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At least 523 records · Page 29Linked to original sources
PubMed1989

Effect of left ventricular volume on right ventricular end-systolic pressure-volume relation. Resetting of regional preload in right ventricular free wall.

Effect of left ventricular (LV) volume on right ventricular (RV) end-systolic pressure-volume relation (ESPVR) was investigated, and the mechanism was examined from a standpoint of the alteration of RV free wall mean fiber length. Twelve cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were controlled independently were used, and RV-ESPVR was determined at three different LV volume levels. At small (10.2 +/- 0.6 ml), middle (15.3 +/- 1.0 ml), and large (20.5 +/- 1.4 ml) LV volume, the slope of the RV-ESPVR was 2.63 +/- 0.13, 2.74 +/- 0.13, and 2.89 +/- 0.12 mm Hg/ml, respectively, and each value was significantly different from the others (p less than 0.01). The volume intercept (V0) of the relation (RV-V0) was significantly decreased with the increment of LV volume (RV-V0 in small, middle, and large LV volume; 3.92 +/- 0.68, 3.39 +/- 0.67, and 2.87 +/- 0.71 ml, respectively; p less than 0.01). In nine hearts, RV free wall lengths in latitudinal and meridional direction were measured at three LV volume levels when RV volume was held constant (16.1 +/- 1.1 ml). RV latitudinal end-diastolic length was significantly augmented with increasing LV volume (latitudinal length in small, middle, and large LV volume; 9.68 +/- 0.55, 9.81 +/- 0.56, and 9.92 +/- 0.55 mm, respectively). RV meridional end-diastolic length also increased significantly with increasing LV volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

The linear relation between oxygen consumption and pressure-volume area can be reconciled with the Fenn effect in dog left ventricle.

We studied the Fenn effect in 12 excised cross-circulated dog left ventricles in control contractility and in a contractility enhanced by dobutamine or depressed by propranolol. The additional oxygen consumption (Vo2) in an ejecting contraction compared with that found in an isovolumic contraction at a comparable end-systolic pressure was considered to constitute the cardiac Fenn effect. We examined whether this load-dependent Vo2 could be reconciled with the linear relation between Vo2 and pressure-volume area (PVA) common for both ejecting and isovolumic contractions that has so far been consistently observed and was presently confirmed. PVA is a specific area in the pressure-volume diagram, represents the total mechanical energy generated by each contraction, and consists of external mechanical work (EW) and mechanical potential energy. Because potential energy is common in the isovolumic and ejecting contractions producing the same end-systolic pressure, PVA of the ejecting contraction is greater by EW than that of the isovolumic contraction. Despite this difference in PVA by EW, the Vo2-PVA relation was always linear and load independent regardless of the isovolumic and ejecting contractions in a given heart in any given contractile state. By contrast, the upward convex Vo2-end-systolic pressure relation was higher for ejecting contractions than the downward convex Vo2-end-systolic pressure relation for isovolumic contractions in each contractile state. The difference of Vo2 between the ejecting and isovolumic contractions was proportional to EW at comparable end-systolic pressure. The slope of the additional Vo2 of ejecting contractions plotted against their EW had a slope close to the slope of the Vo2-PVA relation. Thus, the load-independent linear Vo2-PVA relation can be reconciled with the cardiac Fenn effect.

Animals↗
PubMed1990

Decreased contractile efficiency and increased nonmechanical energy cost in hyperthyroid rabbit heart. Relation between O2 consumption and systolic pressure-volume area or force-time integral.

Both systolic pressure-volume area (PVA) and force-time integral (FTI) have been used as measures of oxygen consumption per beat (VO2) in the isolated left ventricle. The reciprocal of the slope of the VO2-PVA relation has been considered to reflect the chemomechanical energy transduction efficiency of the contractile machinery (contractile efficiency), whereas its VO2 intercept consists of energy cost of excitation-contraction coupling and basal metabolism. To examine whether the increase in myosin isoform V1/V3 ratio in hyperthyroid rabbits decreases contractile efficiency and to determine overall mechanisms of higher oxygen consumption in hyperthyroid hearts, the VO2-PVA and VO2-FTI relations as well as the end-systolic pressure-volume relation were assessed in cross-circulated, isovolumically beating hearts isolated from normal, hyperthyroid, and hypothyroid rabbits. Normalized initial slopes of the rising limb of the curvilinearly fitted end-systolic pressure-volume relation (E'max, ventricular contractility index) were similar for normal and hyperthyroid groups. However, the slopes and VO2 intercepts of the VO2-PVA and VO2-FTI relations were greater in hyperthyroid hearts than in normal hearts. Accordingly, in the hyperthyroid hearts, the contractile efficiency (27 +/- 6%) was lower and left ventricular VO2 for excitation-contraction coupling (0.028 +/- 0.004 ml O2/beat/100 g) was higher than in normal hearts (40 +/- 4% and 0.021 +/- 0.005 ml O2/beat/100 g, respectively). This decreased contractile efficiency in the hyperthyroid hearts was attributable to myosin isoform alteration rather than to increased beta-adrenoceptors because isoproterenol did not affect the slope of the VO2-PVA relation in all groups. In contrast, the slope of the VO2-FTI relation was significantly increased by isoproterenol in all groups. Neither the VO2-PVA nor the VO2-FTI relations in hypothyroid hearts were different from those in normal hearts except for significantly lower VO2 for basal metabolism. We conclude that in hyperthyroid rabbits, the left ventricle has decreased contractile efficiency and increased energy cost of excitation-contraction coupling and that the decreased contractile efficiency in hyperthyroid hearts is probably due to the increased V1/V3 ratio of the myosin isoform component. In addition, this study demonstrates that the VO2-PVA and VO2-FTI relations dissociate depending on the intervention, even in the same isovolumic contraction mode.

Animals↗
PubMed1990

Effects of bigeminies and paired-pulse stimulation on oxygen consumption in dog left ventricle.

In 10 excised, cross-circulated, isovolumically beating dog left ventricles, we examined the effects of bigeminy, including paired-pulse stimulation, on cardiac oxygen consumption (VO2) and evaluated whether the VO2 versus pressure-volume area (PVA) relation obtained from regularly beating hearts in our previous studies could account for the changes in VO2 during bigeminies with various coupling intervals. The extrasystolic interval (ESI) was decreased in four steps from 300 msec (regular rhythm) to paired-pulse stimulation (less than or equal to 210 msec). The sum of ESI and the postextrasystolic interval was always held constant (600 msec); therefore, the number of excitations was 200/min at any ESI. Both VO2 and PVA were measured in four runs: a small volume run at a ventricular volume of 13 ml, a large volume of 12 ml, a calcium run in which contractility was enhanced by CaCl2 at a small volume of 12 ml, and a verapamil run in which contractility was depressed by verapamil at a large volume of 20 ml. In any run, both VO2 and PVA were unchanged at long ESIs (greater than or equal to 250 msec) from each control value at regular rhythm, but VO2 markedly increased at short ESIs (less than or equal to 230 msec). VO2s during bigeminies with various ESIs were comparable with the theoretical VO2 values that were calculated by the VO2-PVA relation at regular rhythm. However, the theoretical VO2 values underestimated the measured VO2 values at the shortest ESIs under a high volume loading and in a high contractile state. This indicates that the PVA concept can be expanded to various arrhythmias unless ESI becomes very short.

Animals↗
PubMed1991

Increased oxygen cost of contractility in stunned myocardium of dog.

Recent studies have shown that myocardial oxygen consumption does not proportionally decrease with the deterioration of contractile function in stunned myocardium. To investigate this disproportion, we studied the end-systolic pressure-volume relation and the relation between oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA, a measure of total mechanical energy) in stunned hearts. In the VO2-PVA relation, VO2 can be divided into PVA-dependent and PVA-independent fractions. In excised cross-circulated dog left ventricles, a 15-minute normothermic global ischemia followed by 60-120 minutes of reperfusion significantly decreased the ventricular contractility index (Emax) by approximately 40%, but the PVA-independent VO2 did not significantly decrease. Oxygen cost of PVA, defined as the slope of the VO2-PVA relation, was slightly decreased in stunned hearts. Restoration of the depressed Emax to the preischemic control level by calcium infusion increased the PVA-independent VO2 to 137 +/- 27% of control level (p less than 0.01). Oxygen cost of contractility, defined as the slope of the relation between PVA-independent VO2 and Emax, increased from 0.0011 +/- 0.0003 to 0.0023 +/- 0.0005 ml O2.ml.mm Hg-1.beat-1 per 100 g myocardium in control and stunned hearts, respectively (p less than 0.01). From these new finding, we conclude that the unchanged VO2, despite the depressed contractility in stunned myocardium, is mainly due to the increased oxygen cost of contractility.

Animals↗
PubMed1992

Basal metabolism adds a significant offset to unloaded myocardial oxygen consumption per minute.

Myocardial oxygen consumption (MVO2) includes components for 1) mechanical energy generation, 2) activation, and 3) basal metabolism. Whereas the first two components are expected to increase in proportion with heart rate, a significant basal level of metabolism would consume oxygen even if the heart rate were zero. Contrary to this expectation, however, a previous study reported that, during unloaded beats, MVO2 per beat (which includes basal metabolism) was independent of heart rate. Accordingly, unloaded MVO2 per minute would extrapolate to zero at zero heart rate; this result is unexpected considering basal metabolism. To resolve this inconsistency, we varied heart rate over a wide range after inducing atrioventricular block in eight isolated cross-circulated canine hearts that contracted isovolumically. We examined whether a term representing rate-independent basal metabolism was needed to describe MVO2 per minute. Mechanical energy generated by the left ventricle was evaluated from the pressure-volume area, which was altered by changing isovolumic ventricular volume over at least five levels at each heart rate. Contractility, evaluated by the slope of the end-systolic pressure-volume relation, did not vary significantly with heart rate in this study. In contrast to the previous report, unloaded MVO2 per beat (i.e., MVO2 extrapolated to a pressure-volume area of zero) was not constant but fell monotonically with increases in heart rate in every heart. We considered that this trend was caused by a significant rate-independent basal level of MVO2 per minute. Multiple linear regression analysis confirmed that this rate-independent basal term differed significantly from zero in seven of the eight hearts studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Stunned myocardium after rapid correction of acidosis. Increased oxygen cost of contractility and the role of the Na(+)-H+ exchange system.

Left ventricular (LV) contractile dysfunction during acidosis has been reported to be almost reversible in crystalloid-perfused hearts after correction of acidosis. In contrast, we have found that, in blood-perfused hearts, contractile function is paradoxically depressed after correction of acidosis with a transient overshoot of contractility during the recovery of pH. To clarify the mechanism of this phenomenon, we measured the LV contractility index (Emax) and the relation between myocardial oxygen consumption (VO2) and systolic pressure-volume area (PVA, a measure of the LV total mechanical energy) before and after induction and rapid correction of acidosis by CO2 loading (pH 7.00) and unloading in 13 excised cross-circulated canine hearts. During the rapid correction of acidosis in six control hearts, a severe transient overshoot of Emax (404% of acidosis) occurred. However, after correction of acidosis, Emax and PVA were lower than the preacidosis values by 46% (P < .01) and 44% (P < .01) at the same LV volume. When the preacidosis Emax level was restored by Ca2+ infusion, the VO2 intercept (PVA-independent VO2) of the linear VO2-PVA relation exceeded the control value by 18% (P < .05) with an unchanged slope. In addition, the oxygen cost of contractility, defined as the slope of the relation between PVA-independent VO2 and Emax, increased by 83% (P < .01) after correction of acidosis, indicating that postacidosis myocardium requires higher VO2 for nonmechanical activities for a unit increase in Emax. Then, we hypothesized that these mechanoenergetic disorders after rapid correction of acidosis would result from Ca2+ overload via accelerated Na(+)-Ca2+ exchange due to the heavily operating Na(+)-H+ exchange system at the time of rapid pH recovery. To examine this hypothesis, dimethylamiloride, a selective Na(+)-H+ exchange inhibitor, was administered just before the correction of acidosis in the other seven hearts. The administration of dimethylamiloride completely prevented both the mechanical and energetic disorders after correction of acidosis. We conclude that rapid recovery of pH paradoxically depresses myocardial contractility and increases the oxygen cost of contractility through an activation of the Na(+)-H+ exchange system.

Acidosis↗
PubMed1967

Evidence that an acute increase in glomerular filtration has little effect on sodium excretion in the dog unless extracellular volume is expanded.

The concept that acute increases in glomerular filtration rate (GFR) will cause large concomitant increases in sodium excretion has been re-examined. In previous work, GFR was elevated by volume expansion, usually with saline infusions. Recent evidence shows that tubular reabsorption is depressed during saline loading; hence, the independent effect of increased GFR on sodium excretion cannot be assessed.TO DETERMINE THE EFFECT OF ACUTE INCREASES IN GFR PER SE ON SODIUM EXCRETION, WE RAISED GFR BY FOUR TECHNIQUES NOT INVOLVING VOLUME EXPANSION: protein feeding, dopamine infusion, intravenous dexamethasone, and cross-circulation. GFR increased acutely by 5 to 85% in these experiments. In 12 of 24 experiments, GFR increased by more than 30%. In all but one experiment, sodium excretion increased by less than 75 muEq per minute. Data from experiments using each of the four techniques were comparable. The results were the same whether mineralocorticoid activity was high or low. In contrast, during saline loading, sodium excretion increased more than 800 muEq per minute with equal or lesser changes in GFR. These results demonstrate that acute increases in GFR per se have little effect on sodium excretion. We suggest that, due to constant fractional sodium reabsorption in the proximal tubule (glomerulotubular balance) and increased distal reabsorption, virtually all of the increase in filtered sodium is reabsorbed when GFR increases. Depression of tubular reabsorption is required for natriuresis.

Absorption↗
PubMed1984

Dynamic changes of multiple forms of serum immunoactive relaxin during pregnancy in the rat.

Relaxin isolated from the ovaries of pregnant rats has a mol wt of 6,500. This study determined the size(s) of the relaxin-immunoactive component(s) in the serum of rats during pregnancy. Peripheral sera from rats on days 15, 17, 19, and 21 of pregnancy were filtered through Sephacryl S-200 columns at 37 C and 4 C. Relaxin immunoactivity eluted in three components designated C1, C2, and C3, which had mol wts of approximately 60,000, 13,000 and 6,500, respectively. The distribution of relaxin immunoactivity among C1, C2, and C3 changed with the day of pregnancy. On day 15 of pregnancy essentially all relaxin immunoactivity was associated with C1. By day 17 approximately 20% of the relaxin immunoactivity was in C2 plus C3, and by day 21 the percentage in each of these two components increased to about 25%. C1 appears to possess relaxin bioactivity since the frequency of intrauterine pressure cycles in nonpregnant rats declined during cross-circulation with day 15 pregnant rats. C1 may not be attributable to the binding of 6,500 mol wt relaxin to a binding protein(s) since relaxin immunoactivity remained associated with a component(s) having a mol wt greater than 28,000 after incubation and gel filtration of day 15 serum in the presence of 2.0 M potassium thiocyanate at 37 C. Moreover, the levels of C1 as well as those of C2 and C3 were markedly increased in the peripheral serum of day-21 rats within 15 min of LH administration. C3 may be the 6,500-mol wt form of relaxin and C2 may be an intermediate in the processing of the 20,000-mol wt rat relaxin precursor to the 6,500-mol wt form of relaxin. The physiological significance, if any, of the multiplicity of relaxin-immunoactive components is unknown.

Animals↗
PubMed2006

Starling-effect-independent lusitropism index in canine left ventricle: logistic time constant.

The logistic time constant (tau(L)) has been proposed as a better index of the rate of left ventricular (LV) relaxation or lusitropism than the conventional monoexponential time constant (tau(E)). However, whether and how the Frank-Starling effect influences tau(L) remains to be elucidated. We compared the effect of LV volume (LVV) loading on both logistic and monoexponential fittings. The isovolumic LV relaxation pressure curves from the maximum negative time derivative of pressure (-dP/dt(max)) were analyzed at 3 different end-points at 4 LVVs of 10, 12, 14, and 16 mL in 8 excised, cross-circulated canine hearts. We found that the logistic fitting was superior to the monoexponential fitting at all LVVs and end-points. LVV loading did not affect tau(L) but affected tau(E) slightly. Although the advancing end-point increased both tau(L) and tau(E), the increases were significantly smaller for tau(L) than for tau(E) at all LVVs. Moreover, the changes in both the amplitude constants and nonzero asymptotes with the advancing end-point were significantly smaller for the logistic fitting than for the monoexponential fitting. We conclude that tau(L) served as a more reliable index of lusitropism that is independent of the change in LVV loading or the Frank-Starling effect.

Animals↗
PubMed1987

Quantitative evaluation of left ventricular regional work from wall tension-regional area loop in canine heart.

We evaluated left ventricular (LV) regional work from a wall tension-regional area (T-A) loop using sonomicrometers in the excised cross-circulated canine left ventricle connected to a volume servo pump. Regional work assessed from a T-A loop closely agreed with the predicted value calculated from LV stroke work and percent regional area under conditions of the control state, dobutamine infusion, and global ischemia. In addition, globally integrated regional work over the entire ischemic and non-ischemic zones agreed closely with LV stroke work either before or after coronary occlusion. These results indicate that LV regional work can be assessed reliably from the T-A loop in both normal and regionally ischemic hearts. Regional work correlated linearly with end-diastolic regional area, indicating a regional Frank-Starling relation, and the slope of this relationship increased with dobutamine infusion and decreased with global ischemia. The correlation between regional work and LV stroke work was also linear and the regression line was the same during the control state and global ischemia, indicating a constant relationship between the work of a specific wall region and LV stroke work regardless of global changes in contractile state. However, after regional ischemia, this regression line apparently shifted downward because T-A loops in the ischemic region were extremely deformed and regional work markedly decreased. From these results, we conclude that T-A loops are a reliable and useful means of assessing regional contractile performance of the LV.

Animals↗
PubMed1989

Right ventricular mechanical and energetic properties.

To formulate right ventricular (RV) mechanical and energetic properties in terms of the time-varying elastance model, Emax and the systolic pressure-volume area (PVA) of RV were measured in the excised cross-circulated heart preparation, while the left ventricle was beating unloaded. Emax of RV was constant, and independent of the RV volume, the stroke volume, the ejection velocity, and the pre-ejection period in the control contractile state. Enhancement of the contractile state with calcium increased Emax, and reduction of the contractile state with propranolol decreased Emax. The whole heart oxygen consumption (Vo2) was linearly regressed on PVA of RV, in both the control and the calcium-enhanced contractile state. Calcium elevated the regression line in a parallel manner. The slope of the regression line was (1.85 +/- 0.19) x 10(-5) ml O2/mmHg ml in the control state, and (1.57 +/- 0.44) in the calcium state. These slope values were similar to those in left ventricle (LV). We therefore conclude that mechanical and energetic properties of RV are similar to those of LV.

Animals↗
PubMed1991

Denopamine (beta 1-selective adrenergic receptor agonist) and isoproterenol (non-selective beta-adrenergic receptor agonist) equally increase heart rate and myocardial oxygen consumption in dog heart.

The effects of denopamine (a beta 1-selective adrenergic receptor agonist) and isoproterenol (a non-selective beta-adrenergic receptor agonist) on heart rate, left ventricular contractility, and left ventricular oxygen consumption (VO2) at the same left ventricular volume were compared in excised cross-circulated dog hearts. Denopamine and isoproterenol increased heart rate and VO2 to a comparable extent at a comparably increased contractility. Moreover, the oxygen cost of contractility which quantifies VO2 for excitation-contraction coupling was the same between the two agents. These findings contradict the previously reported smaller increases in heart rate and VO2 by denopamine than by isoproterenol in open-chest dog hearts, which have been mainly attributed to the beta 1-selectivity of denopamine. Our results suggest that in isolated and denervated hearts, the degree of beta 1-selectivity of a beta-agonistic agent does not directly determine the relative potencies of its inotropic and chronotropic effects and the oxygen cost of contractility.

Adrenergic beta-Agonists↗
PubMed2000

Electrogram characteristics indicative of a recurrent conduction site after ablation of the inferior vena cava-tricuspid annulus isthmus: a study in the canine blood-perfused atrioventricular preparation.

Analysis of the electrograms recorded along the ablation line can identify a recurrent conduction site after ablation of the isthmus between the inferior vena cava (IVC) and tricuspid annulus (TA) for atrial flutter. The present study examined the relationship between the activation sequence and electrogram characteristics using a model of recurrent conduction in the isthmus. The canine heart was isolated (n=8) and cross-circulated with the arterial blood of a support dog. A plaque electrode was placed at the isthmus, and 42 bipolar electrograms (filtered and unfiltered) were recorded during pacing at 120beats/min from the lateral right atrium before and after creating a narrow gap by 2 discontinuous incisions from the TA to the IVC. All bipolar electrodes, with the cathode in the TA side and the anode in the IVC side, were placed perpendicular to the TA. Before creating the incisions, the wavefront (WF) from the pacing impulse traveled uniformly in the isthmus and almost in parallel to the TA, and the filtered electrogram at each site showed a single potential. After creating the incisions, the WF propagated through the gap and spread radially to the area distal to the incisions. In close proximity to the incision lines opposite to the pacing site, the WF advanced from the gap towards the TA and IVC perpendicularly to the TA. Filtered electrograms on the incision lines showed double or split potentials, whereas those on the gap showed a single or fractionated potential. In unfiltered electrograms recorded from the TA to the IVC in close proximity to the incision lines opposite the pacing site, reversal of electrogram polarity was noted at the gap. A single or fractionated potential between double potentials indicates a gap between lines of conduction block. Electrogram polarity reversal along the ablation line indicates the presence of 2 opposing WF arising from the gap.

Animals↗
PubMed2004

[Energy utility of failing heart].

We investigated left ventricular (LV) mechanoenergetics in acute and chronic failing hearts, induced by high Ca(2+), ischemic-reperfusion injury, diabetes mellitus (DM), and hypothyroidism, using cross-circulated excised rat heart preparations. After high Ca(2+) or ischemic-reperfusion, there was a contractile failure associated with a parallel downward shift of the linear relation between myocardial O(2) consumption per beat (VO(2)) and systolic pressure-volume area (PVA). This result indicated a decrease in VO(2) for total Ca(2+) handling in E-C coupling. We found proteolysis of a cytoskeletal protein, alpha-fodrin. A calpain inhibitor significantly suppressed contractile failure, decreased VO(2) for total Ca(2+) handling, and membrane alpha-fodrin degradation. In DM, the LV relaxation rate was significantly slower, resulting in the decreased O(2) consumption per min for total Ca(2+) handling in E-C coupling. In hypothyroidism, there were systolic and diastolic failures associated with the decreased O(2) consumption per beat for total Ca(2+) handling in E-C coupling. The protein level of sarcoplasmic reticulum Ca(2+) ATPase (SERCA2) was significantly lower in DM and hypothyroidism. We conclude that suppression of O(2) consumption for total Ca(2+) handling, mainly utilized by SERCA2, is a major cause of failing hearts, mediated through degradation of membrane alpha-fodrin via activation of calpain or suppressed expression of SERCA2.

Animals↗
PubMed1976

Reversible adrenergic alpha-receptor blocking action of 2,4'-dimethyl-3-piperidino-propiophenone (tolperisone).

The vascular action of 2,4'-dimethyl-3-piperidino-propiophenone hydrochloride (tolperisone hydrochloride), a centrally acting muscle relaxant, was investigated in pentobarbital anesthetized dogs. Tolperisone given intravenously produced a transient hypotension, tachycardia, and hyperventilation. The drug increased the femoral arterial flow, and decreased the superior mesenteric arterial flow following an initial transient increase. When injected directly into femoral and mesenteric arteries, tolperisone caused a rapid increase in both arterial flow (vasodilatation). However, femoral vessels were about 90 times as sensitive as mesenteric vessels to tolperisone. These results indicate that tolperisone shifts the blood volume from mesenteric (visceral) vessels to femoral (skeltal) ones. The femoral vasodilatation produced by i.a. tolperisone was not depressed by the pretreatment with i.a. propranolol, atropine or chlorphenylamine. Tolperisone decreased the contractile force in an isolated and cross-circulated papillary muscle. Tolperisone produced adrenaline reversal and antagonized the pressor response to noradrenaline. Moreover, femoral vasoconstriction caused by i.a. adrenaline was converted to vasodilatation and that caused by i.a. noradrenaline was depressed during an i.a. infusion of tolperisone. These results indicate that tolperisone blocks adrenergic alpha-receptors. The blocking action was rapid in onset, short-lived, and in addition, competitive.

Adrenergic alpha-Antagonists↗
PubMed1988

Release of atrial natriuretic peptide from the isolated, blood-perfused right atrium of the dog.

Release of atrial natriuretic peptide (ANP) was investigated using the isolated right atrium (RA) cross-circulated with heparinized arterial blood of the donor dog. ANP concentration of the blood was measured by radioimmunoassay. The plasma ANP concentration of the arterial blood of the donor dog (ANP-D) which perfused the RA preparation was 111 +/- 18 pg/ml (n = 4), while the ANP concentration of venous blood leaving the RA preparation (ANP-A) was 1680 +/- 220 pg/ml (n = 4). In comparison, the plasma ANP concentration of venous blood leaving the isolated papillary muscle of the right ventricle (ANP-V) was 106 +/- 19 pg/ml (n = 4), which was not significantly different from the ANP-D concentration. When the right atrium was electrically driven at a rate of 100 beats/min, almost the same rate as the spontaneous sinoatrial rate of 98 +/- 6 beats/min (n = 4), the ANP-A concentration was not changed (1630 +/- 160 pg/ml, n = 4). When the driving rate was increased to 200 beats/min, the ANP-A concentration was significantly increased to 2250 +/- 130 pg/ml (n = 4). These results suggest that ANP is exclusively secreted from the atrium, but not from the ventricle, and that release of ANP is directly related to atrial rate.

Animals↗
PubMed1989

The first demonstration of CGRP-immunoreactive fibers in canine hearts: coronary vasodilator, inotropic and chronotropic effects of CGRP in canine isolated, blood-perfused heart preparations.

CGRP-immunoreactive nerve fibers were histologically stained in the endocardium and perivascular layer of coronary vessels of canine hearts. To examine the physiological role of the CGRP in the heart function, effects of exogeneous CGRP on the hearts were studied using canine isolated, blood-perfused heart preparations. CGRP exerted dose-related potent vasodilator effects with a minimal increase in the developed tension of the papillary muscle, but slightly decreased the sinoatrial rate. The vasodilator effects were unaffected by the pretreatment of either atropine or propranolol. These specific functional effects on the coronary artery are well in accordance with the anatomical localization of CGRP. Taken together, CGRP seems to play an important role in the regulation of coronary vascular tone, while it has only a small functional role in inotropism and chronotropism in canine hearts.

Animals↗