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PubMed1999

O(2) cost of contractility but not of mechanical energy increases with temperature in canine left ventricle.

We investigated the effects of myocardial temperature on left ventricular (LV) mechanoenergetics in the excised, cross-circulated canine heart. We used the framework of the LV contractility (E(max))-pressure-volume area (PVA; a measure of total mechanical energy)-myocardial oxygen consumption (VO(2)) relationship. We have shown this framework to be useful to integrative analysis of the mechanoenergetics of a beating heart. In isovolumic contractions at a constant pacing rate, increasing myocardial temperature from 30 to 40 degrees C depressed E(max) and increased the oxygen cost of E(max), which was enhanced by dobutamine, in a linear manner. However, the slope of the VO(2)-PVA relation (reciprocal of contractile efficiency) and its VO(2) intercept remained constant. Q(10) values of E(max), the oxygen cost of E(max), and the oxygen cost of PVA were 0.4, 2.1 and 1.0, respectively, around normothermia. We conclude that the temperature-dependent processes of cross-bridge cycling and Ca(2+) handling integratively depress E(max) and augment its oxygen cost without affecting the oxygen cost of PVA as myocardial temperature increases by 10 degrees C around normothermia.

Animals↗
PubMedDate not supplied

Is there a regeneration stimulator substance in the effluent from perfused partially hepatectomized livers?

An attempt was made to transfer a stimulator substance from the perfusate of partially hepatectomized perfused livers to the portal stump of portacaval-shunted pig recipients. Blood was either cross-circulated with recipients during perfusion or was given by exchange transfusion after 4 hr perfusion. There was an increase in thymidine kinase activity and mitotic indices in biopsies from portacaval-shunted recipients whether perfusions were performed 2 or 4 days after partial hepatectomy. Blood perfused through intact livers did not enhance the regenerative response of portacaval-shunted pigs; in fact it appeared to suppress the normal small response. Approximately 10% of the portacaval-shunted recipients died acutely when perfusate was infused into the portal stump. This did not occur if saline or unperfused blood was used suggesting that some toxic substance accumulated during liver perfusion. In end-stage fulminant hepatic failure, use of blood perfused through a partially hepatectomized animal liver may provide the regenerative stimulus which often appears to be lacking.

Animals↗
PubMed1995

The effect of infused nutrients and absorbed foods on daily food intake in rats.

Studies with crossed intestines rats show that daily food intake is controlled by internal signals that arise at the level of the small intestines or from the absorption of food into the bloodstream and its subsequent metabolism. The gut can produce endogenous signals such as neural messages responding to the presence of nutrients in the wall of the small intestine or in the portal vein leading to the liver. GI hormones can be released from various regions of the small intestine and may partially inhibit food intake. When nutrients bypass the gut and are infused indirectly into the bloodstream, they produce a partial 50% to 80% compensation for the number of calories infused. Clearly, nutrients play a major role in the control of daily intake. Infusion of these nutrients into specific vascular sites suggest that they do not act directly on the brain or the liver to reduce daily intake. Cross-circulation studies suggest that the combination of hormones and nutrients do not affect intake during a single meal. It is possible that nutrients act directly on the gut to inhibit stomach emptying or on the storage tissues, such as muscle or fat, to control daily food intake.

Animals↗
PubMed1988

Ventricular systolic pressure-volume area (PVA) and contractile state (Emax) determine myocardial oxygen demand.

We have briefly reviewed the recent advances in the understanding of primary determinants of cardiac oxygen consumption (Vo2). We focused on our own experimental findings that Vo2 is a function of left ventricular systolic pressure-volume area (PVA), as a measure of total mechanical energy generated by contraction, and the left ventricular contractility index (Emax). We conclude that the cardiac oxygen demand of the ongoing contractions is equivalent to Vo2 and is a precise function of PVA and Emax whether coronary oxygen supply is normal or mildly limited in the excised, cross-circulated dog left ventricle. However, when the coronary oxygen supply is severely limited, Vo2 may not always be equivalent to the oxygen demand capability shown by the heart when its coronary oxygen supply is restored.

Animals↗
PubMed1998

Ventricular pressure-volume area (PVA) accounts for cardiac energy consumption of work production and absorption.

We briefly review that ventricular systolic pressure-volume area (PVA) can predict changes in myocardial O2 consumption (VO2) associated with cardiac work production (positive work) and absorption (negative work). PVA represents the total mechanical energy of cardiac contraction as it is an integral of mechanical energy generated during systole in the cardiac chamber. We have shown that PVA linearly correlates with VO2 under varied pre- and afterload conditions in the left ventricle of the excised cross-circulated canine heart preparation as well as other heart preparations of different species. PVA is the sum of external mechanical work (EW) and mechanical potential energy (PE) which is almost fully convertible to mechanical work without affecting VO2. To compare the energetic effects of cardiac work production and absorption, we varied the timing of the servo pump motion relative to left ventricular (LV) contraction. When the pump fills the LV during diastole and sucks (allows ejection) during systole, cardiac work is produced by the heart, and hence EW > 0. When the pump fills the LV during systole and sucks during diastole, work is absorbed by the heart, and hence EW < 0. The pressure-volume loop rotates counterclockwise when EW > 0. It rotates clockwise when EW < 0. As the result, PVA (= PE + EW) > PE when EW > 0; PVA < PE when EW < 0. We found that VO2 always linearly correlated with PVA regardless of the polarity of EW. Therefore, PVA is the unique determinant of VO2 in a cardiac chamber in a stable contractility.

Animals↗
PubMed1991

Luminal glucose enhances transepithelial Na+ and fluid transports in rat lungs.

The effects of luminal glucose on transepithelial Na+ and fluid transports were investigated in rat lungs. Two preparations were used: isolated, perfused lungs and lungs in situ perfused with blood (cross-circulations), a situation more comparable to that existing in vivo. Unidirectional (efflux from air spaces, J(out)) and net (Jnet) Na+ fluxes and fluid absorption from air spaces were estimated in lungs filled with bicarbonate-buffered solutions containing 10 mmol/l of either mannitol, glucose or alpha-methyl-D-glucopyranoside, or 0.1 mmol/l phlorizin in the presence of glucose. In the presence of mannitol J(out) was estimated to be 7.8 +/- 1.02 pmol cm-2 s-1 in isolated lungs and 9.2 +/- 0.97 pmol cm-2 s-1 in lungs in situ, and Jnet 1.0 +/- 0.33 and 2.5 +/- 0.35 pmol cm-2 s-1, respectively. When glucose replaced mannitol J(out) (+ 30% + 40%), Jnet (+200% + 300%) and fluid absorption (+ 100% + 400%) were enhanced in both preparations. Substituting methyl glucoside for mannitol increased Na+ and fluid absorption rates to the same extent as glucose. Phlorizin, in the presence of glucose, reduced Na+ and fluid transports to values similar to those observed in the presence of mannitol. These changes did not result from modifications of the paracellular permeabilities (assessed with [3H]mannitol).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Cardiovascular and sympathetic responses to intracarotid and intravenous injections of serotonin in rats.

The possible central regulation of cardiovascular system by serotoninergic neurones was investigated in rats by using a cross-circulated head preparation. Intracarotid injections of serotonin (5-HT, 0.1-10 micrograms) consistently produced neurally mediated vasodepression in the recipient body. Although intravenous injections of 5-HT (0.1-1 micrograms) caused similar depressor responses, larger doses (5-10 micrograms) caused biphasic responses, consisting of vasodepression followed by a sustained pressor response. Despite the biphasic blood pressure responses, sympathetic nerve activity was consistently reduced by the intravenous 5-HT. Bilateral vagotomy abolished the vasodepressor responses to intravenous injections of 5-HT (10 micrograms) and made the responses purely pressor, but the vasodepressor responses to intracarotid injections of 5-HT (10 micrograms) were largely unaffected. Following destruction of central noradrenergic neurones by intracerebroventricular injections of 6-hydroxydopamine, the vasodepressor responses to intracarotid 5-HT (1-10 micrograms), but not to the intravenous 5-HT, were significantly reduced. These results suggest that intravenous injections of 5-HT reduce nerve activity by affecting the reflex mechanism via the vagus nerves. On the other hand, the vasodepression and reduction of the nerve activity by the intracarotid injections appears to be of central origin, and the vasodepression could be mediated via noradrenergic mechanisms in the brain.

Animals↗
PubMed1975

The influence of imipramine on dopamine-induced ganglionic inhibition and neurogenic vasodilatation in the dog.

Imipramine potentiates the dopamine-induced inhibition in the paravertebral lumbar ganglia of the dog. Potentiation by imipramine of the dopamine-induced neurogenic vasodilatation in the isolated perfused gracilis muscle, is seen in cross-circulation preparations only, where imipramine is injected into the perfusion circuit of an isolated perfused gracilis muscle, it antagonizes the dopamine-induced neurogenic vasodilatation. When imipramine is injected intravenously into a dog with an autoperfused gracilis muscle, the peripheral antagonism masks the potentiating effect at the ganglionic level, and the dopamine-induced neurogenic vasodilatation is abolished.

Action Potentials↗
PubMed1976

Effects of atrio-ventricular conduction of calcium-antagonistic coronary vasodilators, local anaesthetics and quinidine injected into the posterior and the anterior septal artery of the atrio-ventricular node preparation of the dog.

The effects on atrio-ventricular (A-V) conduction and blood flow of calcium-antagonists (verapamil, nifedipine and diltiazem), local anaesthetics (procaine and lidocaine) and quinidine were investigated in the isolated, cross-circulated A-V node preparation of the dog. The drugs were injected individually into the posterior septal artery (PSA) through which the upper part of the A-V node is mainly perfused or into the anterior septal artery (ASA) through which the lower part of the node and the more distal conduction system are perfused. Single injections into the PSA of nifedipine (0.3-10 mug), verapamil (1-30 mug), diltiazem (1-30 mug), quinidine (30-300 mug), lidocaine (100 mug-1 mg) and procaine (300 mug-3 mg) produced a dose-related increase in the A-V conduction time and with higher doses of these drugs a second or third degree block of A-V conduction occurred. Nifedipine (0.3-30 mug) and verapamil (1-100 mug) injected into the ASA scarcely affected A-V conduction. Quinidine (30 mug-1 mg) and lidocaine (100 mug-3 mg) injected into the ASA prolonged the A-V conduction time in a dose-related manner, although the effects were less prominent than those produced upon injection into the PSA. High doses of quinidine (3 mg) and lidocaine (3-10 mg) injected into the ASA altered the shape of ventricular bipolar electrograms and prolonged the time interval between an electrogram of the right bundle branch and that of the ventricle. The results are consistent with the hypothesis that in excitation of A-V nodal cells a slow calcium current rather than a fast sodium current plays an important role and that in the His-Purkinje-ventricular system the fast sodium current is predominant. Single injections of the 6 drugs into the PSA produced a dose-related increase in blood flow through the PSA. All drugs but nifedipine increased the blood flow in almost the same dose range that caused impairment of A-V conduction. Nifedipine was 10 times more potent in increasing the blood flow than in impairing A-V conduction.

Action Potentials↗
PubMed1994

A further study of the vasodilator and negative inotropic mechanisms of action of nicorandil and its congeners in the canine heart.

The vasodilator and negative inotropic mechanisms of action of nicorandil and its congeners (SG-209, SG-103, and SG-86) were investigated in isolated canine papillary muscle preparations cross-circulated through the anterior septal artery with support dogs. SG-209, SG-103, and SG-86 were obtained by replacement of the nitroxyl group of nicorandil by acetoxyl, nicotinoyloxyl, and hydroxyl groups, respectively. Nicorandil (0.03-10 mumol), SG-209 (0.1-10 mumol), SG-103 (1-30 mumol), and SG-86 (3-100 mumol) all produced an increase in coronary blood flow through the anterior septal artery. Both nicorandil and SG-209 produced a near-maximal increase in coronary blood flow, the latter being about 5.5 times less potent than the former. SG-103 and SG-86 were far less potent than SG-209 in that order. The vasodilator actions of nicorandil and SG-209 were antagonized by glibenclamide given IV to support dogs, but those of SG-103 and SG-86 were not. The pKB values of glibenclamide were 6.34 toward nicorandil and 6.49 toward SG-209. Developed tension of the papillary muscle was reduced by nicorandil, SG-209, and SG-103, but not by SG-86. In this respect SG-209 was about 4.7 times less potent than nicorandil, and SG-103 was much less potent than SG-209. The negative inotropic effects of nicorandil and SG-209 were antagonized by glibenclamide, but that of SG-103 was not.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Ejecting activation differs in energetics from ordinary positive inotropism in the canine left ventricle.

Ventricular ejection is known to have dual effects on the end-systolic pressure: the ejecting deactivation by a relatively large ejection against a low afterload versus the ejecting activation by a relatively small ejection against a high afterload. We studied how the increase in contractility index (Emax) by the ejecting activation would affect myocardial oxygen consumption (VO2). To this end, left ventricular steady-state ejecting contractions were produced with various stroke volumes from a fixed end-diastolic volume in an excised cross-circulated canine heart. The effect of the ejection-activated Emax on VO2 was assessed by the relation between VO2 and pressure-volume area (PVA). PVA is the total mechanical energy generated by ventricular contraction. In contrast to the elevation of the linear VO2-PVA relation in a parallel manner with an enhanced Emax by ordinary positive inotropic agents such as catecholamines and calcium, the ejection-activated Emax did not elevate the VO2-PVA relation. This result indicates that the ejecting activation enhances Emax in an energetically different manner from ordinary positive inotropism in the canine left ventricle.

Animals↗
PubMed1992

Similar oxygen cost of myocardial contractility between DPI 201-106 and epinephrine despite different subcellular mechanisms of action in dog hearts.

The effects of DPI 201-106 (a novel, cyclic AMP-independent positive inotropic agent with Ca(2+)-sensitizing and Na(+)-channel agonistic mechanisms) on myocardial mechanics and energetics were assessed in the excised cross-circulated dog left ventricle. In the first protocol, the relation between left ventricular oxygen consumption (VO2) and systolic pressure-volume area (PVA) was analyzed before and during administration of DPI 201-106. The reciprocal of the slope of the VO2-PVA relation has been shown to reflect the contractile efficiency, and the VO2-intercept consists of the oxygen cost of contractility-dependent excitation-contraction coupling and basal metabolism. DPI 201-106 increased Emax (contractility index) and elevated the VO2-PVA relation in a parallel manner, i.e., the VO2-intercept increased without a change in the slope. In the second protocol, the increase in the VO2-intercept of the VO2-PVA relation for a unit increase in Emax (i.e., oxygen cost of enhanced contractility) was compared between DPI 201-106 and epinephrine in a paired manner in each heart. Epinephrine significantly abbreviated the time to end systole, whereas DPI 201-106 did not, suggesting that the mechanism of inotropic action differed between the two drugs. However, the oxygen cost of enhanced contractility was the same between the two drugs in each heart. Therefore, DPI 201-106 did not alter the contractile efficiency nor spare the oxygen cost of enhanced contractility as compared to epinephrine under the present experimental conditions. This suggests that the Ca(2+)-sensitizing effect of DPI 201-106, if any, is too small to spare the oxygen cost of contractility in the blood-perfused, non-failing dog heart.

Animals↗
PubMed1988

A new cardiotonic agent, OPC-8212, elevates the myocardial oxygen consumption versus pressure-volume area (PVA) relation in a similar manner to catecholamines and calcium in canine hearts.

We studied the effect of a new positive inotropic agent, OPC-8212 (3,4-Dihydro-6-[4-(3,4-dimethoxybenzoyl)-1-piperazinyl]-2(1H)-quinolinon e), on the relation between left ventricular oxygen consumption (VO2) and pressure-volume area (PVA) in excised cross-circulated dog hearts. PVA represents the total mechanical energy generated by ventricular contraction. OPC-8212 increased the contractility index, Emax, by 59% +/- 36% from 7.6 +/- 4.3 to 11.1 +/- 4.6 mmHg/(ml/100 g LV [leftventricle]). OPC-8212 elevated the VO2-PVA relation without a significant change in its slope. Namely, OPC-8212 did not affect the mechanical efficiency of the contractile machinery from the PVA-dependent fraction of VO2 to PVA, but increased the PVA-independent fraction of VO2 which is related with non-mechanical processes of contraction. This effect suggested an increased energy expenditure for excitation-contraction coupling. These results associated with the enhanced contractile state by OPC-8212 were both qualitatively and quantitatively similar to those obtained with catecholamines and calcium in our previous study. This suggests that OPC-8212, catecholamines, and calcium have similar effects on intracellular Ca2+ concentration and enhanced ventricular contractility.

Animals↗
PubMed1988

Paired pulse pacing increases cardiac O2 consumption for activation without changing efficiency of contractile machinery in canine left ventricle.

The relation between cardiac O2 consumption (VO2) and the total mechanical energy (TME) generated by contraction was studied under paired-pulse (PP) pacing and compared with that under single-pulse pacing at the same basic rate as PP pacing and at the double-pacing rate in ten excised cross-circulated canine left ventricles (LV). TME was assessed by the systolic pressure-volume (P-V) area (PVA) defined as the area bounded by the end-systolic and end-diastolic P-V curves and the systolic P-V trajectory. The VO2-PVA relation was linear under PP pacing as well as at control and double heart rates. PP pacing increased LV contractility index Emax from 6.3 +/- 3.3 (SD) to 18.0 +/- 8.6 mmHg/(ml/100 g) and elevated markedly the VO2-PVA relation by increasing the VO2-axis intercept (or PVA-independent VO2) from 0.62 +/- 0.11 to 1.13 +/- 0.35 J.beat-1.100 g-1. However, PP pacing did not change the slope of the VO2-PVA relation at 2.24 +/- 0.53 (dimensionless). The efficiency from PVA-dependent VO2 (total VO2-PVA-independent VO2) to PVA (=TME), calculated as the reciprocal of the slope of the VO2-PVA relation, was also constant at 47 +/- 11% regardless of PP pacing. These results are similar to previous results obtained by positive inotropic interventions with catecholamines and Ca2+. We conclude that PP pacing augments the PVA-independent VO2 for activation without affecting the efficiency of the contractile machinery to generate TME from the PVA-dependent VO2.

Animals↗
PubMed1997

Calcium equally increases the internal calcium recirculation fraction before and after beta-blockade in canine left ventricles.

We studied whether intracoronary Ca administration after beta-blockade would increase the internal Ca recirculation fraction (RF) analogously to the Ca administration before beta-blockade. This was performed in excised cross-circulated canine hearts. We analyzed the exponential decay component of the postextrasystolic potentiation (PESP) following a spontaneous extrasystole. All the PESPs decayed in alternans with atrial pacing at a constant rate. We obtained the time constant (tau(e)) of the monoexponential decay component of the alternans PESP. An increment of intracoronary Ca by 1.5 mmol/l enhanced the left ventricular contractility index Emax (end-systolic maximum elastance) by 2.5 times before and after beta-blockade with propranolol. The intracoronary Ca after beta-blockade slightly but significantly increased tau(e), and hence increased RF calculated from tau(e) by RF = exp(-1/tau(e)). This was analogous to the slightly increased tau(e) and RF with Ca before beta-blockade. We speculate that the myocardial cyclic AMP-dependent phosphorylation level would not significantly alter the effect of intracoronarily administered Ca on myocardial Ca handling, in terms of tau(e) and RF.

Adenosine Monophosphate↗
PubMed1991

Tin compounds inhibit the plasma cell response to metallic tin. Transfer of inhibition by parabiosis.

Injection of metallic tin powder causes intense proliferation of plasma cells in draining lymph nodes of Lewis rats. Pretreatment orally with soluble tin salts prevents this response to subsequently injected metallic tin. In the present work, pretreatment with tin salts by parenteral injection was just as effective as addition to the drinking water. This new approach made the following experiments possible. Poorly soluble tin compounds were found to be inhibitory when injected parenterally. Tin salts injected parenterally into one of two rats joined in parabiotic union prevented the plasma cell response to metallic tin in both parabionts. The transfer of the inhibitory effect via the cross-circulating blood represents significant progress toward understanding the mechanisms involved. The evidence suggests the possibility that tin salts elicit an intermediary substance or process that is responsible for inhibition of the plasma cell response to metallic tin.

Animals↗
PubMed1998

[Intermittent warm blood cardioplegia--an experimental study].

The influence of intermittent warm blood cardioplegia (WBCP) on myocardial function and metabolism was studied. Fourty-two adult mongrel dogs were used. The isolated heart of one dog was perfused by the cross circulation method with another support dog. The dogs then were divided into three groups. In group I (n = 6), the empty beating heart was perfused with warm blood (WB) kept at 36 degrees C for 100 minutes. In group II (n = 7), the arrested heart was perfused with continuous WBCP using modified Fremes solution for 100 minutes. In group III (n = 8), the arrested heart was perfused with WBCP for 10 minutes following a 15-minute non-perfusion period. This perfusion method was repeated four times. The E max, LV developed pressure, +/- LV dp/dt and LVEDP were all measured to evaluated the myocardial function. In addition, the coronary venous blood pH, myocardial oxygen consumption, myocardial lactate extraction, coronary blood flow, myocardial high energy phosphate content and myocardial water content were also studied in order to elucidate the myocardial metabolism. Regarding the myocardial function, no significant difference was observed between the three groups. The results of chemical studies on the myocardial metabolism were as follows: (1) the coronary venous blood pH in group III decreased at the end of the no perfusion period of WBCP. But it thereafter gradually returned to the normal physiological range; (2) the myocardial oxygen consumption in group III increased just after each interruption, but then gradually decreased toward following intermittent WBCP; (3) the myocardial lactate extraction decreased at the end of the non-perfusion period. However, it gradually returned to the control value by the end of each period of WBCP perfusion; (4) after 60 minutes of reperfusion, the coronary venous blood pH, myocardial oxygen consumption and myocardial lactate extraction showed no significant differences between the groups; (5) the coronary blood flow in group III increased significantly after 1 minute of reperfusion; (6) the ATP value in group III decreased significantly after 60 minutes of reperfusion. The ADP and AMP values demonstrated no significant difference between the groups during the same period; and (7) no significant difference was seen in the myocardial water content between the groups after 60 minutes of reperfusion. It is thus concluded that 10 minutes of intermittent WBCP followed by a 15-minute interruption appeared to have no deleterious effect on the myocardial function and metabolism.

Animals↗
PubMed1976

Pulmonary bacterial defense. Effect of the burn wound on transfer of alveolar macrophage activation in rats by parabiosis.

The alveolar macrophage was studied in parabiotic rats using an inbred strain. Parabiotic pairs were sutured together at five weeks of age. Rats were subjected to a full thickness cutaneous burn of 20 per cent of the body surface area at seven weeks of age, and alveolar macrophages were washed from the lungs at six days post burn. The number of alveolar macrophages, their per cent of activation, and their ability to phagocytize and kill P aeruginosa in vitro were significantly increased at six days post burn in the burned controls and in both the burned and unburned members of the parabiotic pairs. No change in the alveolar macrophages was found in either unburned parabiotic pairs or in those which were sham-burned. These results indicate that a humoral or cellular agent produced either within the cutaneous burn wound or elsewhere as a response to the injury, traverses the parabiotic cross circulation to stimulate the alveolar macrophages.

Animals↗