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PubMed1979

Further study of the neurohumoral factor, endorphin, in the mechanism of acupuncture analgesia.

Cross circulation was performed between the femoral arteries and veins of paired rabbits that were entirely conscious. Jaw opening reflex by dental pulp stimulation was used as pain index. When acupuncture was applied to the donor rabbit the pain thresholds of both the donor and recipient were elevated from 30 minutes to one hour after acupuncture stimulation and lasted for another 30 minutes after withdrawal of acupuncture. The analgesic effect in both the donor and recipient was abolished by the pretreatment of naloxone. The increase in the pain threshold of the non-acupunctured recipient was due to an opiate-like, humoral substance generated from the acupuncture donor. The possible role of endorphins in the mechanism of acupuncture analgesia is discussed.

Acupuncture Therapy↗
PubMed1979

Neural and humoral signals for pulmonary ventilation arising in exercising muscle.

This review analyzes attempts to isolate and quantify the neurally and humorally mediated portions of the ventilatory response to moderate exercise. 1. Dejours' "neuro-humoral theory" postulates that, following a change from rest to moderate, constant-load exercise in man, the abrupt initial increase in VE is neurally mediated, and the subsequent gradual rise in VE is humorally mediated. However, no compelling evidence exists to support either of these hypotheses. Moreover, there is a plausible alternative method of partitioning VE into fast and slow components: the steady-state value of VE may be entirely due to the slow component. 2. The similarity between the kinetics of VE and VCO2 during exercise suggests that the ventilatory response may be primarily triggered by a signal that has its origin in the CO2 flux to the lung. Intravenous CO2 loading in resting animals produces such a flux, unaccompanied by possible neural signals arising from contracting muscles. However, experiments of this type have produced drastically conflicting results. 3. With cross-circulation techniques, the ventilatory response to neural signals from exercising limbs can be isolated, by sending the blood leaving these limbs directly into the venous system of another animal. Experiments of this type with anesthetized dogs led Kao and co-workers to conclude that the increase in VE during steady-state exercise is entirely due to neural signals originating in the exercising limbs. 4. In skeletal muscle, the kinetics of VO2 closely follow those of the concentrations of creatine phosphate and free creatine: a sensor of either of these concentrations could thus theoretically serve as a useful "metaboreceptor". The extracellular concentration of K+ in contracting muscles also changes rapidly enough to lead cardio-ventilatory adjustments, and thus might possibly trigger a neural signal involved in their control.

Animals↗
PubMed1998

Lazaroid U74500A is superior to U74006F in preserving rabbit heart for 24 hours.

BACKGROUND: Lazaroid, a series of 21-aminosteroids, has been shown to reduce free-radical-mediated injury after ischemia and reperfusion. Recent in vitro studies have demonstrated that, among the various compounds studied, the most efficient agent was U74500A. The question is whether these findings apply to the whole heart experiencing ischemia-reperfusion injury. In this study we compared the myocardial protective effects of U74006F, the only clinical candidate, and U74500A. METHODS: An isolated rabbit heart preparation perfused with the blood from a support rabbit was used. All hearts were divided into three groups according to the administration of U74500A (4 mg/kg, group A; n = 7), U74006F (4 mg/kg, group F; n = 7), or solvent (group S; n = 7) to the donor rabbit before preservation. After 24 hours of preservation with University of Wisconsin solution at 0 degrees C, all hearts were perfused with cross-circulated blood for 60 minutes with the Langendorff mode followed by 40 minutes in the working mode. RESULTS: After 10 minutes of reperfusion the serum lipid peroxide levels were significantly (p < 0.05) lower in group A (0.62+/-0.31 nmol/mL) than those in group S (2.1+/-1.3 nmol/mL) and group F (1.0+/-0.6 nmol/mL). The aortic flow rate at 10 mm Hg of left atrial pressure was significantly higher in group A (164+/-37 mL/min) than that of other groups (71+/-28 mL/min in group S and 97+/-28 mL/min in group F). There were no significant differences in high-energy phosphate levels after reperfusion among the three groups. CONCLUSION: These data imply that U74500A inhibits lipid peroxidation and prevents ischemia-reperfusion injury more efficiently than U74006F.

Animals↗
PubMed2005

Lillehei, Lewis, and Wangensteen: the right mix for giant achievements in cardiac surgery.

The dawn of open-heart surgery occurred at the University of Minnesota on September 2, 1952, when Dr John Lewis and his surgical team closed an atrial septal defect using total-body hypothermia and inflow stasis. Eighteen months later on March 26, 1954, Dr C. Walton Lillehei and his surgical team used a parent as a biologic oxygenator to repair a ventricular septal defect in a 1-year-old boy. This technique of cross circulation was then used in a total of 45 children during the next 16 months to successfully repair tetralogy of Fallot, atrioventricular canal, and ventricular septal defect. Remarkably, two thirds of these children were discharged from the hospital. Thirty years later, Dr Lillehei reported that 17 of his 27 patients with repair of a ventricular septal defect had survived and were all New York Heart Association class I. These landmark operations in the open heart could not have been achieved by Drs Lewis and Lillehei without the remarkable support that they received from their surgical chief, Dr Owen Wangensteen. Doctor Wangensteen would later state in his book, The Rise of Surgery, that: "The outstanding contribution to the advancement of surgery in the 20th century has been the development of open-heart surgery."

Cardiovascular Surgical Procedures↗
PubMed1995

Left ventricular mechanoenergetics under altered coronary perfusion in guinea pig hearts.

Coronary perfusion pressure (CPP) is well known to affect left ventricular (LV) mechanoenergetics (Gregg's phenomenon). The garden hose effect via the Frank-Starling mechanism caused by coronary distension has long been considered to be the underlying mechanism of this phenomenon. However, recent studies have revealed a close correlation between CPP and the excitation-contraction coupling in myocytes. The aim of this study was to investigate the mechanoenergetic aspects of Gregg's phenomenon by the ventricular contractility (Emax) dependency of the myocardial oxygen consumption (VO2)-total mechanical energy (PVA, systolic pressure-volume area) relationship. Experiments were performed in the excised, cross-circulated guinea pig heart preparation. The protocol consisted of LV volume loading (VOL run), changing coronary perfusion pressure at a fixed LV volume (CPP run) and intracoronary calcium (Ca) infusion also at the same LV volume (Ca run). In all seven hearts, we obtained a linear VO2-PVA relation in VOL run. The VO2-PVA relations in CPP and Ca runs, which equally enhanced Emax, were highly linear and had no significant difference in their slopes, both significantly steeper than in VOL run. These findings suggest no significant difference in the oxygen cost of Emax between CPP and Ca runs. The enhanced LV mechanoenergetics under increasing CPP is characterized by increases in the VO2 component primarily for the excitation-contraction coupling to a greater degree than expected from the mechanical (garden hose) effect.

Animals↗
PubMed1990

Force-time integral does not improve predictability of cardiac O2 consumption from pressure-volume area (PVA) in dog left ventricle.

We have proposed the systolic pressure-volume area (PVA) as a measure of the total mechanical energy generated by ventricular contraction, and we found a closely linear correlation between PVA and cardiac oxygen consumption (VO2). Although the force-time integral (FTI) has long been considered to be the most reliable correlate of cardiac oxygen consumption (VO2), we have already shown that VO2 remained constant although FTI was changed while PVA was kept constant in the excised, cross-circulated dog left ventricle. This means that PVA is superior to FTI as a predictor of VO2. In the present study, we studied whether a linear addition of FTI to PVA could improve the prediction of VO2 from PVA in isovolumic and ejecting contractions with different afterload pressures in the same type of dog left ventricle preparation. Although left ventricular VO2 was always closely correlated with either PVA (r = 0.967, mean after z-transformation) or FTI (mean r = 0.925), multiple regression analysis indicated that PVA alone accounted for as much as 94% (mean) of the variance of VO2 and that FTI linearly added to PVA accounted for an additional few percent of the variance (statistically significant in less than half the cases). We conclude that the addition of FTI to PVA does not improve the predictability of VO2 from PVA in ordinary contractions.

Animals↗
PubMed1993

Oxygen consumption for constant work is minimal at lowest working contractility in normal dog hearts.

We tested whether minimal myocardial oxygen consumption (MVO2) for a given external work would exist in the middle of a normal contractility range as previously predicted theoretically. The left ventricle of the excised cross-circulated dog heart preparation was connected to a volume servo pump. Myocardial contractility in terms of ventricular end-systolic elastance (Emax) was gradually increased from control 8.9 +/- 3.4 (mean +/- SD) to 30.0 mmHg/(ml/100 g) by epinephrine and decreased to 1.8 mmHg/(ml/100 g) by propranolol while heart rate, end-systolic pressure and stroke work were kept constant. MVO2 was determined as the product of total coronary flow and coronary arteriovenous oxygen content difference in each contractile state. We plotted MVO2 values against E(max) values in each heart. The MVO2-E(max) relation for a constant cardiac work showed that MVO2 was minimal at the low end of the covered E(max) range. We conclude that minimal MVO2 for a given cardiac work is generally obtained at the lowest working contractility in normal dog hearts. This conclusion might pose some problems in the previous theoretical prediction as to the contractility that achieves the minimal MVO2 in a given external work.

Animals↗
PubMed1990

New method to determine oxygen cost for contractility.

We developed a new method to determine the oxygen cost for myocardial contractility and applied it to epinephrine in the excised cross-circulated dog heart. We utilized the relation between myocardial oxygen consumption (VO2) and the systolic pressure-volume area (PVA) which represents the total mechanical energy generated by contraction. We first obtained a reference VO2-PVA relation in a baseline contractile state. Then, the end-diastolic and stroke volumes were fixed constant and a global index of ventricular contractility, Emax, was enhanced by infusing epinephrine. The VO2-PVA data point was shifted linearly right-upward with the increases in Emax. From the slopes of both the reference VO2-PVA relation line and the regression line of VO2 on PVA during the gradually increased Emax, we calculated the oxygen cost for contractility, i.e., the ratio of the elevation of the VO2-PVA relation to enhanced Emax in each heart. The ratio was 0.00095 +/- 0.00013 ml O2.ml.mmHg-1.beat-1.100 g LV-2. The result indicates that the oxygen cost for contractility can be reliably and efficiently determined by this new method.

Animals↗
PubMed1995

Ca(2+)-free, high-Ca2+ coronary perfusion suppresses contractility and excitation-contraction coupling energy.

We studied the mechanoenergetic effects of a short-term Ca(2+)-free, high-Ca2+ Tyrode solution coronary perfusion in eight excised, cross-circulated canine hearts. The perfusion protocol consisted of coronary perfusion with Ca(2+)-free Tyrode solution for 10 min followed by high-Ca2+ (16 mM) Tyrode solution for 5 min. This new protocol successfully induced acute contractile failure in seven hearts, without myocardial ultrastructural changes. We studied the end-systolic pressure-volume relation (slope = Emax, a contractility index) and the relation between oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA) in these failing hearts. These hearts had no increase in end-diastolic pressure at a given volume, a 40% decrease in Emax and a proportional decrease in the PVA-independent VO2 for 1-4 h, but no decrease in the oxygen cost of PVA, defined as the slope of the VO2-PVA relation. The oxygen cost of Emax for Ca2+ handling, defined as the slope of the relation between PVA-independent VO2 and Emax, was unchanged in the failing hearts. We conclude that the present protocol induced left ventricular contractile failure, primarily involving the suppression of Ca2+ handling energy for excitation-contraction coupling.

Animals↗
PubMed1990

Pharmacological analysis of cardiac effects of a central cholinergic agent, WEB 1881-FU, in isolated canine heart preparations.

The cardiovascular effects of the novel compound WEB 1881-FU (4-amino-methyl-1-benzyl-pyrrolidine-2-one-fumarate) were investigated using cross-circulated dog atrial preparations. Intravenous injections of WEB 1881 induced a hypotensive effect with slight tachycardia at a large dose in anesthetized dogs. At the same time, it produced slight positive chronotropic and inotropic effects in the isolated atrium perfused with the donor's arterial blood. Direct injections of WEB 1881 into the sinus node artery of the isolated and perfused atrium induced positive chrono- and inotropic effects in a relatively small dose range. At higher doses, it caused biphasic chrono- and inotropic effects, i.e., initial brief negative effects followed by long-lasting positive chrono- and inotropic effects. The negative chrono- and inotropic responses to WEB 1881 were not blocked by atropine in doses which significantly suppressed ACh-induced negative chrono- and inotropic responses. The positive chrono- and inotropic responses to WEB 1881 were significantly inhibited either by a beta-blocker (propranolol) or by an uptake blocker (imipramine). From these results, it is concluded that WEB 1881 has a tyramine-like, catecholamine releasing property. Although a large dose of WEB 1881 has a direct cardiac depressant action, it does not affect muscarinic mechanisms in the heart.

Acetylcholine↗
PubMed1993

A natriuretic factor is released by saline infusion into rat renal artery.

Saline (154 mM NaCl) infused into one renal artery of anesthetized rats produced a prompt and substantial increase in sodium excretion without significant alteration of arterial pressure, renal blood flow, or glomerular filtration rate. A 1-h infusion at rates of 0.0375, 0.05, or 0.1 ml/min increased sodium excretion by the infused kidney from 0.15 +/- 0.04 to 0.70 +/- 0.12, from 0.45 +/- 0.10 to 2.17 +/- 0.40, and from 0.27 +/- 0.06 to 4.29 +/- 0.80 mumol/min, respectively. Natriuresis also occurred in the contralateral kidney. No comparable responses resulted from infusions at 0.0375 ml/min into the jugular vein, inferior vena cava, or carotid artery. Cross-circulation of blood from infused rats increased sodium excretion in uninfused recipients from 0.36 +/- 0.11 to 1.43 +/- 0.43 mumol.min-1.kidney-1. Isovolemic exchange-transfusion of blood from infused donor rats increased sodium excretion in uninfused recipients from 0.30 +/- 0.05 to 0.51 +/- 0.09 mumol.min-1.kidney-1. In both experiments, aortic infusions below the renal artery produced no comparable effect in recipient rats. Infusion of 300 mM glucose was not natriuretic. Infusion of two NaCl loads, 5.8 and 15.4 mumol/min, each at two different rates, increased sodium excretion in proportion to the load of NaCl and not to the rate of infusion. Infusions of a protein-free artificial rat plasma or of 140 mM NaCl, both with the sodium concentration of rat plasma, produced very little increase in sodium excretion. Infusion of 154 mM sodium lactate produced an increase in sodium excretion comparable to that produced by 154 mM NaCl. Reducing the infusion rate of 154 mM NaCl from 0.05 to 0.01 ml/min produced a rapid decline in the rate of sodium excretion. We conclude that renal arterial saline infusion activates a mechanism that increases sodium excretion by the infused kidney and concurrently causes the release of a natriuretic factor. Increased sodium concentration in renal arterial blood was the only stimulus found to produce the effect.

Animals↗
PubMed1984

Failure of changes in intracapillary pressures to alter proximal fluid reabsorption.

To determine the role that peritubular capillary oncotic and hydraulic pressures play in regulating urinary sodium excretion in the euvolemic state, experiments were carried out in rats under conditions which altered these pressures without volume expanding the animal. In cross-circulation experiments, the donor rat was expanded with plasma or Ringer's solution while the recipient rat remained euvolemic. Micropuncture measurements in the euvolemic recipients demonstrated significant increases in efferent plasma flow rate (QEA), capillary hydraulic pressure (Pc), and decreases in mean capillary oncotic pressure (pi c). There were no changes in nephron GFR (SNGFR), absolute proximal reabsorption (APR), or UNaV. In additional studies, peritubular oncotic pressure was lowered markedly by plasmapheresis of the experimental animal. Large decreases in pi c were produced without any change occurring in SNGFR, APR, or UNaV. Measurements of interstitial hydraulic pressure (Pi) with a subcapsular pressure pipet revealed that Pi was unaltered under all of these conditions but rose markedly in rats undergoing a saline-expansion diuresis. Our findings indicate that APR and UNaV can remain constant despite large changes in pi c, Pc, and QEA in nonexpanded animals. Furthermore, the changes in pi c, Pc, and QEA induced in the euvolemic non-diuretic rats were the same as those in the saline-expanded diuretic rats. We conclude that under euvolemic experimental conditions, urinary sodium excretion and APR do not correlate with intracapillary pressures or flow rates in the renal cortex. The only difference found between the nondiuretic and diuretic rats was a rise in Pi in the latter group.

Animals↗
PubMed1989

Effect of ouabain on the relation between left ventricular oxygen consumption and systolic pressure-volume area (PVA) in dog heart.

We studied the effect of ouabain (digitalis) on the relation between left ventricular (LV) O2 consumption (VO2) and pressure-volume (P-V) area (PVA) in 7 excised cross-circulated canine heart preparations. PVA is a measure of the total mechanical energy generated by LV contraction and was obtained as the specific area in the P-V diagram circumscribed by the end-systolic P-V line, end-diastolic P-V curve, and the systolic P-V trajectory. Ouabain (0.11 mg, intracoronary-arterially) increased Emax (LV contractility index) by 58 +/- 44% (mean +/- SD) from 7.8 +/- 3.4 to 12.0 +/- 4.8 mmHg/(ml/100 g LV). PVA correlated linearly with LV VO2 per beat in either the control (r greater than 0.97) or the ouabain run (r greater than 0.96) in individual hearts. Ouabain increased the VO2-axis intercept of the regression line of VO2 on PVA from 0.029 +/- 0.004 in the control run to 0.036 +/- 0.009 ml O2/beat/100 g LV without significantly changing the slope [(1.53 +/- 0.24).10(-5) ml O2/(mmHg/ml)] of the regression line. This slope is equivalent to the contractile efficiency value of 44 +/- 6% from the excess VO2 above unloaded VO2 to PVA. The parallel elevation of the VO2-PVA relation with ouabain was similar to the results produced by epinephrine and Ca2+ in our previous studies. Ouabain, like epinephrine and Ca2+, did not change the contractile efficiency from the PVA-dependent fraction of VO2 to PVA.

Animals↗
PubMed2001

Pulmonary vasoconstriction during regional nitric oxide inhalation: evidence of a blood-borne regulator of nitric oxide synthase activity.

BACKGROUND: Inhaled nitric oxide (INO) is thought to cause selective pulmonary vasodilation of ventilated areas. The authors previously showed that INO to a hyperoxic lung increases the perfusion to this lung by redistribution of blood flow, but only if the opposite lung is hypoxic, indicating a more complex mechanism of action for NO. The authors hypothesized that regional hypoxia increases NO production and that INO to hyperoxic lung regions (HL) can inhibit this production by distant effect. METHODS: Nitric oxide concentration was measured in exhaled air (NO(E)), NO synthase (NOS) activity in lung tissue, and regional pulmonary blood flow in anesthetized pigs with regional left lower lobar (LLL) hypoxia (fraction of inspired oxygen [FIO2] = 0.05), with and without INO to HL (FIO2 = 0.8), and during cross-circulation of blood from pigs with and without INO. RESULTS: Left lower lobar hypoxia increased exhaled NO from the LLL (NO(E)LLL) from a mean (SD) of 1.3 (0.6) to 2.2 (0.9) parts per billion (ppb) (P < 0.001), and Ca2+-dependent NOS activity was higher in hypoxic than in hyperoxic lung tissue (197 [86] vs. 162 [96] pmol x g(-1) x min(-1), P < 0.05). INO to HL decreased the Ca2+-dependent NOS activity in hypoxic tissue to 49 [56] pmol x g(-1) x min(-1) (P < 0.01), and NO(E)LLL to 2.0 [0.8] ppb (P < 0.05). When open-chest pigs with LLL hypoxia received blood from closed-chest pigs with INO, NO(E)LLL decreased from 2.0 (0.6) to 1.5 (0.4) ppb (P < 0.001), and the Ca2+-dependent NOS activity in hypoxic tissue decreased from 152 (55) to 98 (34) pmol x g(-1) x min(-1) (P = 0.07). Pulmonary vascular resistance increased by 32 (21)% (P < 0.05), but more so in hypoxic (P < 0.01) than in hyperoxic (P < 0.05) lung regions, resulting in a further redistribution (P < 0.05) of pulmonary blood flow away from hypoxic to hyperoxic lung regions. CONCLUSIONS: Inhaled nitric oxide downregulates endogenous NO production in other, predominantly hypoxic, lung regions. This distant effect is blood-mediated and causes vasoconstriction in lung regions that do not receive INO.

Administration, Inhalation↗
PubMed1991

Equivalent heart rate during ventricular fibrillation in the dog heart: mechanoenergetic analysis.

We propose equivalent heart rate (eHR) as an estimate of the frequency of contractions of individual myocytes in a fibrillating ventricle by analyzing mechanics and energetics of the ventricle. Using the isolated, cross-circulated dog heart preparation, we determined eHR in two different ways. First, we obtained eHR (eHR1) from myocardial O2 consumption (Vo2)-equivalent pressure-volume area (ePVA) data points during ventricular fibrillation (VF) by utilizing the Vo2-pressure-volume area (PVA) relation in the beating state. PVA is the area surrounded by the end-systolic and end-diastolic pressure-volume relations and the systolic pressure-volume trajectory in the pressure-volume diagram. PVA has been shown to represent the total mechanical energy generated by each contraction. We have recently proposed ePVA as a measure of the total mechanical energy generated by single contractions of all individual asynchronously contracting myocytes in a fibrillating ventricle. ePVA is the area surrounded by the horizontal line at the VF pressure and the end-systolic and end-diastolic pressure-volume relations in the beating state. Second, we measured Vo2 in beating state at various heart rates and Vo2 during VF under a mechanically unloaded condition. By comparing these fibrillating and beating Vo2 values, we determined eHR (eHR2) for the fibrillating state. eHR1 was 216 +/- 27 beats/min and eHR2 was 223 +/- 26 beats/min. These two values were not significantly different. We conclude that the average frequency of contractions of individual myocytes in a fibrillating ventricle is equivalent approximately to 220 beats/min in terms of ventricular energetics.

Animals↗
PubMed1979

Instantaneous pressure-volume relationship of right atrium during isovolumic contraction in canine heart.

We studied the contraction of the right atrium in an excised cross-circulated heart preparation. Atrial volume and instantaneous atrial pressure were measured in a water-filled balloon fitted in the spontaneously contracting right atrium. The relation of instantaneous pressure to volume was analyzed by collecting pressure data from multiple isovolumic contractions with different volumes but measured at multiple identical time points in the contraction cycle. The relation was found to be quasi-linear during most of atrial systole and diastole. A linear regression formula P(t) = K(t)[V- VD(t)] was therefore fitted to the data. K(t) and VD(t) of the regression formula are the slope and the volume axis intercept in the pressure-volume plane, respectively. When the atrium beat spontaneously at a regular sinus rhythm with no inotropic intervention. K(t) increased during systole and decreased during diastole, whereas VD(t) decreased during systole and increased during diastole. The average value of K was 13 +/- 1.7 (SE) mmHg . kg . ml-1 at the end of diastole and 33 +/- 0.02 (SE) mmHg . kg . ml-1 at the end of systole. The average value of VD was 0.303 +/- 0.017 (SE) ml . kg-1 at the end of diastole and 0.212 +/- .025 (SE) ml . kg-1 at the end of systole. Enhancement of contractility with epinephrine or Ca2+ significantly increased the value of K at the end of systole, but it did not significantly affect either K at the end of diastole or VD at the end of systole and diastole.

Animals↗
PubMed1984

Ejection timing as a major determinant of left ventricular relaxation rate in isolated perfused canine heart.

In the present study, we attempted to test the hypothesis that ejection timing rather than peak left ventricular pressure is a primary determinant of ventricular relaxation rate. In cross-circulated isolated canine hearts instantaneous left ventricular volume was controlled by a servo-pump system. To eliminate the effects of end-systolic and end-diastolic volumes and ejection velocity on left ventricular relaxation rate, these parameters were clamped, and only the ejection timing (onset and end of ejection) was altered, keeping the duration of ejection unchanged. Left ventricular relaxation rate was assessed by time constants of left ventricular pressure decline during the isovolumic relaxation phase calculated by both a semilogarithmic method, assuming that the asymptote is zero, and a best exponential fitting method. In 25 runs, a pair of contractions with ejection timings which differed by 53.1 +/- 2.1 (SE) msec were imposed, while end-systolic and end-diastolic left ventricular volumes and ejection duration were unchanged. All pairs of contractions demonstrated early ejection resulted in significantly (P less than 0.001) slowed relaxation as indicated by a prolongation of the time constants of isovolumic left ventricular pressure decay (delta 4.2 +/- 0.7, sec and delta 15.4 +/- 2.1 msec by semilogarithmic plot and the best exponential fit respectively), although peak left ventricular pressures (104.6 +/- 2.4 mm Hg) were even lower than those (116.6 +/- 2.8 mm Hg) in contractions with later ejection timing. Furthermore, in seven experiments, the heart was allowed to eject at five different timings; onset and end of ejection were progressively delayed in steps of 20 or 30 msec.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

[Origin, nature, role and fate of prostaglandins liberated during the expansion of intravascular space in the anesthetized rat].

In experiments in which blood was cross-circulating in rats, the blood pressure of the recipient dropped while that of the donor rose, following the increase of the circulating blood volume, produced by infusion either of saline or blood. The phenomenon was almost imperceptible when binephrectomized animals were used. In experiments in which the blood-bathed organ technique was used, prostaglandin-like substances were detected, released during the rise of the blood pressure, produced by the same stimulus (the expansion), in anaesthetized rats. A significant difference was found between the prostaglandin-like substances detected using the blood-bathed organ technique, in normal rats (5.387 ng per ml of blood plus or minus 0.288 = SEM) and those detected in binephrectomized rats (3.202 ng per ml of blood plus or minus 0.330, p smaller than 0.025). The biologically active substances detected in 25 ml of blood collected during expansion, while the assay organs showed a prostaglandin-like activity, were found to have the chromatographic behaviour and the bioassay properties of PGA, PGE and PGF series. A great quantity of the biologically active substances, having the chromatographic behaviour and the bioassay properties of PGA, PGS and PGF was detected in the rat renal medulla. Sufficient quantities of the released prostaglandin-like substances could escape the pulmonary vascular bed in this species of animal. It was concluded that a great quantity of the released prostaglandin-like substances came from the kidney and their release by this particular mechanism suggested that they play an important homeostatic role on the blood pressure, blood volume, and sodium and water balance regulation.

Animals↗