bluuebunny/crossref_metadata_2025 huggingface dataset:
Renal vascular effects of endoperoxide analogs, prostaglandins, and arachidonic acid
Authors: Feigen L. P. , Chapnick B. M. , Flemming J. E. , Flemming J. M. , Kadowitz P. J.
Published: December 2017

Renal vascular responses to analogs of prostaglandin H2(PGH2) were investigated in anesthetized dogs. The analogs were potent renal vasoconstrictors whose actions were not affected either by indomethacin or by alpha-adrenergic or angiotensin antagonists. The constrictor activity of the analogs approximated that of norepinephrine. Responses to PGD2 were also obtained. This prostaglandin, previously thought to be inactive, was found to cause renal vasodilation similar to that caused by PGA2. Responses to the prostaglandin precursor, arachidonic acid, were of two types. In some animals, the response was marked vasodilation, whereas in others transient vasoconstriction preceded the vasodilation. These studies demonstrate that PGH2 analogs are potent renal vasoconstrictors and that PGD2 possesses renal vasodilating properties. In addition, it is suggested that the rapid vasoconstrictor portion of the arachidonate response may represent effects of endogneously produced PGH2.
Brain blood flow autoregulation and metabolism during halothane anesthesia in monkeys
Authors: Morita H. , Nemoto E. M. , Bleyaert A. L. , Stezoski S. W.
Published: December 2017

Past studies suggest that halothane causes cerebrovascular dilatation and increased cerebral blood flow (CBF); these properties may be relevant to its use for neurosurgical procedures. We studied CBF autoregulation in monkeys during anesthesia with 66% N2O/33% O2 and with 0.5%, 1.0%, and 2.0% inspired halothane at various cerebral perfusion pressures (CPP) achieved by infusion of trimethaphan camsylate or phenylephrine. CBF was measured by monitoring brain xenon-133 clearance after intra-arterial injection of the isotope in saline. CBF autoregulation was intact during N2O/O2 and during 0.5% halothane/N2O/O2 anesthesia at CPPs ranging from 50 to 100 mmHg, but began to fail at 1.0% halothane. Complete loss of autoregulation occurred during 2% halothane/N2O/O2 anesthesia. Estimated brain O2 consumption fell by 30%, 40%, and 50% during 0.5%, 1.0%, and 2.0% halothane anesthesia, respectively, compared to O2 consumption during N2O/O2 anesthesia (100%).
Hemodynamic similarities between the trigeminal and aortic vasodepressor responses
Authors: Kumada M. , Dampney R. A. , Whitnall M. H. , Reis D. J.
Published: December 2017

The hemodynamic changes associated with hypotension elicited by electrical stimulation of the spinal trigeminal complex (trigeminal depressor response, TDR) or the aortic nerve (aortic depressor reflex, ADR) were compared in rabbits anesthetized with urethan. The hypotension associated with each response was accompanied by bradycardia, a marked fall in total peripheral resistance, a small decrease in cardiac output, and a nonuniform decrease in regional vascular resistances, with the order of magnitude of the decrease being femoral greater than mesenteric greater than renal arterial resistance. In individual experiments the percent decrease in heart rate, total peripheral resistance, or regional resistances was plotted against the percent fall in arterial pressure to obtain a pair of regression lines during the TDR and ADR. There was no significant difference in the slope or y-intercept of the regression line between the TDR and ADR for all of the hemodynamic variables examined. In both responses, however, the slope of the femoral resistance/arterial pressure relationship was significantly greater than that of the renal resistance/arterial pressure relationship. We conclude that the TDR is characterized by a pattern of hemodynamic changes similar to that of the ADR.
Effect of regional myocardial ischemia on cardiac pump performance during exercise
Authors: Horwitz L. D. , Peterson D. F. , Bishop V. S.
Published: December 2017

The effect of brief periods of regional ischemia upon left ventricular pump performance was studied in nine dogs standing quietly at rest and during running exercise on a treadmill. Transient occlusions of the left circumflex coronary artery resulted in increase in heart rate at rest (+30 beats/min) but not during exercise. Other changes due to occlusion were similar at rest and during exercise and included decreases in stroke volume (-25% standing, -23% running); in dP/dt max, the maximum first derivative of the left ventricular pressure (-20% standing or running); and in left ventricular peak systolic pressure (-13% standing, -21% running); and rises in left ventricular end-diastolic pressure (+4.5 mmHg standing, +6.3 mmHg running). Cardiac output was unchanged by occlusions at rest but fell (-18%) during occlusions while the dogs were running. Propranolol reduced absolute levels of cardiac performance during exercise occlusions but had no effect at rest. Inotropic agents with ischemia had some effects at rest but did not alter exercise hemodynamics. It is concluded that integrated left ventricular function during ischemia is not impaired by exercise, probably because of beta-adrenergic stimulation of nonischemic myocardium.
Quantitation of anterior descending vs. circumflex venous drainage in the canine great cardiac vein and coronary sinus
Authors: Nakazawa H. K. , Roberts D. L. , Klocke F. J.
Published: December 2017

The fractions of left anterior descending (LAD) and circumflex (LC) inflow drainage into the canine great cardiac vein (GCV) and coronary sinus (CS) have been quantitated by use of a right heart bypass preparation in which GCV outflow was isolated from the remainder of CS outflow. Following direct LAD injection of indocyanine green dye (ICG), 63 +/- 8% (SD) of the total amount of dye recovered appeared in GCV outflow and the remainder in CS outflow. CS recovery of ICG was decreased appreciably by ligation of epicardial venous connections between the LAD and LC beds, but was not affected by selective reductions of LAD or LC inflow. Only 3 +/- 3% of ICG injected into the LC was recovered in GVC outflow under basal conditions, and these low values were not affected measurably by selective reductions of LAD or LC inflow. CS drainage of LAD inflow could be augmented by selective increments of GCV pressure exceeding 7-10 mmHg. Increments of LC drainage in GCV outflow required CS pressures that exceeded GCV pressures by greater than 10 mmHg.
Reflux mechanisms involved in cardiac arrhythmias induced by hypothalamic stimulation
Authors: Evans D. E. , Gillis R. A.
Published: December 2017

Electrical stimulation of widespread areas in the CNS has been shown to cause cardiac arrhythmias, which occur most frequently after cessation of stimulation. To determine the reflex and autonomic mechanism responsible for the poststimulation arrhythmias, we anesthetized cats with chloralose, and recorded arterial pressure, ECG, and cardiac vagal nerve activity. Stimulation of the hypothalamus consistently caused increases in blood pressure and heart rate during stimulation and caused arrhythmias, accompanied by vagal hyperactivity, immediately following stimulation. The arrhythmias were mediated solely by the vagus nerves because vagotomy or propantheline administration prevented them, whereas propranolol did not. Administration of either phentolamine or spinal cord transection prevented both the rise in blood pressure during stimulation and the poststimulation arrhythmias, but sectioning the carotid sinus and aortic depressor nerves had no preventative effect. However, when this denervation was combined with sectioning of vagal afferents, bursts of vagal activity (used as an index of cardiac rhythm disturbances) were prevented in three of six animals. Subsequent administration of phentolamine prevented the bursts in the remaining animals. It is concluded that poststimulation arrhythmias are elicited by the rise in blood pressure occurring during stimulation causing a sudden surge in parasympathetic outflow to the heart. The reflexogenic areas involved appear to be stretch receptors innervated by afferent vagal fibers.
Effects of nitroglycerin on cardiac function and regional blood flow distribution in conscious dogs
Authors: Vatner S. F. , Pagani M. , Rutherford J. D. , Millard R. W. , Manders W. T.
Published: December 2017

The effects of intravenous infusion of nitroglycerin (NTG), 8 and 32 microgram/kg.min for 7 min, and of sublingual NTG, 1.2 mg, were examined on direct and continuous measurements of systemic, coronary, and regional hemodynamics, left ventricular (LV) dimensions, pressures, and myocardial contractility in conscious dogs. NTG induced sustained reductions in LV dimensions and transient increases in heart rate and dP/dt, and decreases in mean arterial pressure. Initially NTG increased cardiac output and flows to the coronary, mesenteric, renal, and iliac beds, while systemic and regional vascular resistances fell. Later, cardiac output, cardiac work, and mesenteric and iliac flows fell significantly below control, and significant vasoconstriction in the systemic as well as mesenteric, iliac, and coronary beds was observed at a time when LV end-diastolic dimensions were still significantly reduced. Peripheral vasoconstriction was not observed with systemic NTG in deafferented dogs or when NTG, 1 microgram/kg.min, was infused intra-arterially into the iliac bed. Thus, systemic NTG induces a biphasic response consisting of initial arteriolar vasodilation followed by vasoconstriction in the mesenteric, iliac, coronary and systemic beds, which is presumably due to longer lasting effects on preload and to secondary reflex responses to the drug.
Normal cardiac myosin ATPase and mechanics in pressure overload with digitalis treatment
Authors: Carey R. A. , Bove A. A. , Coulson R. L. , Spann J. F.
Published: December 2017

Cardiac muscle myosin ATPase activity is depressed and contractile function impaired when the heart is subjected to a chronic pressure overload. Administering digitalis in the presence of chronic pressure overload significantly attenuates the decline in mechanical function. The current study sought to determine if the cardiac muscle myosin ATPase activity of cats treated with digitalis in the presence of pressure overload remains normal in parallel with the mechanical function. Four groups of cats were studied: normal controls (C), animals with pressure-overload hypertrophy with or without failure (HF), normal cats that received treatment with digitalis (D), and animals that received digitalis prior to and together with pressure overload (DHF). Compared to C, the maximum myosin ATPase activity of HF was significantly (P less than 0.05) depressed, but the maximum ATPase activity of D and DHF was not altered significantly (P greater than 0.05) from C. In parallel with the enzyme maximum activity, the papillary muscle isometric rate of force development was significantly (P less than 0.005) depressed in HF compared to C; D and DHF were not significantly (P greater than 0.05) different from C. It is concluded that the depression of myosin ATPase observed in HF is not present when digitalis is administered concomitant with the pressure overload.
Effect of indomethacin on pulmonary vascular response to ventilation of fetal goats
Authors: Leffler C. W. , Tyler T. L. , Cassin S.
Published: December 2017

The effect of indomethacin treatment of the pulmonary vasodilation caused by ventilation of the fetal lung with air was evaluated in anesthetized, exteriorized, fetal goats by means of an open-chest, pump-perfused lung preparation. The decrease in pulmonary vascular resistance that occurs when the fetal lung is ventilated with air consists of two components: 1) a rapid decrease in pulmonary vascular resistance during the first 30 s of ventilation; 2) a slower decline, which continues through the first 10-20 min or more of ventilation. Indomethacin has no effect on the first component. The second component is absent following indomethacin pretreatment. The effect of indomethacin treatment is more pronounced in immature fetuses (less than 90% gestation) than in mature fetuses. Prostaglandin synthase activity appears to be important in the pulmonary vasodilation caused by ventilation of the fetal lungs with air.
Role of tissue hypoxia in local regulation of cerebral microcirculation
Authors: Kontos H. A. , Wei E. P. , Raper A. J. , Rosenblum W. I. , Navari R. M. , Patterson J. L.
Published: December 2017

The mechanism of action of hypoxia on cerebral blood vessels and its role in the regulation of the cerebral circulation were investigated in anesthetized cats. Arterial hypoxia produced marked cerebral arteriolar vasodilation, which was partially reversed by perfusing the space under the cranial window with artificial cerebrospinal fluid (CSF) containing 6-94% oxygen. More marked increase in the local supply of oxygen, via perfusion of the space under the cranial window with fluorocarbon FC-80 equilibrated with 100% oxygen, completely eliminated the vasodilation induced by arterial hypoxia. Fluorocarbon equilibrated with 100% N2 had no effect on the vasodilation. The vasodilation associated with hypotension was completely reversed by perfusion with fluorocarbon equilibrated with 100% oxygen and was unaffected by perfusion with fluorocarbon or CSF equilibrated with gas not containing oxygen. The vasodilation associated with Metrazole-induced seizures was partially reversed by perfusion with fluorocarbon containing oxygen. The results show that hypoxia dilated cerebral blood vessels entirely via a local mechanism, that hypoxia is the dominant mechanism involved in the vasodilation associated with hypotension, and that it is, at least partially, responsible for the vasodilation associated with seizures.
Microbubble elimination during priming improves biocompatibility of membrane oxygenators
Authors: Osada H. , Ward C. A. , Duffin J. , Nelems J. M. , Cooper J. D.
Published: December 2017

We tested the hypothesis that platelet loss following blood contact with foreign materials is partly related to the presence of microbubbles of gas (gas nuclei) trapped in surface defects on the membrane material. Extracorporeal membrane oxygenator perfusions were conducted in two groups of sheep, with use of standard priming techniques for the oxygenator in one group and a new vacuum priming technique in the other group. The vacuum priming technique was developed to eliminate gas nuclei from the oxygenator surface. With denucleation priming, platelet loss during perfusion was markedly reduced, as was thrombus formation on the membrane surface. The platelet particle-size distribution curve showed a shift consistent with platelet aggregation with the standard priming technique but not with the vacuum priming technique. We conclude that the elimination of trapped gas nuclei from the membrane surface during priming reduces the initial interaction between blood elements and the foreign surface.
Mechanisms of vascular changes in skeletal muscle during asphyxia in the cat
Authors: Weissman M. L. , Sonnenschein R. R. , Rubinstein E. H.
Published: December 2017

Vascular responses in the hindlimb muscles of anesthetized paralyzed cats during systemic asphyxia were studied. The cats were ventilated with 10% O2-10% CO2-80% N2 for 10-20 min periods, while blood flow to the skinned hindlimb was monitored (electromagnetic flowmeter). Mean arterial pressure rose and hindlimb flow typically fell during asphyxia, implying increased vascular resistance. After sympathetic denervation of the hindlimb, resistance increased in some groups of animals, and did not change in others during asphyxia. Functional adrenalectomy did not alter these response characteristics. Resistance also did not changes significantly if the control resistance was first increased to the predenervation level by electrically pacing the lumbar sympathetic chain. In contrast, pronounced vasodilatation occurred during asphyxia after blocking of the alpha receptors in the hindlimb (phenoxybenzamine) or after systemic catecholamine depletion (reserpine). We conclude that the vasoconstriction in innervated muscle during asphyxia was caused in part by increased discharge of sympathetic constrictor nerves to the muscle vasculature, with augmentation from a humoral alpha agonist of nonadrenal origin, possibly norepinephrine released from sympathetic nerves throughout the body.
Transient oxygen uptake during myocardial reactive hyperemia in the dog
Authors: Ruiter J. H. , Spaan J. A. , Laird J. D.
Published: December 2017

Oxygen uptake during myocardial hyperemia (MRH) following occlusions of 2.5-30 s was studied in nine anesthetized open-chest dogs by continuous measurement of left anterior coronary blood flow and anterior coronary vein oxygen saturation with electromagnetic flowmeter and fiber-optic catheters, respectively. The ratio of excess oxygen uptake to debt multiplied by 100% was defined as the oxygen repayment ratio (RR) and varied between -50% and +150% (mean 78%). Application of a steady-state Fick formula, as used by previous investigators, results in a profound overestimate of the RR (70-400%, mean 295%). RR is severely distorted by the venous catheter system, and after consideration of these effects we would conclude that the "true" RR in MRH is even lower than we found. Comparing our results with steady-state exercise autoregulation leads us to the following conclusions: 1) chemical kinetic limitations in oxygen release by red blood cells are excluded, 2) a simple direct PO2 regulation of flow is unlikely, but 3) our results are not inconsistent with a more complex integral oxygen regulation or with the metabolic hypothesis.
Dye-dilution cardiac output without blood withdrawal in the conscious rabbit
Authors: Boerboom L. E. , Boelkins J. N.
Published: December 2017

Cardiac output can be measured in the conscious rabbit without blood withdrawal by use of a modified dye-dilution method. Blood flows continuously from the central ear artery through a Silastic catheter that passes through a modified cuvette lumen and back into an ear vein. Blood flow through this shunt was 1.5 ml/min. This modified technique was evaluated by comparison with a simultaneously performed cardiac output measurement using radioactive microspheres and by making consecutive dye-dilution measurements at short time intervals. A correlation coefficient of 0.96 was obtained when comparing dye-dilution and microsphere cardiac outputs. The difference between 11 paired measurements was 7.09 +/- 5.24% (mean +/- SD). Consecutive outputs measured within 3 min of each other by the flow-through technique had a correlation coefficient of 0.99 and a difference between the first and second determinations of 3.52 +/- 2.38%. The method permits dye-dilution cardiac output measurement in the conscious rabbit while avoiding the potential error caused by blood withdrawal from small animals.
Neural pathways of a cardiogenic hypertensive chemoreflex
Authors: Hageman G. R. , Urthaler F. , James T. N.
Published: December 2017

Excitation of a cardiac chemoreceptor with 5-hydroxytryptamine (serotonin) produces a complex autonomic reflex which includes hypertension, changes in heart rate and contractile force, and disturbances of AV conduction. This study examines the afferent and efferent neural pathways of this autonomic reflex in 60 anesthetized dogs. We used cooling and sectioning techniques in 40 of these, and in 20 others recorded afferent neurograms. The most common afferent pathways for the reflex were found in the left and right recurrent cardiac nerves. No preferential efferent routes to the heart were found, although the nature of the reflex cardiac response could be altered by specific nerve interruption. Cyproheptadine (1 mg/kg iv) regularly abolished both the reflex and the chemoreceptor afferent neural traffic, but injection of a 10 times higher concentration of serotonin (1 mg/ml) readily surmounted the blockade and restored the chemoreceptor neural traffic. Thus cyproheptadine interdicts the reflex at the site of its initiation.
Effects of intraventricular angiotensin II mediated by the sympathetic nervous system
Authors: Falcon J. C. , Phillips M. I. , Hoffman W. E. , Brody M. J.
Published: December 2017

Central effects of angiotensin II were studied in rats treated with adrenalectomy, chemical sympathectomy with intravenous 6-hydroxydopamine, or a combination of both. Unrestrained, unanesthetized rats were compared before and after one of the three treatments to determine water drinking and blood pressure responses to intracerebroventricular (ivt) injections of 50 and 500 ng angiotensin II (AII). Adrenalectomy alone did not alter either drinking or pressor response to AIIivt. Peripheral sympathectomy alone resulted in a prolonged latency for pressor response but did not significantly alter drinking response to AIIivt. Results obtained by combined treatment were not significantly different from results obtained by sympathectomy alone. There remained a pressor response to AIIivt after combined treatment. The adrenals do not appear to be involved in mediating pressor response to AIIivt. Furthermore, sympathetic neural activation alone causes the early pressor response to AIIivt. Finally, some other factor(s) in addition to sympathetic neural activation must contribute to the pressor response to AIIivt.
Release of norepinephrine by sympathetic nerve stimulation from rabbit lungs
Authors: Tong E. Y. , Mathe A. A. , Tisher P. W.
Published: December 2017

Rabbit lungs were perfused via the pulmonary artery and norepinephrine (NE) measured in the outflows. The basal NE level was approximately 3 ng/min. Electrical stimulation (50 V, 1 ms, 10 Hz) of the sympathetic nerves doubled the NE release. Hexamethonium (10(-4) and 10(-5) M) had no effect on the release of NE. Administration of a monoamine oxidase (MAO) inhibitor, pargyline (70 mg/kg) resulted in a 20-fold NE increase by nerve stimulation, implying that the bulk of the amine does not reach the systemic circulation due to an active MAO. Methacholine (1 and 10 micrograms/ml) inhibited NE release by nerve stimulation. This inhibition was abolished by atropine (5 micrograms/ml). It is suggested that a muscarinic inhibitory mechanism may regulate the NE release in the lung. PGE2 (100 ng/ml), but not PGS2alpha, (100 ng/ml), depressed NE release during nerve stimulation, whereas indomethacin (10 mg/kg) enhanced NE release before, during, and after nerve stimulation in seemingly normal animals. This indicates the existence of another presynaptic inhibitory mechanism for NE release in the lung: a PGE-mediated inhibition.
Stimulation of arteriolar number by salbutamol in spontaneously hypertensive rats
Authors: Dusseau J. W. , Hutchins P. M.
Published: December 2017

Experiments were performed to study beta2-adrenergic involvement in arteriolar development in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. Newly weaned 20-day WKY and SHR rats were injected with salbutamol, a selective beta2-agonist (50 microgram/day sc, plus 5 mg/100 ml in drinking water), for 20 days. At 40 days, under 2% chloralose-7.5% urethan anesthesia (6 ml/kg), either the cremaster muscle was prepared for in vivo microscopy to estimate the number and diameter of open arterioles or the arterioles were injected with latex to determine the total number of arterioles and their maximal diameters. Control SHRs had 62% (P less than 0.01) fewer open arterioles and a 32% (P less than 0.001) reduction in the total number of arterioles compared to WKY controls. Salbutamol stimulated 67% (P less than 0.001) and 22% (P less than 0.05) increases in total number of the smallest arterioles in the SHR and the WKY, respectively. Salbutamol also significantly reduced the maximum diameter of latex-injected arterioles. These results suggest that the decreased arteriolar density in the cremaster muscle of SHR rats may result from differences in the beta-adrenergic mechanism.
Role of receptor elements in baroceptor resetting
Authors: Sapru H. N. , Krieger A. J.
Published: December 2017

Spontaneously hypertensive rats (SHR), 4 wk of age, were treated with antihypertensive agents for 40 wk. The treatment was withdrawn for 2 wk so that the animals experienced hypertension for about 1 wk. The aortic arch was then perfused and aortic nerve activity was recorded. The threshold pressure was 140 mmHg in these SHR. This threshold pressure was less than that observed in age-matched untreated SHR (160--180 mmHg) but greater than that observed in age-matched Kyoto-Wistar rats (80--120 mmHg), indicating partial baroceptor resetting. No significant changes were observed in the vascular wall in these SHR, and partial baroceptor resetting was completely reversed when short duration of hypertension was reversed. On the other hand, baroceptor resetting in untreated SHR was always accompanied by significant changes in vascular wall, and reversal of baroceptor resetting was contingent upon regression of vascular wall hypertrophy. Partial baroceptor resetting in absence of significant changes in vascular wall may be explained by adaptation of baroceptors to persistent high blood pressure.
An automatic cardiac action potential duration meter
Authors: Lab M. J. , Child R. K.
Published: December 2017

The duration of a cardiac action potential (AP) is measured from the beginning of its upstroke to the end of its asymptotic repolarization phase: the end being given by a point in proportion to the AP amplitude. If the resting potential, AP amplitude, as well as the duration, alter simultaneously, frequent accurate measurements can be extremely tedious. A fully automatic AP duration meter has thus been constructed to cope with these difficulties while measuring within about 2% on a beat-to-beat basis. It is suitable either for brief sampling of AP durations when recording with microelectrodes, which may impale cells intermittently, or for continuous monitoring, as with suction electrodes on intact beating hearts in situ. For example, the device can faithfully track changes in duration during periods of regional myocardial ischemia in intact ventricles in situ while the AP alters its base line, upstroke velocity, amplitude, and duration.
Prevention of salt-induced hypertension in the Dahl strain by 6-hydroxydopamine
Authors: Takeshita A. , Mark A. L. , Brody M. J.
Published: December 2017

Salt-induced hypertension in Dahl's genetically hypertensive rat has been attributed to humoral or renal factors. However, a recent study from our laboratory suggested that neurogenic mechanisms contribute to salt-induced increased in hindquarters vascular resistance in Dahl salt-sensitive (S) rats. In the present study, we examined the hypothesis that (chemical sympathectomy) with 6-hydroxydopamine (6-OHDA) prevents salt-induced hypertension and increased vascular resistance in S rats. Hypertension did not develop during high-salt diet (8% NaCl) in S rats treated with 6-OHDA, (75--100 mg/kg ip), whereas in rats treated with vehicle, hypertension developed after 4 wk of high salt diet. Chow consumption, sodium excretion, and weight gain were not altered by 6-OHDA. Hindquarters vascular resistance and neurogenic vasoconstrictor tone were significantly lower in S rats treated with 6-OHDA than in S rats treated with vehicle. 6-OHDA also significantly reduced responses to direct sympathetic nerve stimulation and tyramine. These results suggest that an intact sympathetic nervous system plays an essential role in the development of salt-induced increase in blood pressure in Dahl S rats.
Extracellular space, water, and ion concentration in the hypertrophied rat myocardium
Authors: Mavroudis C. , Jester J. A. , Jacobs S. , Ebert P. A.
Published: December 2017

Extracellular space (ECS), water, and intracellular ion concentration were determined in the normal and hypertrophied rat myocardium. Theoretical measurements of myocardial ECS based on a mathematical model (9.31%) closely approximated the observed results in the normal myocardium (12.8%) and hypertrophied myocardium (11.7%). Observed results confirmed theoretical considerations of no change in ECS with hypertrophy. ECS and water content were higher in the right ventricle than the left ventricle, but intracellular electrolytes remained unchanged. Myocardial hypertrophy did not alter these relationships.
An explanation of impaired solute mixing in extracellular fluid after hemorrhagic hypotension
Authors: Small A. , Homer L. D.
Published: December 2017

A theory is presented suggesting that the slowed rate of solute dispersion in the extracellular fluid (ECF) space during or after hemorrhagic shock is largely due to a depressed cardiac output, and that mixing may be improved by any fluid therapy that decreases the mean recirculation time for the solute. This theory was tested by comparing solute mixing rates after treatment of shocked anesthetized dogs with either protein-free Ringer solution with Ringer solution containing 5% albumin. The rate of mixing was determined by computer analysis of the disappearance of an ECF tracer from plasma. Compared with Ringer-treated dogs, the albumin-treated group had a faster rate of tracer equilibration, larger cardiac plasma output, and smaller, approximately normal ECF volume. It was concluded that the abnormal dispersion of solute within the ECF space seen during or after hypotension can be corrected simply by restoring the cardiac output, and that albumin-containing fluid may be more effective in this regard than crystalloid solution alone.
Effect of implant duration on in vivo sensitivity of electromagnetic flow transducers
Authors: Astley C. A. , Hohimer A. R. , Stephenson R. B. , Smith O. A. , Spelman F. A.
Published: December 2017

Twenty-three electromagnetic flow transducers with lumen diameters of 3.5-6.0 mm were implanted in rhesus monkeys and baboonss for 12 h to 120 days. Each flow transducer was calibrated 1) in vitro on dialysis tubing with saline before implantation, 2) in vivo the last day of the implant period, and 3) again in vitro after the flow transducer was recovered. Three other flow transducers were implanted on femoral arteries of baboon just central to an arteriovenous Silastic shunt, and were calibrated in vivo daily for 23-47 days. In vitro sensitivity was not affected by implant durations of up to 120 days. In vivo sensitivity fluctuated unpredictably for the first 3-4 wk of implant, after which it followed a systematic course that depended on the lumen size. In vivo sensitivity at any time during implant (after the initial period) could be accurately predicted by knowing either the in vitro sensitivity or the terminal in vivo sensitivity.
Valvar subcoronary aortic stenosis in dogs
Authors: Allard J. R. , O'Neill M. J. , Hoffman J. I.
Published: December 2017

A technique for producing valvar aortic stenosis is described. The noncoronary sinus of Valsalva is plicated externally at a level proximal to the origin of the coronary arteries. The major intraoperative problems are hemorrhage, acute left ventricular failure, and heart block, all of which can be avoided. The survival rate in 26 dogs was 54% and all the survivors remained active. Moderate left ventricular hypertrophy was produced.
Increased free fatty acid turnover in CSF during hypotension in dogs
Authors: Fritschka E. , Ferguson J. L. , Spitzer J. J.
Published: December 2017

Cerebrospinal fluid turnover rates of FFA were investigated using ventriculocisternal perfusion techniques. Seven conscious dogs were perfused over a 6-h period from the lateral ventricle to the cisterna magna with mock cerebrospinal fluid (CSF) containing [14C]palmitate and 100 mumol/l of FFA. One hundred and twenty minutes of perfusion were allowed to establish equilibrium of the FFA concentration in the ventricular space. Moderate hemorrhage hypotension was then induced (MABP greater than 60 mmHg) for 3 h, followed by rapid retransfusion and a final hour of perfusion. Cerebral blood flow did not change significantly (45 +/- 6 before, 53 +/- 6 after hemorrhage, and 47 +/- 5 ml.min-1. 100 g-1 after retransfusion). Cerebral arteriovenous difference of O2, glucose, and pH increased significantly during hemorrhage. Hypotension was accompanied by an increased turnover of FFA from 60 to 120 nmol/min (P less than 0.01) in the CSF. FFA turnover was directly correlated with the fatty acid concentration of the CSF (r = 0.77). It is speculated that the increased fatty acid turnover during hypotension may indicate increased phospholipid turnover and/or increased oxidation by tissues lining the ventricular space.
Humoral regulation of vascular resistance after 30 days of pulmonary artery constriction
Authors: McNamara R. F. , Schmid P. G. , Schmidt J. A. , Lund D. D. , Bhatnagar R. K.
Published: December 2017

In an earlier study of guinea pigs with constriction of the pulmonary artery (PA) for 30 days, hindquarters' vascular resistance was maintained primarily by humoral mechanisms. In the present study, we investigated the contribution of circulating catecholamines, angiotensin II, and other constrictor stimuli to hindquarters' vascular resistance by observing vasodilator responses to specific competitive antagonists. Pressure-flow curves indicated vascular resistances in isolated, perfused, sympathectomized hindquarters of anesthetized guinea pigs. Phentolamine produced significantly greater (P less than 0.05) vasodilatation in animals with constriction of pulmonary artery than in sham animals [Sar1-Ala8]angiotensin II produced no vasodilation in either group. After alpha-adrenergic blockade, papaverine produced similar vasodilatation and similar final perfusion pressures in both groups. It appears that circulating catecholamines and augmented vasoconstrictor responsiveness to norepinephrine are totally responsible for the increased humoral regulation of vascular resistance in this experimental model of right ventricular hypertrophy.
Flow and power output of right ventricle facing load with variable input impedance
Authors: Piene H. , Sund T.
Published: December 2017

The output from the right ventricle (RV) was studied at different load impedances. Isolated cat hearts were perfused with Tyrode solution with erythrocytes. Coronary perfusion pressure and RV end-diastolic pressure were kept constant. The RV pumped into an artificial hydraulic load with independently variable resistance (R) and compliance (C). Mean RV flow (RVO) decreased after R increase or C reduction. For each heart, RVO and mean RV pressure were linearly related. The slope of the regression line is interpreted as an "apparent source resistance" (Rs). Rs was on average 3.4 X 10(3) (dyn.s.cm-5). The static hydraulic power output was maximum at a certain load R (Rm). Rm was C dependent at an average high C of 5 X 10(-5) dyn-1.cm5, Rm was 9.4 X 10(3) dyn.s.cm-5 on average and shifted to 5.4 X 10(3) at low C (avg 0.8 X 10(-5). Theoretical considerations show that Rm/Rs will be equal to total heart period divided by ejection period in the extreme case C leads to infinity, and Rm/Rs leads to 1 when C leads to 0. Experimentally, Rm/Rs was 2.4 (avg) for high C, and approached 1 for low C, which fits the theoretical predictions. The results indicate that high C facilitates the matching between the right heart and the vascular resistance in the lung.
Myocardial relaxation. I. Effect of nitroprusside on the tension prolongation phenomenon
Authors: Gaasch W. H. , Bing O. H.
Published: December 2017

The effects of nitroprusside and cyanide on myocardial relaxation were studied during hypoxia and reoxygenation of isolated rat papillary muscle, and during segmental ischemia and reperfusion in the intact dog heart. Nitroprusside did not affect isolated muscle performance before or during hypoxia. During reoxygenation of hypoxic muscles, the tension prolongation phenomenon (which characterizes abnormal or prolonged relaxation) was only slightly attenuated by the addition of nitroprusside to the muscle bath; in contrast, cyanide (at concentrations that did not prevent the return of tension) abolished tension prolongation during reoxygenation. During reperfusion of ischemic segments in intact hearts, the prolongation of segment tension was not affected by systemic administration of nitroprusside, but was abolished by intracoronary cyanide. Attenuation of the tension prolongation phenomenon by nitroprusside in the isolated muscle may be due to the liberation of cyanide. Inasmuch as nitroprusside did not affect the tension prolongation phenomenon in the intact heart, it is unlikely that the influence of this drug on left ventricular diastolic compliance is mediated through an alteration in the tension prolongation phenomenon.
Laser scanner measurement of central segment performance in isolated cardiac muscle preparations
Authors: Wiegner A. W. , Bing O. H.
Published: December 2017

A laser scanning system has been developed to facilitate the study of isolated cardiac muscle by excluding the possibly damaged tissue at the ends of the preparation. The laser scanner monitors the length of a central segment of the muscle that has been delineated by markers consisting of single loops of 8-0 silk suture. Focused laser light traverses the length of the muscle at 150 Hz. Scattered light is detected by a photodiode and the length of the central segment is calculated electronically. This system provides an accurate measure of central segment length in both resting and active muscle with no apparent damage to the preparation.
Early changes in collateral blood flow during myocardial infarction in conscious dogs
Authors: Jugdutt B. I. , Becker L. C. , Hutchins G. M.
Published: December 2017

We studied the early changes in collateral blood flow (CBF) after acute coronary artery occlusion and the relation of these changes to subsequent necrosis. We measured CBF with 7--9 microns radioactive microspheres before and at various times after circumflex artery occlusion in 42 conscious dogs that were killed 48 h later. CBF increased from 20 s postocclusion to later measurements (5 min, 15 min, 1 h, or 6 h) and did so in both necrotic and nonnecrotic areas of the occluded bed. However, the increase in CBF over time was not gradual, but appeared to occur between 20 s and 5 min, with no further changes for up to 6 h. There was a gradation of CBF in the occluded bed, from periphery to center and subepicardium to subendocardium. Central and subendocardial regions with CBF less than 0.40 ml-min-1-g-1 at 5--15 min postocclusion subsequently showed necrosis whereas epicardial and lateral regions with CBF greater than 0.50 ml/min did not. Thus CBF increases very early throughout the occluded coronary bed, and the level of CBF by 5 min appears to determine whether necrosis ultimately occurs.
Myocardial cation contents during induction of calcium paradox
Authors: Alto L. E. , Dhalla N. S.
Published: December 2017

Myocardial cation contents were measured in isolated rat hearts perfused under various conditions. Reperfusion of Ca2+-deprived hearts produced marked increases in myocardial Ca2+ and Na+ and decreases in Mg2+ and K+ contents. These changes were dependent on the Ca2+ concentration and duration of perfusion during the periods of Ca2+ deprivation and reperfusion. The loss of Ca2+ and K+ contents normally seen after Ca2+-free exposure as well as the reperfusion-induced changes were prevented if the Ca2+-free medium contained low (35 mM) Na+ or was cooled to 21 degrees C. Reperfusion with normal Ca2+, low Na+ medium augmented the increase in myocardial Ca2+ content, while reducing K+ or Mg2+ or increasing Mg2+ in the reperfusion medium had no effect. Addition of verapamil, D600, or propranolol to the reperfusion solution did not alter the reperfusion-induced cation changes observed using control medium. These data suggest that during Ca2+ depletion, the mechanisms responsible for regulating calcium influx are either lost or inactivated, so that reperfusion-induced changes are governed solely by the driving force favoring calcium influx. The occurrence of Ca2+ overload under this condition has been implicated in the irreversible damage to myocardium and contractile failure.
Validation of dynamic radiography in the dog and evaluation of ischemic dyssynergy
Authors: Nellis S. H. , Liedtke A. J. , Heimer M. L. , Shiroff R. A. , Jacobs A. M. , Kenney E. S. , Weidner W. A. , McInerney J. J. , Zelis R.
Published: December 2017

If a collimated radiation detector (sodium iodide crystal) and a collimated X-ray source are positioned at right angles, scattered radiation will be sensed and the detector will generate a signal as tissue enters and leaves the "sensitive volume" formed by the intersection of the field of view of the detector and incident beam. This technique, called dynamic radiography, was used to identify and quantify the components of epicardial motion in anesthetized open-chested dogs. The data so obtained were validated by two independent optical methods: biplane cinematography and a technique that measures the shadow cast by the heart using a light beam-cadmium sulfide photocell. Displacement measured by dynamic radiography appeared to be the time integral of the scalar product of the velocity vector and the vector normal to the surface area within the sensitive volume, i.e., that component of displacement of myocardial mass that was perpendicular to the surface of the myocardium. In other words, the dynamic radiographic signal was proportional to the mass of tissue within the sensitive volume. Good agreement in terms of absolute motion, its direction, and phase was noted between predicted dynamic radiographic signals and those observed. Thus validated, this technique was found to be reliable in quantifying motion abnormalities produced by acute coronary ligation.
Role of carotid sinus and cardiopulmonary reflexes on left ventricular dP/dt in cats
Authors: Shimizu T. , Bishop V. S.
Published: December 2017

Interaction between vagally mediated cardiopulmonary receptors and carotid sinus baroreceptors was studied in regard to cardiac contractility in anesthetized cats using vagal cold block and carotid occlusion. Cold block of the vagi produced a small but significant increase in left ventricular dP/dt and in arterial pressure. Carotid occlusion caused a greater increase in both parameters. The effects of each of these individual procedures were significantly greater when either intervention was tested in combination with the other. Cardiac sympathectomy reduced but did not abolish the reflex increase in cardiac contractility due to either procedure. Subsequent beta-adrenergic blockade eliminated the reflex change in the contractility. The study demonstrates that 1) both cardiopulmonary and carotid sinus baroreceptors participate in the neural control of cardiac contractility with the latter's role being dominant; 2) there is an apparent interaction between the two reflex mechanisms in which one reflex system acts to compensate the other's effects.
Supernormal conduction in the canine bundle of His and proximal bundle branches
Authors: Spear J. F. , Moore E. N.
Published: December 2017

We used close bipolar intramural electrodes and catheter electrodes to study the characteristics of conduction in the bundle of His and proximal bundle branches during premature atrial beats in 17 open-chest anesthetized dogs. The electrophysiological properties of the proximal conducting system were heterogenous. The shortest interval between a normal His bundle response and a premature response that was not accompanied by changes in conduction time (the total recovery time) was 258.8 +/- 23.9 (SD) ms for the proximal His and 310.7 +/- 30.6 ms for the distal His and proximal bundle branches. A period of supernormal conduction, in which the conduction times of premature beats were faster than during earlier or later beats, was localized to the distal portion of the bundle of His and proximal bundle branches. The minimal conduction time during the supernormal period was decreased by 9.6 +/- 4.6% below control diastolic conduction times, and the supernormal period was 61.0 +/- 25.7 ms in duration. The characteristics of the period of supernormal conduction in the distal bundle of His and proximal bundle branches were very similar to those previously found in the peripheral bundle branch-Purkinje system. The mechanism of supernormal conduction in the bundle of His is most probably due to a period of supernormal excitability.
Indirect mean arterial pressure in the anesthetized dog
Authors: Geddes L. A. , Combs W. , Denton W. , Whistler S. J. , Bourland J. D.
Published: December 2017

Using the oscillometric method, indirect mean arterial pressure was measured in 14 pentobarbital-anesthetized dogs (8-24 kg) with mean arterial pressure ranging from 23 to 160 mmHg. The effect of cuff size, in relation to forelimb circumference was investigated. Indirect mean arterial pressure agreed with direct mean arterial pressure when the cuff width was about 40% of the forelimb circumference.
Dependence of pial arteriolar response to hypercapnia on vessel size
Authors: Wei Enoch P. , Kontos Hermes A. , Patterson John L.
Published: December 2017

The responses of pial arterioles to changes in PaCOCO2 were studied in anesthetized cats equipped with cranial windows for the observation of the pial microcirculation. The percentile increase in vessel caliber induced by hypercapnia was size dependent, with the smaller vessels responding more vigorously than the larger ones. In contrast, the vasoconstrictor responses to arterial hypocapnia were size independent. Following topical application of phentolamine (10−5 M), or after ipsilateral extirpation of the superior cervical ganglion, the increase in arteriolar caliber caused by moderate hypercapnia (5% CO2 inhalation) in the larger arterioles (>100 μm in diameter) increased and became equal to that of the smaller arterioles (<100 μm in diameter). The response to hypocapnia was not affected by phentolamine. The results indicate that a major reason for the greater responsiveness of smaller vessels to moderate hypercapnia is the fact that the response of the larger vessels is limited by neurogenic vasoconstriction resulting from increased activity of adrenergic nerves originating from the cervical sympathetic chain. The absence of an influence of the sympathetic nervous system on the responses to hypocapnia is explained by the lack of significant resting neurogenic vasoconstrictor tone in pial arterioles of anesthetized cats.

cat; phentolamine; adrenergic nerves; neurogenic control of cerebral vessels

Submitted on July 20, 1979

Accepted on January 4, 1980
Contribution of viable and nonviable heart myocytes to substrate oxidation
Authors: Long W. M. , Bagby G. J. , Spitzer J. J.
Published: December 2017

An approach is described that allows metabolic data obtained from a mixture of vital dye-excluding (T-) and nonexcluding (T+) myocytes to be extrapolated to a homogeneous cell population. Myocytes from adult dog hearts were dispersed by enzymatic treatment and separated into two fractions: one containing predominantly T-, and the other containing predominately T+ cells. Measuring the oxidation rate and viability of each fraction allows the determination of the rate of oxidation of a homogeneous cell population when palmitate, glucose, or lactate is the oxidizable substrate. The calculated rate of oxidation of these substrates by 100% T- cells was: 0.15, 0.46, and 2.99 nmol . mg protein-1 . min-1, respectively. Oxidation of palmitate and lactate by T+ cells was one-fifth of the T-cell rate. Glucose oxidation of T+ cells was not significantly different from zero. Use of this procedure will permit study of myocardial metabolism when experimental procedures may cause altered cell viability.