of glomerulosa cell suspensions, without any difference in its potency between hypertensive and control rats. The equipotent inhibitory action of ANF on the ANG II- and ACTH-stimulated secretion of Aldo in those cell suspensions suggests that the previously observed alterations in the target cell responsiveness to ANF do not exist in the adrenal zona glomerulosa cells of SHR and Dahl S rats.
Common functional origin for simple and complex responses of atrioventricular node in dogs
Authors: Billette J. , Gossard J. P. , Lepanto L. , Cartier R.
Published: December 2017

The possibility that variations in atrioventricular nodal conduction time observed during transient and steady-state nodal responses share common characteristics was examined in six anesthetized dogs. Atrioventricular conduction times (AV intervals) obtained during transient (incremental atrial pacing rates, short frequency steps, and Wenckebach cycles) and steady state (periodic premature stimulation performed at 5 basic rates) responses were plotted together against the corresponding preceding ventriculoatrial (VA) intervals on a graph for each dog. Despite their diversity, nodal responses consistently resulted in AV intervals that fell within a well-defined, relatively narrow, crescent-shaped zone on the graphs. AV interval variations were small in the long VA interval range and increased slightly but predictably as the VA intervals decreased. AV intervals of transient and steady state nodal responses overlapped markedly. These results show that AV intervals of transient and steady-state nodal responses vary within a given common functional domain despite the diversity of their sequential patterns and suggest that the AV node may be obeying the same set of conduction rules during these very distinct responses.
Regional spinal cord blood flow during sleep-waking cycle in rabbit
Authors: Lenzi P. , Cianci T. , Guidalotti P. L. , Franzini C.
Published: December 2017

Spinal cord blood flow (SCBF) was measured in rabbits during the sleep-waking cycle with the use of radioactive microspheres. The values obtained during wakefulness (W), synchronized sleep (SS), and desynchronized sleep (DS) were 18.1 +/- 2.1, 18.9 +/- 2.6, and 34.4 +/- 2.5 (SE) ml X min-1 X 100 g-1, respectively. Differences relative to SS were not significant in W and were significant at the 0.05 level in DS (modified t test and Bonferroni's method). The increase in blood flow during DS was due to a decrease in vascular resistance. The mechanism of the vasodilation during DS has yet to be identified.
Beat-by-beat modulation of AV conduction. I. Heart rate and respiratory influences
Authors: Warner M. R. , Loeb J. M.
Published: December 2017

We examined the integration of heart rate and neural influences at the atrioventricular (AV) node in conscious dogs. Animals were anesthetized and, under sterile conditions, instrumented to chronically record atrial and ventricular electrograms and blood pressure. In the conscious state, electrocardiogram (ECG), respiration, blood pressure, and electrograms were recorded on a beat-by-beat basis, and heart rate and AV interval were plotted graphically as a function of time. Resting animals exhibited both respiratory sinus arrhythmia and marked oscillations in AV conduction time associated with respiration. During inspiration AV interval was shortened, and during expiration AV interval was prolonged. To obviate the effect of cyclic changes in heart rate, atrial pacing was used to increase heart rate over a wide range both abruptly and linearly. Regardless of the pattern of heart rate change, AV interval oscillated at the respiratory frequency at pacing rates 10-100 beats/min above control. Higher levels of atrial pacing resulted in AV conduction patterns that were correlated with changes in blood pressure. Thus in the conscious dog variations in AV conduction time occur on a beat-by-beat basis in conjunction with respiration; oscillatory activity of AV conduction is not dependent on simultaneous changes in heart rate; and during atrial pacing, autonomic neural activity associated with respiration and blood pressure appears to dynamically modulate AV conduction with respiratory effects predominating at low heart rates and blood pressure effects at high heart rates.
Kinetic study of Na+-K+ pump in erythrocytes from essential hypertensive patients
Authors: Diez J. , Hannaert P. , Garay R. P.
Published: December 2017

The interaction of the Na+-K+ pump with internal Na+ was investigated in erythrocytes from 38 normotensive control subjects and 49 essential hypertensive patients. In six of the hypertensive patients, the Na+-K+ pump exhibited an apparent dissociation constant for internal Na+ (KNa) above an upper normal limit of 7 mmol/l cells. Four of these six hypertensives showed an increase in the maximal rate of ouabain-sensitive Na+ efflux (Vmax), above an upper normal limit of 11 mmol X l cells-1 X h-1. These abnormalities were stable in repeated determinations over 1–3 yr. A kinetic study of other erythrocyte Na+ transport pathways showed that 16 hypertensives had a low apparent affinity of the Na+-K+ cotransport system for internal Na+, 10 hypertensives exhibited increased Na+-Li+ countertransport fluxes, and 11 hypertensives had increased Na+ leak. None of these three abnormalities were observed in the six hypertensives with abnormal pump fluxes. We thus propose to denominate them as Pump (-) hypertensives. Interestingly, four Pump (-) hypertensives exhibited an increased maximal rate of outward Na+-K+ cotransport. Basal erythrocyte Na+ content of Pump (-) hypertensives was within normal range. This suggests that the increased maximal rates of the Na+-K+ pump and Na+-K+ cotransport system compensate the low pump affinity for internal Na+.
Effects of myocardial ischemia on regional function and stiffness in conscious dogs
Authors: Amano J. , Thomas J. X. , Lavallee M. , Mirsky I. , Glover D. , Manders W. T. , Randall W. C. , Vatner S. F.
Published: December 2017

The extent to which cardiac nerves influence responses of regional ventricular function to acute myocardial ischemia was investigated in conscious dogs with intact cardiac innervation (N) and dogs with chronic cardiac denervation (D). Following coronary artery occlusion (CAO) left ventricular (LV) end-diastolic pressure increased more (P less than 0.01) in D (18 +/- 3.2 mmHg) than in N dogs (3.4 +/- 0.7 mmHg), whereas heart rate increased more in N (32 +/- 4.8 beats/min) than in D dogs (16 +/- 3.0 beats/min). In nonischemic zones of D dogs there were greater increases, P less than 0.05, in end-diastolic segment length, systolic segment shortening, and velocity of shortening than in N dogs. In ischemic zones, significantly greater increases in end-diastolic segment length were also observed in the D group, but similar reductions in segmental shortening occurred in both N (-116 +/- 2.8%) and D (-108 +/- 5.2%) dogs. The time constant of isovolumic relaxation was not different in the two groups. However, in ischemic zones of N dogs myocardial stiffness constant (k) increased by 109 +/- 24 from 33 +/- 4.9 and end-diastolic stiffness (Eed) rose by 1527 +/- 310 from 253 +/- 34 mmHg, whereas k increased significantly less (P less than 0.05) in D dogs. Eed of ischemic zones also rose significantly less (P less than 0.05) in D dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
Left ventricular epicardial deformation in isolated arrested dog heart
Authors: McCulloch A. D. , Smaill B. H. , Hunter P. J.
Published: December 2017

We have developed a method for measuring epicardial deformation in the isolated arrested dog heart. A biplane video system was used to record the motion of discrete epicardial markers at midanterior sites (n = 4 hearts) and midposterior sites (n = 1) during quasi-static left ventricular (LV) filling. Experimental procedures, performed at room temperature, were completed within 20 min, and LV pressure-volume curves were repeatable and within the range of data presented by other authors. To obtain a complete description of local deformation, epicardial displacements derived from the video record were analyzed using homogeneous strain theory. Local epicardial strain was nonuniform; the mean ranges of midanterior major and minor extensions were 0–13.9 and 0-7.2%, respectively, for LV filling pressures of 0–20 mmHg. For the midanterior wall, the mean orientation of the major extension was 28–35 degrees below the LV circumference, compared with an orientation of approximately 62 degrees at the midposterior site. The results demonstrate the value of this preparation for studying passive ventricular mechanics and are not consistent with the predictions of mathematical models of ventricular stress and strain, in which it has been assumed that the material properties of the passive myocardium are isotropic.
Evidence that centrally released arginine vasopressin is involved in central pressor action of angiotensin II
Authors: Lon S. , Szczepanska-Sadowska E. , Szczypaczewska M.
Published: December 2017

Five series of experiments were performed on conscious trained dogs to find out whether intracranially released arginine vasopressin (AVP) is involved in mediation of central cardiovascular effects of angiotensin II (ANG II). The dogs were implanted with guide tubes leading to the third cerebral ventricle (ICV) and implanted with the intra-arterial catheters. Blood pressure and heart rate were continuously monitored during intracerebroventricular administration of 1) ANG II alone (250 ng), 2) AVP alone (0.01 ng/min during 10 min), 3) ANG II together with AVP, 4) AVP together with AVP V1-receptor antagonist 1(1-mercapto-4-methylcyclohexaneacetic acid)-8-AVP [MeCAAVP, V1ANT,100 ng/min], and 5) ANG II together with V1ANT. The results revealed that 1) ANG II and AVP applied separately elicited significant, long-lasting increases of blood pressure; 2) the maximum pressor effect after ANG II and AVP applied together did not differ from that after separate application of either of these peptides, but the duration of the pressor response was significantly shorter; 3) pretreatment with V1ANT effectively prevented blood pressure increases elicited by central administration of AVP and ANG II; and 4) after blockade of V1 receptors administration of AVP resulted in a significantly delayed decrease of blood pressure below baseline. The results strongly suggest that 1) centrally released AVP mediates the pressor effect of intracerebroventricularly applied ANG II by means of V1 receptors; 2) intracerebroventricularly applied ANG II and AVP interact to activate the mechanism involved in extinction of their pressor effect; and 3) blockade of central V1 receptors uncovers the hypotensive action of centrally applied AVP.
An analogue of cAMP mimics developmental change in neonatal rat ventricular myocyte sodium current kinetics
Authors: Lipka L. J. , Siegelbaum S. A. , Robinson R. B. , Berman M. F.
Published: December 2017

During development, the voltage dependence of single rat ventricular sodium channels shifts to more negative potentials. This shift is mimicked by coculture of neonatal myocytes with sympathetic neurons or by a 96-h exposure to 8-(4-chlorophenylthio) adenosine 3',5'-cyclic monophosphate (CPT-cAMP). The prolonged exposure to CPT-cAMP suggests that this is not a short-term modulatory effect on the sodium channel, but rather may reflect a trophic action. Here we examine the effect of CPT-cAMP using whole cell recording to investigate further the time period required for the effect. Sodium current was measured in a 50 mM NaCl bath solution at 20 +/- 1 degree C using the whole cell patch-clamp technique after exposure of myocytes to CPT-cAMP (0.25 mM) for 0,0.5,20, or 24 h. The relationship between the time constant of decay (tauh) of the sodium current and test voltage (V1) showed a shift to more hyperpolarizing voltages after exposure to CPT-cAMP for 24 h. In addition, the midpoint of the steady-state inactivation curve (V 1/2) was shifted from -75.8 +/- 1.1 mV (0-h exposure) to -83.3 +/- 1.6 mV (24-h exposure) (P < 0.05). Exposure for 0.5 h to CPT-cAMP did not alter the tauh or V 1/2 of the sodium current. However, exposure to CPT-cAMP for 20 h, followed by a 4-h washout period, produced an effect similar to that of the 24-h exposure. Thus the lack of effect of acute (0.5 h) exposure to CPT-cAMP and the persistence of the effect after washout of CPT-cAMP for 4 h suggest that adenosine 3',5'-cyclic monophosphate may play a trophic role in sodium channel development.
Cardiac transient outward potassium current: a pulse chemistry model of frequency-dependent properties
Authors: Liu L. , Krinsky V. I. , Grant A. O. , Starmer C. F.
Published: December 2017

Recent voltage-clamp studies of isolated myocytes have demonstrated widespread occurrence of a transient outward current (I(to)) carried by potassium ions. In the canine ventricle, this current is well developed in epicardial cells but not in endocardial cells. The resultant spatial dispersion of refractoriness is potentially proarrhythmic and may be amplified by channel blockade. The inactivation and recovery time constants of this channel are in excess of several hundred milliseconds, and consequently channel availability is frequency dependent at physiological stimulation rates. When the time constants associated with transitions between different channel conformations are rapid relative to drug binding kinetics, the interactions between drugs and an ion channel can be approximated by a sequence of first-order reactions, in which binding occurs in pulses in response to pulse train stimulation (pulse chemistry). When channel conformation transition time constants do not meet this constraint, analytical characterizations of the drug-channel interaction must then be modified to reflect the channel time-dependent properties. Here we report that the rate and steady-state amount of frequency-dependent inactivation of I(to) are consistent with a generalization of the channel blockade model: channel availability is reduced in a pulsatile exponential pattern as the stimulation frequency is increased, and the rate of reduction is a linear function of the pulse train depolarizing and recovery intervals. I(to) was reduced in the presence of quinidine. After accounting for the use-dependent availability of I(to) channels, we found little evidence of an additional use-dependent component of block after exposure to quinidine, suggesting that quinidine reacts with both open and closed I(to) channels as though the binding site is continuously accessible. The model provides a useful tool for assessing drug-channel interactions when the reaction cannot be continuously monitored.
Role of K+ in regulating hypoxic cerebral blood flow in the rat: effect of glibenclamide and ouabain
Authors: Reid J. M. , Paterson D. J.
Published: December 2017

We assessed the role of extracellular potassium ([K+]e) on the increase in cerebral blood flow (CBF) during hypoxia, and we tested whether it was affected by glibenclamide or ouabain. Cortical CBF was measured using the hydrogen clearance technique in enflurane-anesthetized rats, and local [K+]e was measured with K+ microelectrodes adjacent to the hydrogen electrode. Eucapnic hypoxia (arterial Po2 approximately 35-40 Torr) increased CBF twofold and caused a modest rise in [K+]e (from 2.9 +/- 0.2 to 3.7 +/- 0.2 mM; mean arterial blood pressure, ABP, 86 +/- 5 mmHg). If ABP fell < 70 mmHg during hypoxia, no increase in CBF was seen, whereas [K+]e increased to > 20 mM. Glibenclamide (10-100 microM intracortically) attenuated [K+]e and CBF during hypoxia (ABP approximately 75 mmHg, P < 0.01). Ouabain (20-1,000 microM) increased [K+]e; however, it did not remove the hypoxic-induced rise in [K+]e. We conclude that glibenclamide-sensitive potassium channels contribute to the accumulation of [K+]e during hypoxia, although an increase in CBF during hypoxia can occur without a marked rise in [K+]e. Furthermore, if ABP falls below the lower limit of autoregulation during hypoxia, there is no increase in CBF, yet there is a large increase in [K+]e.
Endotoxin pretreatment enhances portal venous contractile response to endothelin-1
Authors: Pannen B. H. , Bauer M. , Zhang J. X. , Robotham J. L. , Clemens M. G.
Published: December 2017

To test whether endotoxin pretreatment modulates the portal hemodynamic response to endothelin (ET)-1 and phenylephrine (PE), two potent vasoconstrictors in the portal circulation of the normal liver, rats received intraperitoneal injections of Escherichia coli lipopolysaccharide (LPS; 1 mg/kg body wt) or saline. Livers were isolated after 6 or 24 h and perfused with Krebs buffer containing 5% autologous erythrocytes. Analyses of portal pressure-flow (P-Q) relationships and epifluorescence video microscopy were performed before and after ET-1 (10(-9) M) or PE (10(-5) M) administration. LPS pretreatment increased total portal resistances (Rt), zero-flow pressures (PQ = 0), and linear regression slopes of P-Q relationships, and decreased the sinusoidal diameters (Ds) and sinusoidal volumetric flow (Qv). The response to ET-1 was enhanced 6 and 24 h after LPS administration, leading to greater increases in Rt, PQ = 0, and slope and more pronounced decreases in Dx, red blood cell velocity (VRBC), and Qv. In contrast, PE effects were similar (PQ = 0, slope, Ds) or even attenuated (Rt, VRBC, Qv) in livers from LPS-treated compared with control animals. Thus endotoxin pretreatment increased the portal contractile response to ET-1 but not to PE. This enhanced ET-1 response appeared to occur at sinusoidal and presinusoidal levels and may contribute to endotoxin-induced hepatic microcirculatory failure.
ON THE QUANTITATIVE DETERMINATION OF AMMONIA IN URINE
Authors: Shaffer Philip
Published: December 2017

Page 337, line 23, for gm. read mg.

Page 346, line 27, for 25 per cent, read 2.5 per cent.
THE PHYSIOLOGY OF THE MAMMALIAN AURICLE
Authors: Wiggers Carl J.
Published: December 2017

III. The Time Relations of Auricular Systole

I. THE EVENTS OF AURICULAR SYSTOLE AND THEIR RELATION TO VENTRICULAR SYSTOLE
Pancreatic secretion in vitro in "Cl–-free," "CO2-free," and low-Na+ environment
Authors: Rothman S. S. , Brooks F. P.
Published: December 2017

Pages 790–796: S. S. Rothman and F. P. Brooks. "ug/hr" should read "mg/hr" wherever present.
Intrarenal blood flow distribution in the desert quail following salt loading
Authors: Braun EJ
Published: December 2017

The total-kidney glomerular filtration rate (GFR) falls when birds are salt loaded. This fall in GFR is caused by glomerular intermittency. The nephrons that stop filtering are small, surface nephrons without loops of Henle. Larger nephrons with loops of Henle in the deeper regions of the kidney continue to filter during salt loading. Microfil casts were made of the renal microvasculature of the desert quail, Lophortyx gambelii, in an attempt to determine at what points intrarenal blood flow is regulated to cause glomerular intermittency. Casts of the renal vasculature were made in quail that were hydrated and in quail that were salt loaded. The results indicate that the small, surface nephrons stop filtering during salt loading because of a vasoconstriction at the level of the afferent arterioles of these nephrons. At the same time, blood flow is maintained to the large nephrons with loops of Henle. Reducing GFR at the expenses of excreting wastes can be viewed as a mechanism to conserve body water during periods of water deprivation.
Parathyroid hormone and renal excretion of phosphate and calcium in normal starlings
Authors: Clark NB , Braun EJ , Wideman RF
Published: December 2017

The renal handling of calcium, phosphate, sodium, and potassium was studied in normal and parathyroid extract (PTE)-injected starlings, Sturnus vulgaris. The birds were anesthetized with Equi-Thesin and infused intravenously with 2.5% mannitol containing [14C]inulin. Normal starlings actively reabsorb all four of these substances. After intravenous administration of 50 IU PTE/100 g body wt, the relative phosphate clearance (CPO4/CIn) as well as tubular transfer of phosphate (TPO4) increased significantly. Phosphate secretion occurred and usually persisted longer than 2 h. The relative calcium clearance also rose after PTE, but the TCa did not shift. This probably indicates that the tubular transport maximum (Tm) for calcium had been exceeded. The relative clearances of sodium and potassium also increased after PTE; however, only the rise in CNa/CIn was significantly different from the controls. The glomerular filtration rate (CIn) also increased significantly after PTE, but this effect was transient and cannot explain the longer lasting effects of PTE on excretion of phosphate, calcium, or sodium.
Subcellular calcium transport in failing hearts due to calcium deficiency and overload
Authors: Lee SL , Dhalla NS
Published: December 2017

Mitochondrial and heavy microsomal fractions were isolated from rat hearts perfused for different intervals with Ca2+-free medium, as well as from hearts reperfused with control medium after perfusion with Ca2+-free medium. Contractile failure due to intracellular calcium deficiency produced by perfusing the isolated rat hearts with Ca2+-free medium resulted in a marked decline of calcium binding and uptake activities of the mitochondrial fraction without any effect on the microsomal fraction. On the other hand, inability of the rat hearts to recover their contractile force due to intracellular calcium overload produced by reperfusion for 10 min with control medium after 5-20 min of perfusion with Ca2+-free medium was associated with decreased microsomal calcium-binding and uptake activities and increased mitochondrial calcium-binding and uptake activities. When the hearts perfused with Ca2+-free medium in the presence of low sodium (35 mM) for 5 min were reperfused with control medium, the contractile force recovered completely, and appreciable augmentation in mitochondrial calcium transport or depression in microsomal calcium transport as seen in conditions of intracellular calcium overload did not occur. These results suggest dramatic alterations in calcium-transporting properties of mitochondria and sarcoplasmic reticulum in hearts failing due to intracellular calcium deficiency and calcium overload, respectively.
Influence of dietary sodium on renin activity and arterial pressure during anesthesia
Authors: Fray JC , Siwek LG , Strull WM , Steller RN , Wilson JM
Published: December 2017

The effect of pentobarbital anesthesia on plasma renin activity (PRA) and mean arterial pressure (MAP) was studied in chronically catheterized dogs maintained on normal or low-sodium intake. Within 1 min of administration, pentobarbital caused a rapid fall in MAP which was followed by a restoration of MAP toward control within 5 min. Thirty minutes after induction of anesthesia, PRA was unchanged in sodium-replete dogs and elevated two-fold in sodium-depleted dogs. MAP was significantly lowered (20 mmHg) in normal salt dogs and only slightly decreased in low-salt dogs 30 min after pentobarbital. MAP returned to preanesthetic control value in dogs given converting enzyme inhibitor before anesthesia. Surgical stress or cutaneous electrical stimulation causey hexamethonium. These results indicate that change in PRA and MAP of pentobarbital-anesthetized dogs is significantly influenced by the sodium intake of the animal and by the degree of surgical stress.
Oxygen-induced changes in pulmonary superoxide dismutase assayed by antibody titrations
Authors: Crapo JD , McCord JM
Published: December 2017

Previous studies have demonstrated a 50% increase in pulmonary superoxide dismutase (SOD) activity in oxygen-adapted rats and have suggested that SOD plays a significant role in the development of "tolerance". To further study these events, the cuprozinc SOD was purified from rat liver and found to be similar to previously purified cuprozinc superoxide dismutases. A rabbit antisera to rat cuprozinc SOD was produced and used to perform antibody titrations of SOD in the lungs of rats exposed to 85% O2 for 5 days. The absolute amount of cuprozinc SOD increased 41% by antibody titration which accounted for most, if not all, of the 48% increase demonstrated in total SOD activity. Spectrophotometric assays at pH 7.8 and 10.0 of pure rat cuprozinc SOD and crude lung homogenates suggest that there is also a manganese SOD present, but the role of that SOD in the development of oxygen tolerance has not been established.
Effects of increased O2 and CO2 on acid secretion by dogfish gastric mucosa in vitro
Authors: Kidder GW
Published: December 2017

The gastric mucosa of the dogfish (Squalus acanthias), as usually prepared for in vitro chambered experiments, shows a secretory rate (JH) of about 2 mueq/cm2-h, but a potential difference (PD) of zero. Raising PCO2 from 0.05 to 0.1 atm increases JH by 40% and causes the development of a PD of about 2 mV, mucosal surface positive. Increasing PO2 from 0.9 to 1.9 atm in a hyperbaric chamber (at constant PCO2 = 0.1 atm) doubles JH and increases PD to 5 mV. Transepithelial resistance falls by 20% at high PO2. It appears that the dogfish gastric mucosa, like that of the frog, is rate limited by CO2 diffusion into the tissue from the usual 5% mixture and is also rate limited by the usual O2 levels (unlike the frog), presumably due to its thicker structure and higher O2 consumption. The mucosal-positive PD, which is reversed from all other mucosae studied, is readily explained by separate electrogenic H+ and Cl- pumps, but less readily by schemes embodying a neutral HCl pump. It is not yet known whether the hyperbaric conditions are sufficient to ensure O2 sufficiency.
Motor innervation of the toad iris (Bufo marinus)
Authors: Morris JL
Published: December 2017

The sphincter pupillae muscle cells in the iris of Bufo marinus contract autonomously in response to bright light, causing a rapid constriction of the pupil. A strong sympathetic beta-adrenergic inhibition of the sphincter pupillae is apparent in this species. The inhibitory fibers can originate in the second, third, or fourth ventral spinal roots. No strong, consistent excitatory innervation of the toad iris was detected, even by transmural stimulation of the isolated iris. Pupilloconstriction occasionally resulted from stimulation of the 3rd or 5th cranial nerves, but the effect was small (10-20% of the magnitude of the light response) and inconsistent. It therefore appears that the toad must regulate pupillary diameter by balancing myogenic contraction, in direct response to light, against neurogenic (sympathetic) relaxation of the sphincter pupillae.
Penile pressures and muscle activity associated with erection and ejaculation in the dog
Authors: Purohit RC , Beckett SD
Published: December 2017

A needle-tipped polyvinyl catheter or subminiature pressure transducer was implanted in the corpus cavernosum penis (CCP), corpus spongiosum penis (CSP), or bulbus glandis to determine the pressure during coitus in 42 dogs. Silver ring electrodes were implanted in the ischiocavernosus (IC) and bulbospongiosus (BS) muscles to monitor the electromyographic (EMG) activity of these muscles. The CCP pressure increased from 26 mmHg in the quiescent state to 161 mmHg at mild erection of the penis in the presence of a receptive female. During the intromission phase of coitus, the mean peak CCP pressure was 5,296 mmHg in the dogs with implanted catheters and 7,434 mmHg in the dogs with implanted transducers. The CCP pressure peaks during intromission were more in phase with the contractile activity of the IC muscles than with the BS muscles. Anesthesia of IC muscles with lidocaine significantly reduced the CCP pressures and the dogs with low pressures were unable to copulate because of insufficient erection for intromission, which indicated that the IC muscles were the source of energy for the high CCP pressure. The mean peak CSP and bulbus glandis pressures during the intromission phase of coitus were 579 and 1280 mmHg, respectively. The contractile activity of the BS muscles was in phase with the CSP pressure peaks. Anesthesia of BS muscles with lidocaine reduced the peak CSP and bulbus glandis pressures during attempted coitus. The mean rupture pressure of the CCP was 86,615 mmHg.
Age-related changes in Na+ excretion in saline-loaded spontaneously hypertensive rats
Authors: Mullins MM , Banks RO
Published: December 2017

The ability of 6- to 7-, 12- to 13-, and 16- to 17-wk-old spontaneously hypertensive rats (SHR) to excrete an acutely administered, isotonic saline load (equivalent to 4.5% body wt) was evaluated. Female SHR from two different colonies were studied. Age-matched female Wistar (W) and Wistar-Kyoto (WKY) rats served as controls. At age 6 wk, the fraction of administered Na+ load excreted by either SHR colony after 60 min was significantly lower than in the Wistar rats but not significank, one colony of SHR excreted significantly more sodium after 60 min than the other rats. Glomerular filtration rate during control periods was positively correlated with age in one SHR colony; no age-related changes were observed in glomerular function in the other groups. These data 1) suggest that WKY rats are more appropriate than the Wistar rats as controls for renal function in the SHR, 2) demonstrate that the ability of the SHR to excrete an acutely administered sodium load is equal to or greater than normotensive WKY controls, and 3) demonstrate that with respect to renal function parameters, the SHR is not a homogenous strain.
Kallikreinlike activity in perfusates and urine of isolated rat kidneys
Authors: Roblero J , Croxatto H , Garcia R , Corthorn J , De Vito E
Published: December 2017

In the perfusate and the urine produced during perfusion of isolated rat kidneys a kallikreinlike enzyme similar to that found in the kidney was detectable by bioassay 15-25 min after the beginning of the perfusion. The source of the kallikrein activity was the kidney itself, since before the perfusion was started the blood remaining in the kidneys was washed out and the perfusion medium was free of kallikrein and its precursors and substrates. The kallikreinlike activity of the perfusate was characterized by a) an oxytocic effect on isolated rat uterus, b) a kininogenase activity on kininogen II, c) an esterase activity on N-benozyl-L-arginine ethyl ester, and d) a hypotensive effect on anethetized rats. These properties were inhibited by diisopropyl activity in the perfused kidney was lower than that in the nonperfused organ, but the total amount of kallikrein activity released to the excreted urine and the perfusate was significantly greater than the corresponding activity that disappeared in the kidney. This result is in keeping with the concept that the renal tissue is able to synthesize kallikrein.
Hepatic cell integrity in hypodynamic states
Authors: Carlson RP , Lefer AM
Published: December 2017

Changes in liver integrity were studied in isolated perfused cat livers during simulated shock conditions (i.e., combined hypoxia, acidosis, and ischemia) or under the influence of each hypodynamic state separately. The combined hypodynamic stimuli depressed carbon clearance 51% and significantly elevated lactic acid dehydrogenase (LDH) and cathepsin D activities in the perfusate. The perfused liver was more seriously affected by hypoxia than by acidosis or ischemia alone. Reticuloendothelial clearance was depressed 20% and 25% in acidosis and hypoxia, respectively. Hypoxia also induced a 3-fold increase in cathepsin D and a 13-fold increase in LDH activities in the perfusate. After 150 min of hypoxia or ischemia, free cathepsin D in liver tissue increased significantly. The impairment of liver cell integrity (i.e., of Kupffer and parenchymal cells) occurred between 60 and 90 min during simulated shock conditions, indicating that the liver is stable for 60 min when it is exposed to hypoperfusion. The perfused liver is sensitive to local stimuli that predominate in circulatory shock, particularly hypoxia. These stimuli promote the release of lysosomal and cytoplasmic enzymes as well as depress phagocytosis by the reticuloendothelial system, phenomena that exacerbate the shock state.
Inhibitory effects of catecholamines in canine cardiac Purkinje fibers
Authors: Posner P , Farrar EL , Lambert CR
Published: December 2017

The effect of catecholamines over a wide range of concentrations was studied on 42K uptake and efflux, as well as on spontaneous rate in canine cardiac Purkinje fibers. Low levels of catecholamines (less than 10(-10) M epinephrine; less than 10(-9) M norepinephrine) decreased automaticity. This negative chronotropic effect was blocked by phentolamine and mimicked by phenylephrine. These low levels of epinephrine and norepinephrine also inhibited 42K uptake by Purkinje fibers but had no effect on 42K efflux. The inhibition of 42K uptake was blocked by phentolamine and verapamil and mimicked by phenylephrine. The data indicate an alpha-receptor-mediated negative response of rate and 42K uptake to low levels of catecholamine. The end result is discussed in terms of a competitive increase in the influx of Ca2+ rather than Na+ and an indirect inhibition of the Na+-K+ pump.
Calcium-dependent resistance to stretch and stress relaxation in resting smooth muscles
Authors: Siegman MJ , Butler TM , Mooers SU , Davies RE
Published: December 2017

Mechanical responses to stretch and length-tension relations were examined in rabbit taenia coli, mesenteric vein, aorta, and myometrium and in guinea pig taenia coli made atonic by incubation in Krebs-bicarbonate solution at 20-22 degrees C. When stretched 10% of the length at which maximum active tension is observed (Lo) in 0.5 s, the muscles showed a transient large force (resistance to stretch) that decayed to a new constant level within minutes (stress relaxation). The resistance to stretch decreased markedly in Ca2+-free [disodium ethylene glycolbis-(beta-aminoethylether)-N,N-tetraacetic acid (EGTA)] Krebs but was restored in normal Krebs solution. Calcium removal did not affect the passive length-tension curve. The absence of Ca2+ did not change the steady-state force maintained by the muscle; thus stretch resistance was not due to tone. Blockade of Ca2+ influx associated with electrical activity with 5-[3,4-dimethoxyphenethyl)methylamino]-2-(3,4,5-trimethoxyphenyl-2-isoprop ylvaleronitrile (D-600) and of Ca2+ release from intracellular sites with thymol (1 mM) completely blocked contraction but did not alter the responses to stretch, thus dissociating the responses to stretch from these processes and tension development. The Ca2+-dependent stress relaxation showed a dependence on muscle length similar to that for active tension development. Except at long muscle lengths, where connective tissue markedly affects length-tension relations, most of the "viscoelasticity" of these smooth muscles is dependent on calcium and may be largely due to the straining of crossbridges that are attached, but not generating a net force, in the resting state.
Pentose cycle activity of the isolated perfused rat lung
Authors: Bassett DJ , Fisher AB
Published: December 2017

Pentose cycle activity was estimated in isolated rat lungs under varying conditions of glucose oxidation. Lungs were perfused for 100-120 min with a Krebs-Ringer-bicarbonate buffer, pH 7.4, containing 1-14C- or 6-14C-labeled glucose and ventilated with 95% O2:5% CO2. Based on 14C specific yields in either 14CO2 or perfusate lactate plus pyruvate, pentose cycle flux in control lungs was 5.3 mumol of glucose per hour per gram dry weight (11-12% of glucose utilization). Pentose cycle activity was unaltered by perfusion with 0.8 mM 2,4-dinitrophenol. Perfusion with phenazine methosulfate, an artificial hydrogen acceptor, resulations of the pentose cycle based on 14C yields in tissue lipids (both the fatty acid and deacylated fractions) gave values 2-3 times higher than measurements based on 14CO2. This study indicates that pentose cycle activity in the lung accounts for a significant fraction of glucose utilization and this pathway readily responds to metabolic perturbation.
Effects of ions on amylase release by dissociated pancreatic acinar cells
Authors: Williams JA , Cary P , Moffat B
Published: December 2017

Dissociated acinar cells prepared from guinea pig and mouse pancreas were intact on the basis of structure, ion content, and their ability to increase release of amylase in response to bethanechol and the calcium ionophore A23187. Guinea pig but not mouse acinar cells increased amylase release in response to caerulein. An increase in the concentration of K+ in the medium, which increases amylase release from whole pancreas, did not increase release. The effect of varying the ionic content of the medium on basal and stimulated amylase release was studied. Bethanechol and caerulein were still able to stimulate amylase release when Ca2+ was omitted from the medium, whereas stimulation induced by A23187 was abolished. Elevation of the concentration of Mg2+ did not affect basal or stimulated amylase release. Removal of Na+ from the medium initially had no effect on amylase release although bethanechol-stimulated release by mouse cells was inion of the HCO3- or Cl- content of the medium did not affect cholinergic stimulation of secretion. It is concluded that stimulated amylase release by isolated acinar cells is relatively independent of the ionic constituency of the bathing medium.
Effects of angiotensin, vasopressin, and methoxamine on cardiac function and blood flow distribution in conscious dogs
Authors: Heyndrickx GR , Boettcher DH , Vatner SF
Published: December 2017

A comparison was made of the effects of vasopressin (ADH), methoxamine (MX), and angiotensin II (AN) on coronary and left ventricular dynamics, cardiac output, and regional blood flow distribution in intact, consci9us dogs. At an equal percent pressure elevation, ADH reduced cardiac output and cardiac rate the most, while AN had the least effect. After denervation of arterial baroreceptors, ADH still reduced heart rate, while AN increased it, suggesting nonbaroreceptor negative and positive chronotropic effects, respectively. A differential pattern on peak dP/dt was also observed, with ACH causing a greater reduction than MX while AN did not decrease dP/dt. With heart rate held constant, AN did not reduce dP/dt, suggesting a direct positive inotropic effect since dP/dt should have fallen slightly due to reflex mechanisms, as was observed with MX and ADH. ADH induced the greatest increase in coronary resistance (140%), while the least (46%) was observed with AN, which could be explained, in part, by the differential effects observed on cardiac rate and contractility. The greatest increase in resistance in the iliac bed occurred with ADH (30%), and the least with AN (34%). Conversely, the greatest constriction in the renal bed occurred with AN (95%), and lesser amounts were observed with ADH (36%) and MX (35%). Thus ADH, MX, and AN exert potent yet differential vasoconstricting actions on peripheral beds. In addition, while all three agents elicited coronary vasoconstriction, the differential effects on coronary vascular resistance appeared to be due predominantly to a difference in chronotropic and inotropic actions.