Decrease In Systemic Pressure Research Articles

Influence of beta-rhythm neurofeedback on the functional state of the cardiovascular system of athletes

BACKGROUND: The study of the effects of urgent and long-term adaptation of the cardiovascular system of athletes under the influence of beta-rhythm neurofeedback expands its corrective and restorative potential for use in the practice of sports medicine and rehabilitation.
 AIMS: Study of the restorative and rehabilitation potential of the influence of beta-rhythm neurofeedback on the functional state of the cardiovascular system of athletes.
 MATERIAL AND METHODS: The course of neurofeedback on the beta rhythm of the brain consisted of 10 sessions, including a graphical and game version of the representation of the controlled parameter (beta rhythm) on the computer monitor screen, the success of controlling the beta rhythm with the specified conditions of voluntary muscle relaxation during the session was supported by visual and auditory biological feedback. Registration of indicators of the cardiovascular system was carried out before and after the 1st, 5th and 10th sessions of the course, the dynamics during the course and individual sessions is represented by the growth rate (%) of the indicators.
 RESULTS: A course of neurofeedback on the beta-rhythm of the brain of 10 sessions were young athletes (n=1020) aged 1821, representatives of cyclic, acyclic and game sports in the preparatory period of the training cycle.
 The effects of urgent adaptation in athletes at the 1st session of the neurofeedback course according to the beta-rhythm of the brain are reflected by positive changes in the strengthening of the vagal influence of the parasympathetic nervous system on the functional state of the cardiovascular system, expressed in a decrease in heart rate, systemic pressure, performance and pumping functions of the heart, in the transition of the type of regulation of blood circulation from the unfavorable hyperkinetic type to the physiological ― eukinetic ― type. At the same time, the load on the peripheral vascular bed increased, especially on its precapillary section.
 The effects of long-term adaptation at the 10th session of the neurofeedback course according to the beta-rhythm of the brain are represented by systemic rearrangements with an increased influence of the parasympathetic nervous system in the functioning of the cardiovascular system of athletes, reflected in the maximum decrease in heart rate throughout the course, in an equivalent decrease in systemic pressure, stabilization of performance and pumping function of the heart, achievement and preservation of the eukinetic type of regulation of blood circulation, achievement of a stable stable state of the central and peripheral vascular bed with a slight response to environmental factors.
 CONCLUSION: A course of neurofeedback on the beta-rhythm of the brain of 10 sessions helps to reduce stress in the functioning of the cardiovascular system of athletes by enhancing the vagal influences of the parasympathetic nervous system, has a positive effect on heart rate, systemic pressure, performance and pumping function of the heart; promotes the transition from an unfavorable hyperkinetic to a physiological eukinetic type of circulatory regulation; has a positive effect on adaptive changes in indicators of general and peripheral vascular resistance. The revealed effects of the course of neurofeedback on the beta-rhythm of the brain are of a pronounced corrective and restorative nature during the intense functioning of the cardiovascular system of athletes and can be used in sports rehabilitation and rehabilitation practice.

Modeling and analysis of steam-water two-phase flow distribution and wall temperature distribution in parallel heated pipes with different manifold types

In solar tower receiver, boiler water-wall and various heat exchangers, the uneven distribution of two-phase flow often occurs among parallel heated pipes, which seriously reduces the operating efficiency and may further induce heat transfer deterioration and soaring wall temperature. In this paper, a coupling model for the flow distribution and heat transfer process of steam-water two-phase flow in parallel heated pipes was established based on the discrete methods. In the present model, two main improvements were proposed as below. On one hand, the calculated equations for the pressure drop and the phase distribution of two phase fluid in both the combining T-junction and dividing T-junction were established to consider the coupling effects of the inlet manifold and outlet manifold on the flow distribution characteristics. On the other hand, the calculation module for the heat transfer and wall temperature along the branch pipes was also coupled in the present model with considering of different heat transfer regions (saturated nucleate boiling region, liquid deficient region, and superheated steam region) along the pipe. The present model was then verified and used to investigate the effects of system pressure, inlet fluid flow, inlet steam quality and manifold type on the flow distribution characteristics of high temperature and high pressure steam-water in parallel vertical upward pipes, and the effect of the uneven distribution of the gas-liquid two phases on the system safety was analyzed and evaluated. It was found that gas phase preferentially enters the first branch pipe near the inlet of the dividing manifold affected by buoyancy, and this results that the inlet steam quality of the corresponding branch pipe is always obviously higher than that of the subsequent pipes. As the system pressure decreases, the outlet fluid enthalpy distribution and outlet wall temperature distribution among branch pipes become more uneven. Moreover, the outlet fluid enthalpy and outlet wall temperature of the branch pipes closer to the inlet of the dividing manifold increase sharply with the decrease of system pressure. In the U-type parallel pipe system, the branch pipes away from the inlet of the dividing manifold are more prone to wall overheating at the outlet, while the opposite is true for the Z-type parallel pipe system.

Experimental study on the condensation characteristics of nitrogen with non-condensable gas

The non-condensable gas at the top of the main condenser of the distillation section, such as helium or neon, would lower the heat transfer efficiency and the productivity of the air separation plant. Current research mainly focuses on the study of the water vapor condensation mechanism with non-condensable gases, while those on cryogenic fluids are rare. In this work, an experimental setup was designed to study the condensation mechanism of pure nitrogen vapor and nitrogen vapor mixed with helium on the vertical plate. The experimental data of pure nitrogen vapor is in good agreement with the results calculated by the classical Nusselt model, which demonstrates that the experimental system has high reliability. The influences of the mass fraction of helium and system pressure on the condensation heat transfer coefficient are analyzed. Results show that even a very low mass fraction of helium can cause the condensation heat transfer coefficient of nitrogen vapor to decrease obviously. The deviation between the heat transfer coefficient of the nitrogen-helium mixture and pure nitrogen increases with the increases of the helium mass fraction and the decrease of system pressure. A new condensation heat transfer correlation for nitrogen with helium is developed that the deviations of most of its predictions are within 20% compared to the experimental data.

Adenosinergic regulation of the cardiovascular system in the red-eared slider Trachemys scripta

Few studies have investigated adenosinergic regulation of the cardiovascular system in reptiles. The haemodynamic effect of a bolus intra-arterial adenosine injection (2.5μMkg−1) was investigated in nine anaesthetised red-eared sliders (Trachemys scripta). Adenosine caused a transient bradycardia, which was accompanied by systemic vasodilatation as evidenced by an increase in systemic flow and a decrease in systemic pressure. Meanwhile, pulmonary flow fell significantly. Both the bradycardia and increase in systemic conductance were significantly attenuated by theophylline (4mgkg−1), demonstrating an involvement of P1 receptors. These results suggest that adenosine is likely to play a significant role in reptile cardiovascular physiology. In turtles specifically, adenosinergic regulation may be particularly relevant during periods of apnoea.

Recovery of methane from hydrate reservoir with gaseous carbon dioxide using a three-dimensional middle-size reactor

Three groups of hydrate-bearing sediment samples with/without underlying gas were prepared using a three-dimensional middle-size reactor to investigate the favorable conditions for methane recovery from hydrate reservoir with gaseous CO2. The experimental results indicated that hydrate reservoir with underlying free gas, high saturation of free gas and low saturation of water is appropriate for recovering CH4 with CO2. For the replacement mechanism, it is assumed that the CO2–CH4 replacement chiefly includes two parts: CH4 hydrate dissociation and mixed hydrate re-formation from the dissociated water and free water. In the re-formed hydrate, CO2 molecules mainly occupy the large cage and CH4 molecules mainly occupy the small cage. A kinetics model was constructed to describe the replacement process, which considers not only the kinetic reaction of CH4–CO2 replacement but also the reaction between CO2 and free water. The calculated results agree well with the experimental data. The influencing factors on the replacement rate were also discussed according to the developed model. It is found that the replacement rate and the mole fraction of CH4 in gas phase increase with the increase of initial CO2 mole fraction, the decrease of system pressure, and the increase of diffusion coefficient of CH4 in hydrate layer.

Silica-Grafted Diethylzinc and a Silsesquioxane-Based Zinc Alkyl Complex as Catalysts for the Alternating Oxirane−Carbon Dioxide Copolymerization

A novel zinc silsesquioxane complex ([(c-C5H9)7Si7O11(OSiMePh2)]2Zn4Me4 (1)) has been used as a model compound for silica-grafted zinc catalysts in the copolymerization of cyclohexene oxide and CO2. Complex 1 exists as a dimer in the solid state and is moderately active in the copolymerization, and polycyclohexene carbonates have been obtained with a carbonate content of 79−98%. Polymerizations with ZnEt2-treated silica particles resulted in polymer particles with Mn and Mw values and carbonate contents comparable to those of the polymers obtained with 1. It was further demonstrated that CO2 consumption can be followed online by monitoring the decrease of system pressure during the reaction. CO2 consumption has been interpreted in relation to both polycarbonate and cyclic carbonate formation. These measurements represent the intrinsic kinetics of this reaction, which appear to be directly related to CO2 pressure.

Evidence that neurotensin mediates postprandial intestinal hyperemia in the python,Python regius

Digestion of large meals in pythons produces substantial increases in heart rate and cardiac output, as well as a dilation of the mesenteric vascular bed leading to intestinal hyperemia, but the mediators of these effects are unknown. Bolus intra-arterial injections of python neurotensin ([His(3), Val(4), Ala(7)]NT) (1 - 1,000 pmol/kg) into the anesthetized ball python Python regius (n = 7) produced a dose-dependent vasodilation that was associated with a decrease in systemic pressure (P(sys)) and increase in systemic blood flow (Q(sys)). There was no effect on pulmonary pressure and conductance. A significant (P < 0.05) increase in heart rate (f(H)) and total cardiac output (Q(tot)) was seen only at high doses (>30 pmol/kg). The systemic vasodilation and increase in Q(tot) persisted after beta-adrenergic blockade with propranolol, but the rise in f(H) was abolished. Also, the systemic vasodilation persisted after histamine H(2)-receptor blockade. In unanesthetized pythons (n = 4), bolus injection of python NT in a dose as low as 1 pmol/kg produced a significant increase in blood flow to the mesenteric artery (177% +/- 54%; mean +/- SE) and mesenteric conductance (219% +/- 74%) without any increase in Q(sys), systemic conductance, P(sys), and f(H). The data provide evidence that NT is an important hormonal mediator of postprandial intestinal hyperemia in the python, but its involvement in mediating the cardiac responses to digestion may be relatively minor.

Endothelin-1 causes systemic vasodilatation in anaesthetised turtles(Trachemys scripta) through activation of ETB-receptors

The effects of endothelin-1 (ET-1) on systemic and pulmonary circulation were investigated in anaesthetised freshwater turtles (Trachemys scripta) instrumented with arterial catheters and blood flow probes. Bolus intra-arterial injections of ET-1 (0.4-400 pmol kg(-1)) caused a dose-dependent systemic vasodilatation that was associated with a decrease in systemic pressure (P(sys)) and a rise in systemic blood flow (Q(sys)), causing systemic conductance (G(sys)) to increase. ET-1 had no significant effects on the pulmonary vasculature, heart rate (fh) or total stroke volume (Vs(tot)). This response differs markedly from mammals, where ET-1 causes an initial vasodilatation that is followed by a pronounced pressor response. In mammals, the initial dilatation is caused by stimulation of ET(B)-receptors, while the subsequent constriction is mediated by ET(A)-receptors. In the turtles, infusion of the ET(B)-receptor agonist BQ-3020 (150 pmol kg(-1)) elicited haemodynamic changes that were similar to those of ET-1, and the effects of ET-1 were not affected by the ET(A)-antagonist BQ-610 (0.15 micromol kg(-1)). Conversely, all effects of ET-1 were virtually abolished after specific ET(B)-receptor blockade with the ET(B)-antagonist BQ-788 (0.15 micromol kg(-1)). The subsequent treatment with the general ET-receptor antagonist tezosentan (15.4 micromol kg(-1)) did not produce effects that differed from the treatment with ET(B)-antagonist, and the blockade of ET-1 responses persisted. This present study indicates, therefore, that ET(B)-receptors are responsible for the majority of the cardiovascular responses to ET-1 in Trachemys.

The role of nitric oxide in the regulation of the systemic and pulmonary vasculature of the rattlesnake, Crotalus durissus terrificus

The functional role of nitric oxide (NO) was investigated in the systemic and pulmonary circulations of the South American rattlesnake, Crotalus durissus terrificus. Bolus, intra-arterial injections of the NO donor, sodium nitroprusside (SNP) caused a significant systemic vasodilatation resulting in a reduction in systemic resistance (Rsys). This response was accompanied by a significant decrease in systemic pressure and a rise in systemic blood flow. Pulmonary resistance (Rpul) remained constant while pulmonary pressure (Ppul) and pulmonary blood flow (Qpul) decreased. Injection of L-Arginine (L-Arg) produced a similar response to SNP in the systemic circulation, inducing an immediate systemic vasodilatation, while Rpul was unaffected. Blockade of NO synthesis via the nitric oxide synthase inhibitor, L-NAME, did not affect haemodynamic variables in the systemic circulation, indicating a small contribution of NO to the basal regulation of systemic vascular resistance. Similarly, Rpul and Qpul remained unchanged, although there was a significant rise in Ppul. Via injection of SNP, this study clearly demonstrates that NO causes a systemic vasodilatation in the rattlesnake, indicating that NO may contribute in the regulation of systemic vascular resistance. In contrast, the pulmonary vasculature seems far less responsive to NO.

Use of a tantalum-178 generator and a multiwire gamma camera to study the effect of the Mueller maneuver on left ventricular performance: Comparison to hemodynamics and single photon emission computed tomography perfusion patterns

During the Mueller maneuver, there is a decrease in intrathoracic pressure and an increase in transmural left ventricular pressure. The changes in loading conditions cause transient left ventricular dysfunction. This study examined the effects of the Mueller maneuver on left ventricular performance using tantalum (Ta)-178 (half-life 9.3 min) and a multiwire gamma camera. First-pass radionuclide angiograms were obtained at baseline and during Mueller maneuver in 41 patients aged 58 ± 10 years. In 34 patients, stress single photon emission computed tomography (SPECT) myocardial perfusion imaging with thallium-201 or sestamibi was also performed. Hemodynamic measurements during the Mueller maneuver ( n = 10) showed a decrease in systemic pressure (139 ± 25 mm Hg vs 123 ± 24 mm Hg, p < 0.001) and pulmonary artery pressure (24 ± 6 mm Hg vs 14 ± 12 mm Hg, p = 0.01) and an increase in heart rate (67 ± 10 bpm vs 75 ± 14 beats/min, p = 0.001). Among the 34 patients who had perfusion imaging, the left ventricular ejection fraction remained unchanged or increased in 17 patients (group 1) (48% ± 19% vs 49% ± 21%, p not significant) and decreased (≥5%) in 17 patients (group 2) (55% ± 13% vs 40% ± 16%, p = 0.001). The stress SPECT images showed no or only fixed defects in 11 (65%) patients in group 1 and 3 (18%) patients in group 2 ( p = 0.02), and reversible defects in 6 (35%) patients in group 1 and 14 (82%) patients in group 2 ( p = 0.04). Group 2 had more regional dysfunction (measured as regional ejection fraction) than group 1 in the anterior wall and inferior walls ( p < 0.05, each). In 31 regions with regional dysfunction the SPECT images showed reversible defects in 18 (58%) segments and fixed defects in 8 (26%) segments. Thus the Mueller maneuver causes transient left ventricular dysfunction in many patients with coronary artery disease, especially those with stress-induced myocardial ischemia.

In pigs, inhaled nitric oxide (NO) counterbalances PAF-induced pulmonary hypertension

In 6 anesthetized mechanically ventilated pigs we have studied the effects of inhalation of 80 ppm of nitric oxide (NO) before and after platelet-activating factor (PAF) administration (50 ng/kg iv). Our results show that NO inhalation causes a decrease in pulmonary arterial pressure and in heart rate without affecting other circulatory parameters. PAF administration causes a pulmonary hypertension and a prompt and brief decrease in systemic pressure. Inhalation of NO reduces the pulmonary hypertension, without completely reversing PAF-dependent vasoconstriction. PAF administration to pigs pretreated with indomethacin produces a lesser increase in pulmonary vascular pressure. In this case, NO inhalation can restore to baseline values. Pretreatment of 3 of the 6 pigs with N G-nitro- l-arginine-methyl-ester did not prevent the prompt and brief PAF-induced systemic hypotension. In conclusion, our results show that NO reduces basal pulmonary vascular tone, acts as a pulmonary vasodilator on PAF-preconstricted vessels and is not involved in the brief systemic hypotension consequent to PAF administration.

Effect of Hemodilution and Resuscitation on Tumor Interstitial Fluid Pressure, Blood Flow, and Oxygenation

Hemodilution due to hemorrhage may increase tumor blood flow (TBF) by lowering blood viscosity and decrease tumor interstitial fluid pressure (TIFP) by moving fluid from the interstitium to the vascular compartment and by lowering microvascular pressure (MVP), mainly due to the decrease in systemic pressure. To test this hypothesis, we measured mean arterial blood pressure (MABP), TIFP, hematocrit, relative TBF (RBC flux), and intratumor p O2 during hemorrhage and volume restitution in severe combined immunodeficient mice, bearing LS174T human colon adenocarcinoma xenografts. MABP and TIFP significantly decreased after 0.2 ml of blood (∼12% of blood volume) was withdrawn. MABP decreased from 87.5 ± 3.9 mmHg (mean ± standard error) to 59.8 ± 4.8 mmHg (n = 5, P = 0.01) within 2.5 rain after the withdrawal of blood and then returned to control value within 10 min. TIFP gradually decreased from 18.7 ± 2.3 mmHg to 11.3 ± 0.9 mmHg after 1 hr (n = 8, P = 0.01), while RBC flux increased by a factor of 1.99 ± 0.38 (n = 5, P = 0.02). The systemic hematocrit decreased from 51.2 to 45.9% (n = 7, P = 0.02). Tumor oxygenation did not significantly improve (median pO2 = for control, 28 mmHg, and median p O2 after blood withdrawal, 32 mmHg; P = 0.14). When 0.2 ml blood was withdrawn and replaced (within 2.5 min) with the same volume of normal saline, MABP significantly decreased from 86.4 ± 2.4 mmHg to 65.6 ± 4.6 mmHg (n = 11) at 1 hr post-treatment (P = 0.001). TIFP decreased, but not significantly, from 24.2 ± 2.9 mmHg to 20.4 ± 2.4 mmHg (P = 0.35). Blood withdrawals in excess of 0.3 ml significantly decreased MABP and TIFP without recovery during 1 hr of observation. Volume restitution with hyperoncotic/hyperosmotic 6.0% Dextran 70 and 7.5% saline had effects attributable to a direct transmission of systemic pressure to the tumor microcirculation and to a lowering of tumor venous resistance. These effects appear to be common to saline blood restitution and volume top-load with Dextran 70. In conclusion, mild hemorrhage (withdrawal of ∼12% of blood volume) can significantly lower TIFP without a reduction in TBF and pO2.

Acute and chronic effects of flosequinan on resting and exercise haemodynamics in congestive heart failure.

1 The acute and chronic (8 weeks) haemodynamic responses to oral flosequinan have been investigated in 12 male patients of mean age 58.9 years with congestive heart failure of N.Y.H.A. classes II and III. 2 Flosequinan 125 mg orally significantly reduced right atrial pressure, pulmonary artery pressure and pulmonary wedge pressure prior to and following 8 weeks chronic treatment (125 mg daily). A significant decrease in systemic pressure and an increase in heart rate were also observed with acute flosequinan prior to chronic treatment. A reduction in systemic vascular resistance and an increase in cardiac index reached significance in response to flosequinan 125 mg orally following 8 weeks of therapy. 3 In the erect position, flosequinan reduced pulmonary wedge pressure and tended to reduce systemic vascular resistance, without decreasing mean arterial pressure. 4 Following chronic treatment, there was a trend towards a reduction in pulmonary wedge pressure and an increase in cardiac index, otherwise resting and exercise haemodynamics were unchanged. 5 The response to flosequinan was similar at week 1 and after 8 weeks of treatment for all of the haemodynamic parameters. 6 Flosequinan increased bicycle exercise times and attenuated exercise-induced increases in pulmonary arterial and systemic pressures. There was a trend towards an increase in treadmill exercise time. 7 Sublingual glyceryl trinitrate (0.5 mg) and oral flosequinan (125 mg) had similar effects on right atrial pressure, pulmonary arterial and pulmonary wedge pressures at 5 min and 2 h respectively post-dosing. A small additive effect on pulmonary arterial and wedge pressures was observed.

Effects of dopexamine on hemodynamics and oxygen consumption after beta blockade in lambs

Dopexamine is a synthetic catecholamine with predominantly beta 2 and dopaminergic adrenergic receptor activities. We investigated its effects on systemic and myocardial hemodynamics and oxygen consumption (VO2) in a newborn species and studied its predominant mechanism of action. Prospective dose-response study with each animal serving as it own control. Eight chronically instrumented, unanesthetized lambs, 9 to 11 days of age. After surgical instrumentation and recovery for 72 hrs, animals were infused with dopexamine at increasing doses (1, 10, and 100 micrograms/kg/min) for 5 mins each before and after beta 1 (metoprolol) and beta 1, beta 2 (propranolol) adrenergic receptor blockade. All studies were performed during normoxia. Heart rate (HR) increased with increasing infusion rates of dopexamine and systemic arterial pressure and vascular resistance decreased. Cardiac index, left ventricular pressure development, and systemic VO2 were unchanged, as was the rate x pressure product. Left circumflex coronary artery blood flow and myocardial VO2 were unaltered. After beta 1-blockade, dopexamine produced an increase in HR and decreased systemic arterial pressure and vascular resistance. After beta 1-adrenergic receptor blockade, no change was noted in systemic or myocardial VO2, coronary blood flow, or rate x pressure product. After beta 1, beta 2-blockade with propranolol, increasing infusion rates of dopexamine resulted in decreases in systemic pressure and vascular resistance. Dopexamine produced significant cardiovascular effects mediated primarily by beta 2-adrenergic receptors, and also produced residual peripheral arterial vasodilation after combined beta 1- and beta 2-blockade. The latter finding suggests that dopaminergic receptor stimulation may partly mediate dopexamine's effects in newborn lambs.

The effects of high (sodium meglumine diatrizoate, Renografin-76) and low osmolar (sodium meglumine ioxaglate, Hexabrix) radiographic contrast media on diastolic function during left ventriculography in patients

Although a majority of studies indicate superior hemodynamic and clinical profiles of low osmolar compared with high osmolar contrast media, the effect of these agents on diastolic left ventricular function has not been examined. We prospectively examined hemodynamic, electrocardiographic, and echocardiographic indices of left ventricular function in patients undergoing contrast ventriculography with a high osmolar, ionic, monomeric contrast, diatrizoate (Renografin-76) compared with a low osmolar, ionic, dimeric contrast, ioxaglate (Hexabrix). Thirty patients were randomized to each group. There were no clinical differences between the two groups. The decrease in systemic pressures was significantly greater with diatrizoate after left ventriculography (−38.5 ± 3.5 versus −18.2 ± 2.3, p < 0.001) and selective left coronary angiography (−29.5 ± 2.4 versus −17.4 ± 2.6, p < 0.001). In addition, left ventricular end-diastolic pressure increased significantly more with diatrizoate (7.3 ± 0.9 versus 2.7 ± 0.8 mm Hg for ioxaglate, p < 0.001). QT interval prolongation occurred in both patient groups. Diatrizoate decreased systemic vascular resistance, and increased cardiac output and left ventricular ejection fraction more than ioxaglate, while simultaneously increasing left ventricular end-diastolic volume and altering the peak atrial filling velocity. Negative dp dt ( p < 0.05), but not Tau, computed by the logarithmic or derivative methods, was reduced by diatrizoate. These data indicate that significant alteration of diastolic filling patterns occurs with high osmolar compared with low osmolar contrast agents. Although the clinical significance of this observation is currently unknown, these data further support the reported hemodynamic superiority of the low osmolar, dimeric contrast agent ioxaglate during contrast angiography.

Pulmonary hypertension in lambs with congenital diaphragmatic hernia: Vasodilator prostaglandins, isoprenaline, and tolazoline

After antenatal induction of diaphragmatic hernias in fetal lambs, prostaglandins D2, E1, and I2 were compared to tolazoline, or isoprenaline, for the treatment of pulmonary hypertension. When rendered hypoxic, these, and normal lambs, showed an increase in pulmonary artery pressure, a decrease in systemic pressure, and a decrease in pulmonary blood flow. All of the drugs altered that response, but to different degrees. None of the drugs tested was consistently successful in reversing the adverse affects of hypoxia, but prostaglandin D2 came closest to the ideal vasodilator, decreasing the pulmonary artery pressure in all seven hypoxic lambs having a diaphragmatic hernia. There was a concomitant increase in pulmonary blood flow in six; in the remaining lamb the decrease in blood flow induced by the hypoxia was arrested. At the same time, there was an increase in systemic artery pressure in three, the decrease was arrested in two, but the decrease continued in the other two. Isoprenaline was a more effective drug than tolazoline, producing an increase in pulmonary blood flow in five of the seven lambs, with minor decreases in systemic pressure in five. Tolazo-line improved blood flow in three of six lambs (not all lambs survived the full study), with a marked decrease in systemic pressure in four of them. Prostaglandin D2 seems to be a useful drug for the treatment of patients having diaphragmatic hernias and pulmonary hypertension, and warrants further study. Isoprenaline was the most effective of the readily available drugs tested in this animal model.

Renal artery stenosis in heart failure

Captopril, an oral angiotensin-converting enzyme inhibitor, has proven to be effective in the management of congestive heart failure (CHF). 1 Several trials have documented short- and long-term hemodynamic and clinical improvement with captopril therapy, including increased exercise tolerance. 2,3 However, captopril may fail to improve or be detrimental to renal function 4 in some patients, particularly if accompanied by marked decreases in systemic pressures. Recent reports have described captopril-induced renal insufficiency in patients with bilateral renal artery stenosis or unilateral stenosis in a solitary kidney 5 and in renal transplant recipients with hypertension. 6 Herein we describe certain findings in 6 of 89 patients with significant CHF seen in a 10-month period in whom a diagnosis of significant renal artery stenosis was made.

Inhibition of indium-111 platelet accretion onto venous thrombi in dogs by prostacyclin.

The known platelet anti-aggregant effects of prostacyclin (epoprostenol) suggest that it may have therapeutic potential in conditions in which the platelet plays a pathophysiological role. The growth of venous thrombi is one such condition. We have attempted to determine, in a canine model of fresh venous thrombosis, whether prostacyclin infusion inhibits platelet accretion in vivo and how this in vivo event related to hemodynamic and in vitro platelet anti-aggregant effects. Gamma camera imaging over thrombi for accretion of indium-111-labeled platelets disclosed that prostacyclin, at an infusion rate of 50 ng/kg per min, inhibited platelet accretion in vivo and resulted in a 95 +/- 4% decrease in in vitro adenosine diphosphate-induced platelet aggregation, and a decrease in mean arterial pressure to 86 +/- 4% of pre-infusion values. Step-wise decrements of prostacyclin infusion demonstrated that platelet accretion occurred in vivo at infusion rates of approximately 10-20 ng/kg per min and correlated with an in vitro adenosine diphosphate-induced aggregation of 54 +/- 13% of control values. Thus, prostacyclin, in a dose that causes only a mild decrease in systemic pressure, can completely inhibit platelet uptake onto fresh venous thrombi in the dog, and this inhibition correlates closely with in vitro adenosine diphosphate-induced platelet aggregation. The potential therapeutic implications of these findings are discussed.

Inhibition of baroreflex bradycardia by aortic nerve excitatory afferents in dogs.

In dogs anesthetized with morphine-chloralose, low-frequency high-intensity stimulation of the aortic nerve (AN) causes a modest reflex tachycardia and a rise in systemic pressure. Stimulation of the carotid sinus nerve or raising pressure in the isolated carotid sinus causes reflex bradycardia and a fall in systemic pressure. Combined stimulation of these reflexes resulted in less bradycardia and a smaller decrease in systemic pressure than the sum of the responses to separate stimulation (P less than 0.001). This suggests that the opposing reflexes interact in a manner whereby the carotid baroreflex responses are inhibited by the AN stimulation. This interaction occurs in the medullary centers and appears to involve primarily suppression of the vagal efferents to the heart. Baroreflex inhibition of sympathetic vasomotor activity also appears to be suppressed by AN stimulation. It is concluded that aortic cardiac sympathetic activity and in part by suppressing baroreflex-induced bradycardia.

Coronary hemodynamics during percutaneous transluminal coronary angioplasty

The hemodynamic consequences of multiple transient occlusions (9.8 ± 3.7 seconds) of the left anterior descending coronary artery were assessed in 15 conscious patients during percutaneous transluminal coronary angioplasty. Thermodilution coronary venous blood flow, measured in the great cardiac vein, decreased from control values of 75.9 ± 24 ml/min to 50.9 ± 21.9 with coronary occlusion (probability [p] < 0.00001) and increased to 101.6 ± 34.3 after release of occlusion (p < 0.00001). Changes in coronary sinus blood flow, measured simultaneously, reflected the alterations in the great cardiac vein. Restoration of postocclusion blood flow to control values occurred in 18.2 ± 6.7 seconds, and is compatible with reactive hyperemia rather than sustained improvement in resting coronary blood flow. Flow repayment during reactive hyperemia exceeded flow debt incurred during coronary occlusion by 288.4 ± 106 percent (p < 0.05). The increase in reactive hyperemic flow after initial coronary occlusion (24.2 ± 15.7 ml/min) was less than that after final occlusion (42.2 ± 10.1, p < 0.05). This suggests an initial limitation of reactive hyperemia by persistent coronary stenosis. In all patients, reactive hyperemia accentuated the trans-stenotic coronary ostial to distal coronary arterial pressure gradient. Compared with a control value of 53.5 ± 7.7 percent, the great cardiac vein oxygen saturation transiently decreased to 49.3 ± 7.0 percent (p < 0.001) on release of the occlusion and then increased to 62.5 ± 5.2 percent (p < 0.001) during reactive hyperemia. A small reduction in aortic pressure from 96.4 ± 10.2 mm Hg to 89.9 ± 10.9 mm Hg(p < 0.00001) was observed during occlusion. A reduction in first derivative of left ventricular pressure (dP/dt) during coronary occlusion, in three patients in whom it was measured, suggests that the decrease in systemic pressure is due to transient ischemic myocardial dysfunction rather than to peripheral arteriolar vasodilation. These observations are relevant to the performance of coronary angioplasty, and to the understanding of the physiology of transient coronary occlusion in conscious patients.