bluuebunny/crossref_metadata_2025 huggingface dataset:
Androgen-mediated sex differences of cardiovascular responses in rats
Authors: Baker P. J. , Ramey E. R. , Ramwell P. W.
Published: December 2017

Sex differences in the systemic depressor response to arachidonic acid (50 or 150 microgram/kg iv) were observed in intact and castrated anesthetized Sprague-Dawley rats. The rank order of responsiveness was: castrate males, castrate females, females, males; all four groups were significantly different (P less than 0.05) at the higher dose. Castrated males pretreated with testosterone (1 mg/kg sc) 5 or 7 days previously gave a response at the higher arachidonate dose levels that was of the same order as that obtained with intact males. Similar treatment of castrate males with androgen potentiated (P less than 0.05) the vasopressor action of norepinephrine (0.25 microgram/kg) on day 7 after the testosterone pretreatment. In contrast, treatment with depot estradiol (100 microgram/kg sc) in castrate males produced no significant change in the response to either of the vasoactive compounds on both days 5 and 7 after pretreatment. These data suggest that testosterone may be a significant factor in the development of sex differences in the cardiovascular systems of rats.
Alteration in heart rate response to hemorrhage in conscious dogs with volume overload
Authors: LeWinter M. M. , Karliner J. S. , Covell J. W.
Published: December 2017

The heart rate response to hemorrhage was studied in conscious dogs before and up to 2 mo after the establishment of volume overload due to systemic arteriovenous (a-v) fistulas. Before a-v fistula, heart rate increased markedly during hemorrhage. When hemorrhage was preceded by dextran infusion, bleeding resulted in a gradual reduction in heart rate. The a-v fistula caused marked increases in resting heart rate, central venous pressure, pulse pressure, and blood volume. During hemorrhage, heart rate initially remained constant, but then declined abruptly from the resting value of 121 +/- 3.7 beats/min to a nadir of 89 +/- 6.5 beats/min (P less than 0.01). Although mean arterial pressure decreased markedly, there was no significant change in pulse pressure, and central venous pressure tended to stabilize with the heart rate decline. The abrupt heart rate decline was prevented by atropine but unaltered by propranolol. The response was observed as early as 5 days after a-v fistula. We conclude that an alteration in the heart rate response to hemorrhage appears early during volume overload. This alteration appears to be reflex in nature and to be mediated by the parasympathetic nervous system.
Central interaction between the baroreceptor reflexes from the carotid sinus and aortic arch
Authors: Kendrick J. E. , Matson G. L. , Lalley P. M.
Published: December 2017

The cardiovascular response to combined stimulation of the aortic nerve (AN) and carotid sinus nerve (CSN) with trains of electrical stimuli was studied in dogs under morphine-chloralose anesthesia. Combined stimulation of both nerves ipsilaterally resulted in systemic arterial depressor responses and cardiac slowing that were 59% and 77% greater (P less than 0.05) than the respective sum of the responses to separate stimulation of these nerves. The depressor response to combined stimulation of these nerves contralaterally was not different (P greater than 0.05) from the sum of the separate responses. However, cardiac slowing to contralateral stimulation of the nerves remained 43% greater (P less than 0.05) than the sum of the individual responses. The results suggest that an interaction between the aortic and carotid baroreceptor reflexes occurs centrally, which causes a greater than additive effect on the autonomic output. The degree of interaction between the reflexes did not change as the delay between the stimulus trains was varied over an interval of 0 and 100 ms. At intervals greater than 100 ms the reflex responses were additive.
Pressor response buffering by beta-adrenergic and cholinergic vasodilation in tranquilized dogs
Authors: Evans J. M. , Knapp C. F. , Lowery T. R.
Published: December 2017

Buffering of alpha-receptor-mediated pressor responses by beta-adrenergic or cholinergic vasodilation in tranquilized, chronically instrumented gos was investigated. Increases in aortic pressure were produced in the same animal by intravenous injections of phenylephrine in the control state and in three successive experimental states by 1) pacing the heart to remove the reflex capability to lower heart rate, 2) pacing the heart and beta-blockade to remove beta-adrenergic vascular buffering, and 3) beta-blockade plus atropine to also remove cholinergic vascular buffering. The pressor response in each experimental state was greater than that in the state preceding it. With the combined beta-adrenergic and cholinergic blockade, the pressor response to an alpha-receptor stimulation was three times greater than that of the control state. From an analysis of the components of the pressor response, cardiac output, and peripheral resistance, it is suggested that normal buffering of an alpha-mediated pressor response may include beta-adrenergic and cholinergic vascular dilation in addition to a decrease in heart rate.
Hypophysectomy and saralasin on mesenteric vasoconstrictor response to vasopressin
Authors: Pang C. C. , Wilcox W. C. , McNeill J. R.
Published: December 2017

The dose-response relationship of the mesenteric resistance vessels to vasopressin was studied in anesthetized laparotomized cats before and after hypophysectomy and again during the plateau phase of the response to a prolonged infusion of [Sar1-Ala8] angiotensin II (saralasin), a competitive antagonist of angiotensin II. Hypophysectomy and saralasin each caused an increase in superior mesenteric arterial conductance. Before hypophysectomy infusion of 0.5 mU/(min.kg) of vasopressin caused mesenteric conductance to decrease from 0.168 to 0.156 ml/(min.kg.mmHg), a change of only 0.012 units. After hypophysectomy, the same dose reduced conductance from 0.227 to 0.179 mU/(min.kg.mmHg), a change of 0.048 units. During the plateau phase of the response to saralasin, 0.5 mU/(min.kg) of vasopressin reduced conductance from 0.281 to 0.201 ml/(min.kg.mmHg), a change of 0.079 units. Hypophysectomy and saralasin had little effect on the mesenteric vasoconstrictor response to high doses of vasopressin (2.0-10 mU/(min.kg). The ineffectiveness of low doses of vasopressin on the mesenteric resistance vessels of the intact anesthetized, surgically stressed animal may be due in part to the already constricted state of the bed caused by endogenous vasopressin and angiotensin and in part due to an opposing vasodilator influence, the reflex withdrawal of the vasoconstrictor effect of endogenous vasopressin.
Distribution of cardiac output during induced isometric exercise in dogs
Authors: Crayton S. C. , Aung-Din R. , Fixler D. E. , Mitchell J. H.
Published: December 2017

Studies were designed to characterize the distribution of cardiac output during induced isometric exercise in anesthetized dogs. The response to isometric exercise involved significant increases in heart rate (+12 +/- 3%(SE)), mean arterial pressure (+13 +/- 2%), cardiac output (+26 +/- 8%), and respiratory minute volume (+75 +/- 26%); total peripheral resistance did not change significantly. Significant changes in blood flow were observed during isometric exercise in kidneys (-18 +/- 6%) and contracting limb muscles (+453 +/- 154%). Flow to liver (hepatic artery), spleen, brain, and myocardium remained near control values. Section of spinal dorsal roots L6-L7 abolished the responses to isometric exercise except for the increase in flow to exercising limb muscles. Alpha-adrenergic receptor blockade abolished the decrease in renal blood flow during isometric exercise; however, the increase in flow to exercising limb muscles was not affected by either alpha- or beta-adrenergic blockade.
External mechanical work from relaxing ventricle
Authors: Suga H.
Published: December 2017

The possibility has been proposed earlier that the specific pressure-volume (P-V) area bounded by the left ventricular end-systolic and end-diastolic P-V curves and the isovolumic relaxation part of the P-V loop represents mechanical potential energy that has been built during systole and is stored at end systole in the wall of the ventricle. In the present study on canine left ventricles, as much as 70% of the P-V area was actually converted into external mechanical work when ventricular volume was allowed to decrease at an appropriate speed (about 55 ml/s in 70 g left ventricle) during relaxation. Less external work was extracted from the same P-V area when the speed of volume reduction was either higher or lower than that speed. These results indicate that the P-V area is equivalent to a form of potential energy, which is wasted with isovolumic relaxation but most of which is convertible to external mechanical work if the ventricle is allowed to eject against an appropriately decreasing afterload during relaxation.
Prostaglandin E release from dog skeletal muscle during restricted flow exercise
Authors: Young E. W. , Sparks H. V.
Published: December 2017

Prostaglandin E (PGE) release from the anterior calf muscles of anesthetized dogs was measured during and following exercise. Blood flow was held constant at 15.5 +/- 1.6 (SEM) ml.min-1. 100 g-1 and the muscles were stimulated for 20 min at a frequency of 4 Hz. PGE release dropped from a resting level of 11.4 +/- 3.8 ng.min-1.100 g-1 to 6.5 +/- 2.0 ng.min-1.100 g-1 during exercise (P less than 0.05). Following exercise, PGE release slowly returned to and eventually exceeded the resting level over a 60-min period. Return of vascular resistance to control was even more prolonged. Indomethacin (5 mg/kg) caused 1) an increase in resting resistance (40%), 2) a drop in PGE release (48% at rest), and 3) a more rapid return of vascular resistance to control following exercise. PGE release does not appear to contribute to the vasodilation during exercise, but can account for the portion of vascular resistance recovery not blocked by indomethacin. The remaining prolonged vasodilation could be explained by another as yet unidentified vasodilator(s). This preparation exhibits tonic prostaglandin release that causes a vasodilation at rest.
Low-frequency viscoelastic properties of canine femoral artery in vivo
Authors: Sipkema P.
Published: December 2017

Mechanical properties of the canine femoral artery in vivo are measured as a function of frequency (0.0025--0.1 Hz) and as a function of mean pressure (10--16 kPa). Sinusoidal pressure variations are generated with a servo-controlled occluder system. The absolute value of the Young's modulus increases with mean pressure (E = 0.63 X 10(5) exp(0.211P)-N.m-2) at 0.05 Hz; where P is pressure. At heart rate frequencies (average value 2.22 Hz) this relation is: E = 1.25 X 10(5) exp(0.175P) N.m-2. The phase angle of the Young's modulus is independent of pressure at both frequencies. At 0.05 Hz we found: phi = 0.189 - 0.00788 P radians and at 2.22 Hz: phi = 0.0723 + 0.000428 P. The slope of both lines is not significantly different from zero slope (alpha = 0.05). Frequency dependence is studied at a constant pressure level (Pr, average value 14.3 kPa) just below the animals' mean pressure levels (average value 15.9 kPa). The frequency behavior of the elastic modulus is fitted with a function with two poles and two zeros (poles at 0.003 and 0.038 Hz; zeros at 0.0022 and 0.03 Hz).
Noncholinergic vasodilator innervation in the feet of ducks
Authors: McGregor D. D.
Published: December 2017

Vasomotor responses to nerve stimulation were studied in the feet of Pekin ducks (Anas platyrhynchos) and domestic chickens (Gallus domesticus). The birds were killed and the feet isolated and perfused with a Krebs solution. Electrical stimulation of pedal nerves gave vasoconstrictor responses that were abolished by injecting guanethidine and by treating birds with reserpine. After guanethidine or reserpine, nerve stimulation resulted only in vasodilatation, which was unaffected by hexamethonium. Vasodilator responses to nerve stimulation were not blocked by hyoscine or atropine, which blocked responses to acetylcholine, nor by metiamide, which blocked vasodilatation in response to histamine. Responses to nerve stimulation were blocked by tetrodotoxin. Isoprenaline produced vasoconstriction that was blocked by phentolamine and also weak vasodilator responses that were antagonized by propranolol. It is concluded that the vasoconstrictor innervation is adrenergic. The identy of the vasodilator neurotransmitter is unknown; it is apparently not acetylcholine, a catecholamine, or histamine.
Hemodynamic and plasma catecholamine responses to hyperthermic cancer therapy in humans
Authors: Kim Y. D. , Lake C. R. , Lees D. E. , Schuette W. H. , Bull J. M. , Weise V. , Kopin I. J.
Published: December 2017

Cancer patients, treated with hyperthermia (to 41.5 degrees C) under thiopental and fentanyl anesthesia, had smaller increases in heart rate and cardiac index and lesser decreases in mean arterial pressure than those reported in normal volunteers. At basal body temperature anesthesia did not alter catecholamine levels. Increasing body temperature to 39.5 degrees C and 41.5 degrees C resulted in parallel increases in heart rate and cardiac index that were directly related to the increases in plasma norepinephrine levels. At basal temperature cutaneous venous plasma norepinephrine levels exceeded those of arterial; mixed-venous plasma levels were intermediate. At 39.5 degrees C and 41.5 degrees C there were sequential increases in plasma norepinephrine. The increases in mixed-venous and arterial norepinephrine were significantly greater than in cutaneous venous blood. The differential increases in norepinephrine levels in cutaneous venous, mixed-venous, and arterial blood indicate that during hyperthermia sympathetic nerve activity in skin is decreased while that in other areas is increased, suggesting that alterations in sympathetic activity modulate the hemodynamic changes that attend hyperthermia in man.
Preservation of left ventricular function by insulin in experimental catecholamine cardiomyopathy
Authors: Werner J. C. , Lee J. C. , Downing S. E.
Published: December 2017

We have shown previously that insulin reduces myocardial injury associated with norepinephrine (NE) infusion in the rabbit (Am. J. Pathol. 93:399--353, 1978). In the present study, left ventricular function (LVF) was assessed from afterload curves obtained by progressive aortic constriction 2--4 days following NE infusion. The initial slope of the function curves (SFC), maximum dP/dt and left ventricular end-diastolic pressure at 120 mmHg ((LVEDP120) were used for comparison. In 4 controls, SFC averaged 23.8 mmHg/cmH2O. In 10 rabbits given NE, the mean slope was 8.4 (P less than 0.01). However, animals pretreated with insulin before being given NE did not differ from controls (SFC, 19.7 mmHg/cmH2O). These performance data were supported by measurements of LVEDP120, which were 2.8, 12.3 and 3.1 cmH2O, respectively (P less than 0.05 and less than 0.02). In spite of the higher LVEDP, max dP/dt120 was significantly lower in the NE group than in the group given insulin. Histological findings and postmortem measurements of LV volume and mass were consistent with the observed differences in LVF. It is concluded that NE damage reduces LVF and this is largely prevented by pretreatment with insulin.
Desensitization of the cholinergic receptor at the sinoatrial cell of the kitten
Authors: Jalife J. , Hamilton A. J. , Moe G. K.
Published: December 2017

The hyperpolarizing effects of long periods of vagal stimulation were studied in kitten sinoatrial node-vagus nerve preparations. Verapamil (2.2 x 10(-6) M) was used to arrest spontaneous pacemaker activity, thus permitting uninterrupted observation of the time course of cholinergically mediated hyperpolarizations. With progressively longer vagal trains the hyperpolarization was not maintained but decreased, rapidly at first, and then more gradually despite continuous vagal stimulation. Similar decay of the cholinergic effect was also observed during continuous iontophoretic application of acetylcholine (ACh) or carbamylcholine (CCh). The results show that, for the most part, the decay of the hyperpolarizing response cannot be due to "fatigue" of nerve terminals, to a gradual reduction in the driving force for K+, or to hydrolysis of ACh by cholinesterase. These experiments demonstrate the development of desensitization of the cholinergic receptor at the sinoatrial cell membrane. The data fit the "cyclic reaction" model proposed by Katz and Thelsleff (J. Physiol. London 138:63-80, 1957) for the neuromuscular junction.
Intracellular chloride activity in quiescent cat papillary muscle
Authors: Spitzer K. W. , Walker J. L.
Published: December 2017

Intracellular chloride activity (alpha iCl) was measured in quiescent cat papillary muscles with chloride liquid ion-exchanger microelectrodes. Muscles were superfused in bicarbonate-buffered solutions containing a control concentration of chloride (146.1 mM) and either 2.7, 4.4, or 5.4 mM potassium. The resulting mean membrane potentials were -96.2, -86.8, and -80.6 mV, respectively. In contrast, alpha iCl and the chloride equilibrium potential were unchanged by these alterations in external potassium and remained stable at 11 mM and -60 mV for up to 10 h following removal of the tissue from the animal. This value of alpha iCl is approximately 2-4 times greater than that predicted assuming chloride is passively distributed. The upper limit of intracellular interference was estimated from low external chloride superfusion and found to be no greater than 2-3 mM. Prolonged exposure to bicarbonate-free solutions buffered with N-2-hydroxyethyl piperazine-N'-2-ethanesulfonic acid (HEPES) did not reduce the apparent value of alpha iCl, suggesting that intracellular interference from intracellular bicarbonate does not significantly influence the measurement of alpha iCl. These results suggest that chloride can move into cat papillary muscle against an electrochemical gradient.
Critical closing and critical opening phenomena in the coronary vasculature of the dog
Authors: Sherman I. A. , Grayson J. , Bayliss C. E.
Published: December 2017

Direct measurements of coronary venous outflow in a right-heart bypass preparation were used to study the critical closing (CC) and critical opening (CO) phenomena in the anesthetized dog heart. Arterial pressure was lowered rapidly by hemorrhage, and CC pressure was the pressure at which coronary flow stopped completely. Shed blood was returned immediately or after 3 min of ischemia. The pressure at which coronary flow resumed (CO pressure) was measured. Coronary flow stopped at a mean aortic pressure of 14.3 mmHg. Vasodilator drugs and ischemic lowered CC pressure to 10.5 and 10.2 mmHg, respectively. Aortic pressure of 47.3 mmHg was needed to resume coronary flow following perfusion arrest. A brief period of ischemia did not significantly change the CO pressure. These results confirm the presence of CC phenomenon in dog heart and show that CC pressure can be altered by ischemia or vasodilators. It is suggested that the high value of CO pressure may be responsible for myocardial injury associated with ischemic cardiac arrest during open-heart surgery.
Accuracy of methods for calculating cerebral blood flow from intracarotid xenon-133 injection
Authors: Marc-Vergnes J. P. , Celsis P. , Charlet J. P. , Setien G.
Published: December 2017

The accuracy of the three commonly used methods, the initial slope analysis, the stochastic analysis, and the compartmental analysis, for calculating mean cerebral blood flow from xenon-133 clearance curves was studied with the use of computer-generated and real curves. The accuracy of calculation was affected by the cutoff time of the curve, by the level of the compartmental blood flows to white and gray matter and by the ratio of these flow levels, by the relative weight of gray matter, and by the choice of the method of calculation. None of the methods was clearly superior to the others. Each had its own defects that render it more or less suitable for different situations. All three methods generally overestimated mean cerebral blood flow. This overestimation was greater the lower the flow. A curve-fitting index was devised which can be used to check the validity of the bicompartmental model when using compartmental analysis. This same index can provide, though not always, an estimate of the error in the calculation of mean cerebral blood flow when an optimization method is used.
Transcapillary Starling forces using membrane osmometry
Authors: Christian J. L. , Brace R. A.
Published: December 2017

Membrane osmometry was used to estimate the four transcapillary Starling pressures in subcutaneous tissue of rats, guinea pigs, and dogs. Isolated subcutaneous tissue samples were either placed on a large-pore or small-pore osmometer that measured the interstitial fluid pressure (Pif) and the difference between the interstitial fluid pressure and the interstitial protein osmotic pressure (Pif-pi if), respectively. The colloid osmotic pressure of the interstitial fluid (pi if) was obtained from the difference in these two pressures. A plasma sample placed on the small-pore osmometer yielded the colloid osmotic pressure of the plasma proteins (pi c). Finally the capillary pressure (Pc) was calculated from the three other Starling forces. In the rat, guinea pig, and dog, respectively, the estimated Starling forces were as follows: Pif -2.2, -2.1, and -4.8 mmHg; pi if, 7.3, 4.8, and 4.4 mmHg; pi c, 21.3, 19.5, and 19.2 mmHg; and Pc, 11.8, 12.6, and 10.0 mmHg. A comparison with data obtained in other studies using different methods shows good agreement and strongly supports membrane osmometry as a method for measuring the Starling pressures in subcutaneous tissue.
Left ventricular free wall and intraventricular pressure-sarcomere length distributions
Authors: Grimm A. F. , Lin H. L. , Grimm B. R.
Published: December 2017

Sarcomere lengths were measured after pentobarbital anesthesia at five sites through the wall of the formaldehyde solution-fixed cadmium-arrested closed-chest rat left ventricle. Sections (250 micron) were cut from endocardium to epicardium with a freezing microtome. Selected sections were sonified, mixed with a gelatin-water solution, and placed on a glass slide. Sarcomere lengths were measured with an optical microscope at five sites through the wall. Sarcomere lengths progressively increased from section I (endocardium site) to section III (middle site) and IV. Sarcomere lengths were again shorter in section V (epicardium site). There was a progressive increase in sarcomere lengths with increasing intraventricular pressures. Sarcomere lengths did not significantly exceed optimum length.
Carotid baroreflex regulation of plasma renin levels
Authors: Ammons W. S. , Santiesteban H. L. , Koyama S. , Manning J. W.
Published: December 2017

The influence of carotid sinus pressure (CSP) on plasma renin activity (PRA) was studied in vagotomized, alpha-chloralose-anesthetized salt-deprived (<1 meq Na+/day) or salt-loaded (100-125 meq Na+day) cats. Changes in renal vascular resistance were produced by varying the pressure in the isolated perfused carotid sinus while maintaining renal blood flow constant in one kidney. Renal flow-pressure determinations were made at high, medium, and low CSP. Venous blood samples were withdrawn for PRA determination by radioimmunoassay after 10 min at each CSP. Low CSP resulted in an increased renal resistance and a dramatic elevation of the PRA in both groups. High CSP also resulted in an increase in PRA (due to contralateral variable-flow kidney) accompanied by a decrease in renal vascular resistance. No difference was found between PRA during medium CSP ad initial control PRA. Propranolol blocked the increase in PRA during low CSP but had no effect on the elevated PRA during high CSP. It is concluded that low CSP produced an increase in PRA that was associated with a reflex activation of renal sympathetic nerves.
Progressive myocardial dysfunction associated with increased vascular resistance
Authors: Franciosa Joseph A. , Heckel Richard , Limas Catherine , Cohn Jay N.
Published: December 2017

To study heart failure from a myocardial lesion, we injected glass beads into the circumflex coronary artery of 11 conscious dogs and followed hemodynamics for 10 mo. Heart rate remained unchanged. Control mean arterial pressure of 112.3 ± 3.0 (SE) mmHg was unchanged at 1 and 3 mo, but rose to 127.2 ± 8.5 to 84.0 ± 7.6 ml . kg-1 . min-1 at 10 mo (P < 0.02), but was unchanged at 1 and 3 mo. Left ventricular end-diastolic pressure (LVEDP) averaged 4.6 ± 0.8 mmHg at control and rose to 11.8 ± 1.4 mmHg at 1 mo and 14.9 ± 2.5 mmHg at 10 mo (both P < 0.01). Systemic vascular resistance rose significantly by 10 mo. The ratio of stroke work to LVEDP fell from 13.1 ± 0.1 at control to 3.8 ± 0.5 by 10 mo (P < 0.01). In this dog model, left ventricular dysfunction is manifest early by increased LVEDP and later by high systemic vascular resistance with low cardiac output, thus suggesting a role of the peripheral circulation in the progression of heart failure.
Myocardial adenosine and coronary resistance during increased cardiac performance
Authors: McKenzie Jack E. , McCoy Frank P. , Bockman Emma L.
Published: December 2017

The relation between myocardial adenosine content and coronary vascular resistance was studied in the open-chest dog. Cardiac performance was increased by aortic constriction or by intravenous infusion of isoproterenol. Coronary blood flow was measured by the microsphere tracer technique. In control animals, adenosine content and coronary vascular resistance were 0.22 ± 0.03 nmol/g and 1.9 ± 0.11 mmHg ⋅ ml-1 . min ⋅ 100 g, respectively. A range of myocardial oxygen consumptions of 5.3-24 ml O2 ⋅ min-1 ⋅ 100 g-1 was elicited. This was associated with a range of coronary blood flows of 33-166 ml ⋅ min-1 . 100 g-1. There was a significant negative correlation between coronary vascular resistance and the log of the myocardial adenosine content (r = 0.77). There was no transmural gradient in adenosine content in the control and aortic-constricted groups, but there was a significant adenosine gradient in the isoproterenol-infused group in which coronary input pressure was decreased. The hearts were not ischemic, as indicated by low myocardial lactate contents and a stable coronary sinus blood pH. These results provide support for a role of adenosine in the local control of the coronary circulation during increased cardiac performance.
Control of hepatic arterial blood flow: independence from liver metabolic activity
Authors: Lautt W. Wayne
Published: December 2017

This investigation tested the hypothesis that hepatic arterial blood flow is not dependent on hepatic metabolism, but rather is controlled in a manner that tends to maintain total hepatic blood flow constant. Cats anesthetized with pentobarbital sodium received SKF 525 A or 2,4-dinitrophenol (DNP), respectively, to inhibit or stimulate metabolism. Blood flows and oxygen uptake of the liver and gut were determined by use of a hepatic venous long circuit and noncannulating electromagnetic recording of hepatic arterial blood flow. In both sets of experiments the hepatic arterial blood flow. In both sets of experiments the hepatic artery constricted sufficiently to offset elevated portal venous blood flow, thereby maintaining total hepatic blood flow constant. The reduced hepatic arterial conductance occurred with DNP despite elevated metabolic rate and reduced oxygen in the portal and hepatic veins. Altered gut metabolism correlated with altered vascular conductance in the gut; hepatic arterial conductance changes did not correlate with changes in liver metabolic activity. The data confirmed the hypothesis. It is suggested that for hormonal homeostatis it is essential that total hepatic blood flow be regulated because hepatic clearance is flow dependent.
Effects of anesthesia on carotid sinus reflex control of arterial hemodynamics in the dog
Authors: Cox R. H. , Bagshaw R. J.
Published: December 2017

The detailed characteristics of the carotid sinus reflex control of regional pressure-flow relations were compared in dogs anesthetized with chloralose, pentobarbital, or halothane. The carotid sinuses were isolated and perfused under conditions of controlled pulsatile pressure. Pressure and flow were measured in the ascending aorta and the celiac, mesenteric, renal, and iliac artery. Mean arterial pressure and peripheral resistance were highest under chloralose and lowest under halothane. For cardiac output this relation was reversed. Set point values of reflex gain and overall range of control were similar under chloralose and halothane and lowest under pentobarbital. These results were found both before and after bilateral cervical vagotomy. Operating point values of regional resistance were generally largest with chloralose and smallest with halothane. Operating point sensitivities of regional resistances were generally smallest under pentobarbital and similar under chloralose and halothane. Vagotomy was associated with increases in set point values of mean arterial pressure, set point gain, and overall range of control under all three anesthetics. With chloralose as a reference, halothane does not depress cardiovascular reflex mechanisms. Carotid sinus reflexes under halothane were as sensitive and well maintained as they were under chloralose. These reflexes were significantly depressed under pentobarbital compared with chloralose.
Effect of taurine on calcium paradox and ischemic heart failure
Authors: Kramer J. H. , Chovan J. P. , Schaffer S. W.
Published: December 2017

The loss of mechanical function in rat hearts subjected to either the calcium-paradox or global ischemia heart failure models was found to correlate with decreases in myocardial taurine levels. Therefore, the effect of taurine treatment was assessed in the two failure procedures. The presence of taurine protected against loss of mechanical function resulting from the calcium paradox and prevented both the large decline in sarcolemmal ATPase activities and the increase in sarcolemmal calcium binding normally associated with this model. Parallel studies on reperfused, taurine-untreated ischemic hearts showed only minor changes in these sarcolemmal functions. Taurine treatment normalized the slight increase in calcium binding associated with ischemia, but had no observable effect on recovery of mechanical function. Although taurine returns selected parameters of the sarcolemma toward normal in both models, it only improves mechanical function in the paradox model. This suggests that calcium paradox-induced heart failure is more closely associated with sarcolemmal dysfunction than ischemic heart failure.
Regional left ventricular wall thickness early and late after coronary occlusion in the conscious dog
Authors: Sasayama S. , Gallagher K. P. , Kemper W. S. , Franklin D. , Ross J.
Published: December 2017

Regional wall thickness and endocardial segment lengths in normal and ischemic zones of the left ventricle were measured simultaneously with ultrasonic-dimension gauges before and after chronic circumflex artery occlusion in conscious dogs. After 3 wk, end-diastolic segment lengths (EDL) in normal zones increase 10% (P less than 0.01), shortening increased 22% (P less than 0.05), and end-diastolic wall thickness (EDWT) was reduced by 12.8% (P less than 0.01). In ischemic zones at 3 wk, EDL was reduced by 15.4% (P less than 0.01), and subendocardial shortening recovered slightly to 15% of control; EDWT increased 11% at 3 days postocclusion and thereafter remained near control values (change not significant), but systolic wall thickening improved substantially, reaching 38% of control at 3 wk. Thus, tissue loss and slight return of function occurred in the ischemic subendocardium, whereas overall wall function (as reflected by regional wall thickening) improved considerably over time. These findings suggest that recovery of function in the outer layers of the wall after myocardial infarction modifies the close correlation between regional subendocardial segment and wall thickening dynamics observed acutely.
Sodium and angiotensin in the pathogenesis of experimental renovascular hypertension
Authors: Seymour A. A. , Davis J. O. , Freeman R. H. , DeForrest J. M. , Rowe B. P. , Stephens G. A. , Williams G. M.
Published: December 2017

The effects of simultaneous angiotensin blockade and sodium depletion on the development of one-kidney renovascular hypertension were studied in rats. In sodium-replete rats, systolic blood pressure (SBP) increased from 102 +/- 2 to 153 +/- 11 mmHg by the 12th day after unilateral nephrectomy and subsequent partial occlusion of the renal artery with a 0.22-mm silver clip. When changes in body fluid volume were minimized by sodium restriction in a second group of rats, the increase in SBP from 98 +/- 4 to 149 +/- 7 mmHg after clipping was not different from that in sodium-replete animals. Inhibition of the angiotensin-converting enzyme with SQ 14,225 during sodium restriction prevented the SBP from increasing above 101 +/- 3 mmHg by the 12th day after nephrectomy and clipping. Once SQ 14,225 administration was discontinued, SBP rose significantly to 148 +/- 5 mmHg within 5 days. Because previous studies have shown that neither sodium depletion nor angiotensin blockade alone prevented the development of one-kidney renovascular hypertension, it is concluded that the increase in blood pressure resulting from renal artery constriction and contralateral nephrectomy was prevented only by suppression of both the renin-angiotensin system and body fluid volume.
Myocyte and nonmyocyte RNA polymerase activity and chromatin template function
Authors: Taylor P. B. , Tang Q.
Published: December 2017

Myocardial and nonmyocardial cell nuclei were isolated from ventricles of adult male Wistar rats by means of sucrose density centrifugation. RNA polymerase activity in myocyte nuclei was approximately 80-90% higher than in nonmyocytes. Total myocyte chromatin template activity using Escherichia coli RNA polymerase was linear and about onefold greater than the nonmyocyte fraction over a fivefold range of chromatin concentrations. Preincubation time required for RNA polymerase to form a stable binding complex with chromatin was at least 40 min for myocyte and 30 min for nonmyocyte nuclear subsets. Titration of chromatin against a fixed amount of RNA polymerase (5 micrograms) showed that 5 micrograms of myocyte chromatin (as DNA) and 8 micrograms of nonmyocyte chromatin (as DNA), respectively, were required to saturate the enzyme. These results indicate that myocyte chromatin can support greater enzyme binding than can nonmyocyte chromatin. The distribution of DNA fragments from isolated myocyte and nonmyocyte nuclei were similar when alkaline sucrose density centrifugation was used. Chromatin prepared from these nuclear subsets showed no difference in degree of DNA fragmentation. These observations indicate that compared with nonmuscle cells, myocytes from adult rat hearts have higher RNA polymerase activity, greater overall chromatin template function, and higher binding capacity for RNA polymerase. Collectively, these data suggest that adult cardiac muscle cells should have a larger potential for RNA synthesis than nonmuscle cells.
High-affinity substance P binding sites in rat sympathetic ganglia
Authors: Niwa M. , Shigematsu K. , Plunkett L. , Saavedra J. M.
Published: December 2017

Substance P binding sites were characterized and quantitated in single rat sympathetic ganglia by incubation of tissue sections with 125I-Bolton-Hunter substance P, autoradiography, image analysis coupled with computer-assisted microdensitometry, and comparison with 125I standards. The prevertebral celiac-superior mesenteric sympathetic ganglia contained clusters of high-density, high-affinity substance P binding sites [maximum binding (Bmax) 7.12 +/- 0.20 pmol/mg protein; affinity constant (Ka) 2.08 +/- 0.02 X 10(9) M-1]. In the paravertebral superior cervical sympathetic ganglia, the number of high-affinity substance P binding sites was substantially lower (Bmax 1.38 +/- 0.04 pmol/mg protein; Ka 1.71 +/- 0.03 X 10(9) M-1). Future studies should address the issue of whether the substance P binding sites identified in prevertebral ganglia of the rat serve as receptors for the peptide presumed to be released by terminals of sensory neurons.
Effects of reestablishing blood flow on extent of myocardial infarction in conscious dogs
Authors: Murdock R. H. , Chu A. , Grubb M. , Cobb F. R.
Published: December 2017

The effects of permanent circumflex coronary artery occlusion (PO) compared with reestablishing blood flow (OR) at 2 and 6 h after occlusion on the final extent of histological infarction (HI) was assessed in chronically instrumented awake dogs. The relationships between the extent of left ventricular ischemia measured by microsphere techniques and HI in the PO group were used as models to predict the expected infarction in the 2- and 6-h OR groups. Mean HI (+/-SD) in the PO and 6- and 2-h OR groups was 21 +/- 13, 19 +/- 10, and 13 +/- 12% of left ventricular weight, respectively; values were not significantly different. The extent of HI in samples grouped according to epicardial and endocardial layers and ischemic blood flow ranges (0-15, 16-30, 31-50, 51-75% of control region blood flow) was reduced in the 2-h but not 6-h OR group. Analysis of individual animals using total ischemic region blood flow to epicardial and endocardial layers demonstrated that OR at 2 h but not 6 h reduced infarction in most animals but not in certain animals with the largest ischemic regions.
Humoral factors may mediate increased rat hindquarter blood flow in portal hypertension
Authors: Korthuis R. J. , Benoit J. N. , Kvietys P. R. , Townsley M. I. , Taylor A. E. , Granger D. N.
Published: December 2017

Chronic portal hypertension is associated with systemic hypotension and reduced peripheral vascular resistance. Although it is well established that splanchnic and renal vascular resistances are reduced, the contribution of possible alterations in skeletal muscle hemodynamics in portal hypertension is unknown. The present study was designed to determine if skeletal muscle vascular resistance was reduced and blood flow increased in portal hypertensive rats. In portal hypertensive animals, hind-quarter blood flow was significantly increased while vascular resistance was significantly reduced. The fall in resistance in the portal hypertensive animals was associated with an increase in the capillary filtration coefficient, suggesting that an increase in functional exchange vessel surface area occurred. Cross perfusion of control hindquarters with portal hypertensive blood resulted in a 38% reduction in hindquarter vascular resistance. Raising the plasma glucagon concentration to levels reported in portal hypertensive animals resulted in no change in blood flow or vascular resistance in control hindquarters. Skeletal muscle vascular sensitivity to norepinephrine was assessed by constructing dose-response curves in control and portal hypertensive animals. Mean ED50 values were not different. The results of these studies indicate that skeletal muscle vascular resistance is reduced in portal hypertension and humoral factors, but not glucagon, are primarily responsible for the skeletal muscle hyperemia associated with portal hypertension.
Effect of arteriolar dilation on coronary artery diameter distal to coronary stenoses
Authors: Schwartz J. S. , Bache R. J.
Published: December 2017

Previous studies have suggested that worsening hemodynamic severity of coronary stenoses in response to distal arteriolar dilation may be related to dilation of the normal epicardial artery adjacent to the stenosis resulting in increasing percent stenosis. To test this hypothesis we used sonomicrometry to continuously measure external circumflex coronary artery diameter distal to snare stenoses of varying severity in 19 open-chest dogs and 5 awake, chronically instrumented dogs. Arteriolar dilation produced by release of a transient coronary occlusion or by intracoronary injection of adenosine caused a decrease in circumflex coronary diameter distal to the stenosis. Regression analysis showed that circumflex diameter and pressure distal to the stenosis were directly related (mean r: transient occlusion, 0.86 +/- 0.04; adenosine, 0.97 +/- 0.01). The close relationship between pressure and diameter suggests that the decrease in diameter in response to arteriolar dilation was a passive effect. Passive coronary narrowing distal to a stenosis suggests that a similar effect may occur within a compliant stenosis, thus partly explaining the increase in severity of compliant stenoses in response to arteriolar dilation.
Electrical conductivity and its use in estimating an equivalent pore size for arterial endothelium
Authors: O'Donnell M. P. , Vargas F. F.
Published: December 2017

Transport characteristics of capillary endothelia have been studied in numerous preparations. Little is known, however, regarding transport across the ultrastructurally similar arterial endothelium. The present studies describe a method for determining endothelial electrical resistance in the isolated, Ringer-perfused rabbit aorta. By use of silver-silver chloride electrodes, total resistance (RT) of the vessel wall was found to be 18.4 +/- 6.5 omega . cm2 (mean +/- SD; n = 10) in response to transmural passage of constant current pulses. After detergent removal of the endothelium, outer layer resistance (Rol) was 8.7 +/- 5.1 omega . cm2. Endothelial resistance (Re) was calculated to be 9.7 +/- 4.1 omega . cm2, since RT = Rol + Re. Combination of Re with previously measured hydraulic conductivity of this endothelium yielded an equivalent endothelial pore radius of 85 A, whereas a fractional pore area of 6.5 X 10(-4) was estimated from conductivity data. An alternative analysis demonstrated an endothelial slit width of 102 A. Re is similar to electrical resistances of leaky epithelia, frog mesenteric capillary, and frog muscle capillary, suggesting similar permeability characteristics in both arterial and capillary endothelia.
In vitro myocardial performance after lethal and nonlethal doses of endotoxin
Authors: McDonough K. H. , Brumfield B. A. , Lang C. H.
Published: December 2017

The present study was initiated to determine whether the myocardial effects of an in vivo injection of endotoxin into rats were correlated with the dose and thus the lethality of the endotoxin administered. All animals in this study were used 4 h after a bolus injection of 1,000, 100, 10, or 1 microgram/100 g body wt of Escherichia coli endotoxin. At this time, mean arterial blood pressure had returned to control levels but cardiac output was still depressed at the three higher doses as previously reported [Am. J. Physiol. 248 (Regulatory Integrative Comp. Physiol. 17): R471-R478, 1985]. Intrinsic function of the myocardium was assessed using the isolated perfused working heart preparation. Cardiac output and pressure development were measured at varying preloads and at two levels of aortic outflow resistance. In vitro approaches were chosen for this study to eliminate peripheral vascular changes and humoral or neural alterations that might influence myocardial performance in vivo. Results indicate that coronary vascular resistance was increased in all hearts from endotoxin-treated animals compared with controls. In addition, myocardial performance was impaired at several doses of endotoxin, and the degree of dysfunction was dependent on the dose of endotoxin administered. Dysfunction, i.e., a depression in cardiac output times peak systolic pressure, was evident at the two higher doses in which there was 50 and 10% lethality by 24 h and also in the lower dose of 10 micrograms/100 g, which was nonlethal. Cardiac output appeared to be very sensitive to the consequences of endotoxin administration. Defects in myocardial performance could be revealed by increasing preload or afterload stress on the hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
Augmentation of sarcolemmal Ca by anionic amphiphile: contractile response of three ventricular tissues
Authors: Langer G. A. , Rich T. L.
Published: December 2017

The anionic amphiphile dodecyl sulfate was used at the concentration of 100 microM, below the concentration at which membrane permeability is compromised. In rat myocardial tissue culture dodecyl sulfate induced a large increase in Ca uptake in the intact cells, of which 84% was distributed in a rapidly exchangeable (t1/2 less than 18 s) and 16% in a slowly exchangeable (t1/2 = 17 min) compartment. Dodecyl sulfate induced a large increase in Ca bound to isolated sarcolemmal membrane of these cells. This increase in membrane binding and the distribution in whole cells is consistent with insertion of dodecyl sulfate in the sarcolemma (SL) with subsequent Ca binding to its anionic head group. With perfusate extracellular calcium concentration ([Ca]o) equal to 1 mM, dodecyl sulfate produced greater than 60% increase in active force in ventricular tissue from adult rabbit and neonatal rat but virtually no increase in adult rat ventricle. Preperfusion with 0.1 mM [Ca]o or 10(-6) M ryanodine markedly increased the relative response of adult rat ventricle to dodecyl sulfate. After a quiescent period in rabbit ventricle, dodecyl sulfate caused a progressive increase of force of each beat compared with control; i.e., the treppe response was increased at each successive beat. This did not occur in adult rat ventricle. These results further clarify the different quantitative role of SL-bound versus sarcotubular Ca in the hearts of different species.
Unilateral and bilateral sympathetic effects on cerebral blood flow during normocapnia
Authors: Busija D. W.
Published: December 2017

The purposes of this study were to 1) determine the effects of unilateral and bilateral sympathetic stimulation on cerebral blood flow (CBF) during normocapnia and 2) explore the mechanism by which bilateral effects are greater than unilateral effects. In anesthesized rabbits, CBF (15-microns microspheres) and internal carotid artery blood flow (ICBF) were determined during a prestimulation period and electrical stimulation of one or both superior cervical ganglia (8 or 16 Hz, 10 V, 2 ms). Resting CBF ranged from 26 to 34 ml X min-1 X 100 g-1. Unilateral stimulation did not reduce CBF at 8 Hz, but stimulation at 16 Hz reduced ipsilateral blood flow to the cerebrum by 21 +/- 5% (n = 6 from each group). In contrast, bilateral stimulation reduced blood flow to cerebrum by 22 +/- 5 and 40 +/- 4% at 8 and 16 Hz, respectively (P less than 0.05, unilateral vs. bilateral; n = 6 for each group). Similarly, unilateral stimulation at 8 Hz did not reduce ipsilateral ICBF or affect contralateral ICBF. However, bilateral stimulation at 8 Hz reduced ICBF by 51 +/- 6% on both sides. We conclude that 1) bilateral effects of sympathetic nerves on CBF are greater than unilateral effects, and 2) this difference in response may be due to activation of two overlapping sets of sympathetic nerves and release of more neurotransmitter during bilateral sympathetic stimulation.