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At least 469 records · Page 26Linked to original sources
PubMed1987

Fluid absorption by rat lung in situ: pathways for sodium entry in the luminal membrane of alveolar epithelium.

1. The purpose of the investigation was to characterize the luminal membrane and the paracellular pathway of rat lung alveolar epithelium. Experiments were performed on lungs in situ instilled with isotonic, buffered Ringer solution and perfused with blood from a donor rat using cross-circulation technique. 2. The rate of active Na+ transport was 4.4 pmol/(cm2s). The fluid absorption was 156 nl/s, and was unaffected by the presence of protein in the instillate (166 nl/s). In the absence of Na+, fluid absorption was zero. Amiloride (10(-3) M) reduced fluid absorption by 60%. Amiloride, combined with absence of D-glucose, arrested fluid absorption completely. Phloridzin at the luminal side reduced fluid absorption whilst phloretin had no effect. Amiloride together with phloridzin (10(-3) M) also arrested absorption. Thus, there are two entry systems for Na+ in the luminal membrane: Na+ channels and a Na+-D-glucose symport. These results show that alveolar fluid absorption is due to cellular activity. 3. Substitution of Cl- with gluconate not only stopped fluid absorption, but led to slight reversal of net fluid movement. 4. Passive unidirectional flux of Na+, determined with 22Na+, was 9.9 pmol/(cm2s) and that of Cl-, determined with 36Cl-, was 12.4 pmol/(cm2s). These fluxes were based on an assumed alveolar surface area of 5000 cm2. Transference numbers calculated from these figures are close to those in free solution, suggesting a neutral or weakly charged intercellular junctional pathway. The D-mannitol permeability in the paracellular pathway was 1.7 X 10(-8) cm/s. 5. It is a consequence of the proposed mechanism for fluid absorption that it becomes inoperative if the normally high reflexion coefficients for Na+ and Cl- are lowered in pathological states. In such conditions pulmonary oedema may develop depending on the net balance of passive mechanical and colloid-osmotic forces. 6. An explanation of the reversal of fluid transport at the time of birth is presented.

Absorption↗
PubMed1971

A portal blood factor as the humoral agent in liver regeneration.

It was demonstrated, by use of extracorporeal cross-circulation, that a humoral factor responsible for liver regeneration does not arise from the liver remnant. While intact livers of normal rats incorporated [methyl-(3)H]- thymidine in proportion to the amount of liver removed in the partner, the greatest response occurred after a total hepatectomy. Evidence from portacaval-shunted,partially hepatectomized animals connected to normal members indicates that the factor is in portal blood and that the onset of regeneration is the result of a quantitative imbalance between the available portal blood factor and the number of liver cells present.

Animals↗
PubMed1984

Effects of bile and bile salt infusions on renal function in dogs.

A previous study in dogs indicated that 4 h of acute biliary obstruction was associated with an increment in the glomerular filtration rate (GFR), renal perfusion, and urinary sodium excretion. These effects could also be transmitted to a "recipient" dog following 2 h of cross circulation. In this study we examined the possible role of bile and bile products in reproducing these effects. The i.v. infusion of 15 mL of undiluted gallbladder bile produced a marked diuresis and natriuresis, while arterial pressure and GFR declined. Bile diluted as much as 1/100 in isotonic saline could produce an effect when infused intravenously. When bile diluted to 1/250 was infused into th left renal artery at 0.5 mL/min, a diuretic and natriuretic response was obtained. GFR and renal blood flow declined with more concentrated solutions, though blood pressure remained normal. Dialysis of bile, or prior incubation with cholestyramine or plasma, failed to uncover a renal vasodilator effect. Following the first two procedures, the diuretic properties of infused bile were lost. The infusion of small amounts of synthetic bile salts (taurocholate or glycocholate) into the left renal artery caused marked increments in urinary sodium excretion without any change in renal hemodynamics. The infusion of bilirubin was without effect on renal function. Taurine and glycine, the amino acids present in the conjugated bile acids, were injected i.v. Both caused marked diuresis and natriuresis, but only glycine increased GFR and renal perfusion. The plasma levels of these substances, however, were unchanged following 4 h of acute biliary obstruction. We conclude that while bile salts probably cause the diuresis of biliary obstruction, the mechanism for the increase in GFR has not yet been identified.

Animals↗
PubMed1986

Response of rat jejunum to changes in sodium and volume balance.

Initial studies determined whether a renal factor facilitates decreased jejunal absorption following volume expansion of the anesthetized rat. Volume expansion (VE) decreased jejunal absorption to the same extent in both normal and nephrectomized animals. Furthermore, VE of a donor animal failed to alter jejunal absorption in a recipient following cross circulation. Thus, a hormonal factor is not implicated in the jejunal response to VE. Additional experiments demonstrated that rats ingesting a high-Na diet exhibited levels of jejunal absorption lower than animals fed a normal-Na diet. High-Na animals were not volume expanded. Plasma aldosterone concentrations and plasma renin activity were reduced in high-Na animals. Bilateral adrenalectomy-nephrectomy inhibited jejunal absorption. However, neither bilateral adrenalectomy nor bilateral nephrectomy alone inhibited jejunal absorption. Furthermore, inhibition of angiotensin formation in adrenalectomized animals failed to alter jejunal absorption. Decreased jejunal absorption in high-Na animals is not due to volume expansion or to inhibition of the renin-angiotensin-aldosterone axis.

Adrenalectomy↗
PubMed2004

Calpain inhibitor-1 protects the rat heart from ischemia-reperfusion injury: analysis by mechanical work and energetics.

We hypothesized that calpain inhibitor-1 protected left ventricular (LV) function from ischemia-reperfusion injury by inhibiting the proteolysis of alpha-fodrin. To test this hypothesis, we investigated the effect of calpain inhibitor-1 on LV mechanical work and energetics in the cross-circulated rat hearts that underwent 15-min global ischemia and 60-min reperfusion (n = 9). After ischemia-reperfusion with calpain inhibitor-1, mean end-systolic pressure at midrange LV volume and systolic pressure-volume area (PVA) at midrange LV volume (total mechanical energy per beat) were hardly changed, although they were significantly (P < 0.01) decreased after ischemia-reperfusion without calpain inhibitor-1. Mean myocardial oxygen consumption per beat (Vo(2)) intercepts (PVA-independent Vo(2); Vo(2) for the total Ca(2+) handling in excitation-contraction coupling and basal metabolism) of Vo(2)-PVA linear relations were also unchanged after ischemia-reperfusion with calpain inhibitor-1, although they were significantly (P < 0.01) decreased after ischemia-reperfusion without calpain inhibitor-1. There were no significant differences in O(2) costs of LV PVA and contractility among the hearts in control (or normal) postischemia-reperfusion and postischemia-reperfusion with calpain inhibitor-1. Western blot analysis of alpha-fodrin and the immunostaining of 150-kDa products of alpha-fodrin confirmed that calpain inhibitor-1 almost completely protected the proteolysis of alpha-fodrin. Our results indicate that calpain inhibitor-1 prevents the heart from ischemia-reperfusion injury associated with the impairment of total Ca(2+) handling by directly inhibiting the proteolysis of alpha-fodrin.

Animals↗
PubMed2006

Transcoronary gene transfer of SERCA2a increases coronary blood flow and decreases cardiomyocyte size in a type 2 diabetic rat model.

The Otsuka Long-Evans Tokushima fatty rat is an animal model of Type 2 diabetes mellitus (DM), which is characterized by diastolic dysfunction associated with decreased sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a). The aim of this study was to examine whether gene transfer of SERCA2a can influence coronary blood flow and cardiomyocyte diameter in this model. DM rats were injected with adenovirus carrying SERCA2a (DM+SERCA) or beta-galactosidase gene (DM+betaGal). Coronary blood flow was measured in cross-circulated excised hearts 3 days after infection. Although in all groups coronary blood flow remained unchanged even if left ventricular (LV) volume or intracoronary Ca(2+) infusion was increased, the DM+SERCA group showed a sustained increase in coronary blood flow compared with the other groups. This result suggests that the sustained high coronary blood flow is a specific response in SERCA2a-overexpressed hearts. Although the LV weight-to-body weight ratio (LV/BW) and cardiomyocyte diameter were higher in the DM and DM+betaGal groups than in the non-DM group, in the DM+SERCA group, these measurements were restored to non-DM size. The percentages of collagen area in the three DM groups was significantly higher than results shown in non-DM rats, and there were no significant differences in collagen area percentage among the three DM groups. These results suggest that a lowered LV/BW by SERCA2a overexpression is due mainly to reduced size of cardiomyocytes without any changes in collagen area percentage. In conclusion, in DM failing hearts, SERCA2a gene transfer can increase coronary blood flow and reduce cardiomyocyte size without reduction in collagen production.

Adenoviridae↗
PubMed2004

Na+/Ca2+ exchange inhibition protects the rat heart from ischemia-reperfusion injury by blocking energy-wasting processes.

We have recently reported that exposure of rat hearts to high Ca(2+) produces a Ca(2+) overload-induced contractile failure in rat hearts, which was associated with proteolysis of alpha-fodrin. We hypothesized that contractile failure after ischemia-reperfusion (I/R) is similar to that after high Ca(2+) infusion. To test this hypothesis, we investigated left ventricular (LV) mechanical work and energetics in the cross-circulated rat hearts, which were subjected to 15 min global ischemia and 60 min reperfusion. Sixty minutes after I/R, mean systolic pressure-volume area (PVA; a total mechanical energy per beat) at midrange LV volume (mLVV) (PVA(mLVV)) was significantly decreased from 5.89 +/- 1.55 to 3.83 +/- 1.16 mmHg.ml.beat(-1).g(-1) (n = 6). Mean myocardial oxygen consumption per beat (Vo(2)) intercept of (Vo(2)-PVA linear relation was significantly decreased from 0.21 +/- 0.05 to 0.15 +/- 0.03 microl O(2).beat(-1).g(-1) without change in its slope. Initial 30-min reperfusion with a Na(+)/Ca(2+) exchanger (NCX) inhibitor KB-R7943 (KBR; 10 micromol/l) significantly reduced the decrease in mean PVA(mLVV) and Vo(2) intercept (n = 6). Although Vo(2) for the Ca(2+) handling was finally decreased, it transiently but significantly increased from the control for 10-15 min after I/R. This increase in Vo(2) for the Ca(2+) handling was completely blocked by KBR, suggesting an inhibition of reverse-mode NCX by KBR. alpha-Fodrin proteolysis, which was significantly increased after I/R, was also significantly reduced by KBR. Our study shows that the contractile failure after I/R is similar to that after high Ca(2+) infusion, although the contribution of reverse-mode NCX to the contractile failure is different. An inhibition of reverse-mode NCX during initial reperfusion protects the heart against reperfusion injury.

Animals↗
PubMed2007

Targeted gene transfer increases contractility and decreases oxygen cost of contractility in normal rat hearts.

The aim of this study was to examine how global cardiac gene transfer of sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) can influence left ventricular (LV) mechanical and energetic function, especially in terms of O(2) cost of LV contractility, in normal rats. Normal rats were randomized to receive an adenovirus carrying the SERCA2a (SERCA) or beta-galactosidase (beta-Gal) gene or saline by a catheter-based technique. LV mechanical and energetic function was measured in cross-circulated heart preparations 2-3 days after the infection. The end-systolic pressure-volume relation was shifted upward, end-systolic pressure at 0.1 ml of intraballoon water volume was higher, and equivalent maximal elastance, i.e., enhanced LV contractility, was higher in the SERCA group than in the normal, beta-Gal, and saline groups. Moreover, the LV relaxation rate was faster in the SERCA group. There was no significant difference in myocardial O(2) consumption per beat-systolic pressure-volume area relation among the groups. Finally, O(2) cost of LV contractility was decreased to subnormal levels in the SERCA group but remained unchanged in the beta-Gal and saline groups. This lowered O(2) cost of LV contractility in SERCA hearts indicates energy saving in Ca(2+) handling during excitation-contraction coupling. Thus overexpression of SERCA2a transformed the normal energy utilization to a more efficient state in Ca(2+) handling and superinduced the supranormal contraction/relaxation due to enhanced Ca(2+) handling.

Animals↗
PubMed1977

End-diastolic and end-systolic ventricular volume clamper for isolated canine heart.

We devised a servo-controlled pump system which can clamp both end-diastolic and end-systolic volumes of the left ventricle of an excised, supported canine heart at desirable values in the face of changing patterns of ejection and filling. The system consists of a Bellofram cylinder and a powerful electromagnetic shaker which is driven by a position servo circuit. A water-filled balloon placed in the ventricle was connected to the water housing of the cylinder. As the ECG triggered the system, a fixed amount of water reciprocated between the heart and the cylinder in a programmed manner. The onset, duration, and speed of ejection and those of filling can be programmed separately. The performance of this pump system was tested in experiments on 15 cross-circulated hearts and proved satisfactory for precise analysis of the instantaneous pressure-volume relation in the ventricle.

Animals↗
PubMed1979

Left ventricular systolic pressure-volume area correlates with oxygen consumption.

In 13 excised, cross-circulated canine hearts, we studied the correlation between left ventricular oxygen consumption per beat (MVO2) and the magnitude of a specific pressure-volume (P-V) area circumscribed by the end-systolic and end-diastolic P-V relationship curves and the systolic segment of the P-V trajectory of a left ventricular contraction. The pressure and volume load of the ventricle were changed with a volume servo pump in order to alter the P-V area, and MVO2 was measured (after each change in the pressure and volume load). In the data collected from both isovolumic and ejecting contractions of each left ventricle contracting with a stable inotropic background, we found a linear correlation between MVO2 and the P-V area. The average correlation coefficient was 0.92 +/- 0.016 (SE). Linear regression analysis yielded the formula: MVO2 (ml/beat) = alpha[P-V area (mmHg.ml/beat)] + b, where alpha, the slope coefficient, was (1.53 +/- 0.14) x 10(-5) and b, which probably represents the basal O2 consumption, was 0.019 +/- 0.003 ml/beta. We propose that the P-V area as defined above may be a good index of ventricular oxygen consumption under a given inotropic background.

Animals↗
PubMed1983

Heart rate-independent energetics and systolic pressure-volume area in dog heart.

Left ventricular (LV) systolic pressure-volume area (PVA), a new measure of total mechanical energy for the contraction, linearly correlates with its oxygen consumption per beat (VO2) regardless of contraction mode in a canine heart with stable chronotropism and inotropism. PVA is the area in the pressure-volume (PV) diagram circumscribed by the end-systolic and end-diastolic PV relation curves and the systolic segment of the PV loop and has dimensions of energy. We investigated whether primary changes in heart rate would affect the VO2-PVA relation. In the excised cross-circulated canine heart with left ventricular load controlled with a servo pump, we changed heart rate by pacing to compare the VO2-PVA relations at low [124 +/- 17 (SD) min-1] and high (193 +/- 23) heart rates. In 15 left ventricles, VO2 (ml O2 X beat-1 X 100 g LV-1) was (1.75 +/- 0.57) X 10(-5) PVA (mmHg X ml X beat-1 X 100 g LV-1) + 0.031 +/- 0.011 (ml O2 X beat-1 X 100 g LV-1). The VO2-PVA relation was virtually independent of heart rate in individual hearts. We conclude that the load-independent VO2-PVA relationship is not affected by chronotropism in a given canine left ventricle.

Animals↗
PubMed1984

Oxygen consumption and pressure-volume area of abnormal contractions in canine heart.

Oxygen consumption rates (VO2) of isovolumic and normally ejecting contractions are closely correlated with their systolic pressure-volume areas (PVA) in a stable canine left ventricle. PVA is the area in the pressure-volume (PV) diagram that is circumscribed by the end-systolic and end-diastolic PV relation curves and the systolic segment of the PV loop trajectory. We studied whether VO2s of abnormally loaded ejecting contractions were similarly correlated with their PVAs. Various abnormally ejecting contractions were produced in the left ventricle of the cross-circulated canine heart. VO2 and PVA data of the various abnormal contractions and the isovolumic and normally ejecting contractions were pooled together, to which the correlation and regression analyses were applied. They could be fitted by a linear regression analyses were applied. They could be fitted by a linear regression line with a high correlation coefficient and a slight scatter in each heart. We therefore conclude that PVA is the primary correlate of VO2, not only in the isovolumic and normally ejecting contractions but also in various abnormally loaded contractions in a given canine left ventricle with a stable contractile state.

Animals↗
PubMed1986

Left ventricular regional work from wall tension-area loop in canine heart.

To quantitatively evaluate left ventricular (LV) regional work, LV pressure-volume relation and wall tension-regional area (TA) relation were analyzed in the excised cross-circulated left ventricle connected to a volume servo pump system. Wall tension was calculated using Laplace's law for a spherical model, and regional area was determined from orthogonal segment lengths measured with pairs of ultrasonic crystals. Data were obtained by changing LV end-diastolic volume or stroke volume before and after dobutamine infusion and before and after global ischemia. Regional work, assessed from the area within a TA loop during one cardiac cycle, correlated well with simultaneously obtained LV stroke work under all of the above experimental conditions (r = 0.90 +/- 0.09 to 0.97 +/- 0.02), and the linear regression line was not altered by changes in stroke volume, end-diastolic volume, or contractile state. Furthermore, measured regional work (RWm) proved to agree closely with the predicted value (RWp) calculated from LV stroke work and regional area [RWm = 0.91 RWp - 0.69 (mmHg . ml), r = 0.93]. Thus we conclude that TA relation may be useful for quantitative evaluation of regional work of the LV wall.

Animals↗
PubMed1986

Peak isovolumic pressure-volume relation of puppy left ventricle.

We studied peak isovolumic pressure-volume (PV) relation of the left ventricle in 3-mo-old mongrel puppies. A puppy heart was excised and cross circulated with an adult dog. Left ventricular pressure and volume were measured with a water-filled balloon. Peak isovolumic PV curve in control contractile state was convex upward, reaching a maximum pressure of 130 mmHg. Epinephrine (0.6 microgram/min intracoronary) shifted the curve leftward and up to a maximum pressure of 160 mmHg. Propranolol (0.8 mg intracoronary) shifted it rightward and down to a maximum pressure of 110 mmHg. These PV curves were reasonably fitted by an asymptotic equation: P = A (1 - exp[-B (V - Vd)]), where V was normalized volume for 100 g left ventricle and Vd (6 ml/100 g) was V at which peak pressure was zero. A and B are regression coefficients. A was 149, 169, and 120 mmHg, and B was 0.16, 0.19, and 0.06 ml, respectively, in control, enhanced, and depressed contractile states. These changes in A and B were statistically significant. We conclude that the puppy left ventricular peak isovolumic PV curve is convex upward and shifts sensitively with inotropic changes.

Animals↗
PubMed1986

Ventricular suction under zero source pressure for filling.

We quantified ventricular suction flow, volume, and pressure under hydrostatically zero source pressure for filling. A large-bore electromagnetic flow probe was placed in the valve-free mitral annulus of the dog heart that had been excised and was cross circulated with the left atrium widely opened. With the heart immersed in a blood pool, ventricular suction flow and transmural pressure were measured. After a rapid ejection flow [peak: 110 +/- 47 (SD) ml . s-1 . 100 g left ventricle-1] during systole, a slow suction flow (peak: 26 +/- 20 ml . s-1 . 100 g-1) occurred during diastole despite the zero source pressure for filling. Peak transmural pressure during ejection was 6 +/- 3 mmHg, and peak negative transmural pressure during suction was 2 +/- 1 mmHg. Suction volume, which was equal to ejection volume in steady state, was 8 +/- 3 ml/100 g left ventricle. Increases in paced heart rate markedly decreased suction volume by curtailing diastolic filling time. Epinephrine, propranolol, calcium, and verapamil variably changed suction volume, and these effects were primarily accounted for by the accompanied heart rate changes.

Analysis of Variance↗
PubMed1987

Transient vs. steady end-systolic pressure-volume relation in dog left ventricle.

We compared transient slope of end-systolic pressure-volume line (T-Emax) with steady Emax (S-Emax) in isolated cross-circulated canine left ventricles. T-Emax is the slope of the end-systolic pressure-volume line (ESPVL) determined from the last steady-state ejecting contraction (SEC) and the first transient isovolumic contraction produced by end-diastolic volume clamp. S-Emax is the slope of ESPVL determined from five steady-state contractions by linear regression analysis. We obtained three T-Emax values in the same contractile state by changing ejection fraction (EF) of SEC to three levels (range 14-58%) from the same end-diastolic volume. T-Emax variably increased with EF in any contractile state. The ratios of the three T-Emax values to the same S-Emax value was 1.08 +/- 0.04 (11 ventricles, means +/- SE) for high EF, 0.87 +/- 0.06 for middle EF, and 0.69 +/- 0.07 for low EF in control contractile state. These ratios decreased under epinephrine and increased under propranolol. We conclude that T-Emax depends not only on EF but also on contractile state in isolated dog left ventricles.

Animals↗
PubMed1987

Relation between oxygen consumption and pressure-volume area of in situ dog heart.

We studied the relation between O2 consumption (VO2) and the systolic pressure-volume area (PVA) in the left ventricle of open-chest dogs. PVA and the slope (Emax) of the end-systolic pressure-volume line were determined by an abrupt occlusion of the ascending aorta. VO2 linearly correlated with PVA in control contractile state, where Emax was 15.8 +/- 4.4 (SD) mmHg/ml with intact reflexes and 11.5 +/- 1.2 mmHg/ml with blocked reflexes. Emax and the VO2 axis intercept of the VO2-PVA line were greater in the in situ heart than in the excised cross-circulated dog heart in our previous study. Enhancement of contractile state by dobutamine increased Emax by 60-80% and shifted the VO2-PVA line upward, increasing the VO2 axis intercept by 38% with intact reflexes and by 79% with blocked reflexes. The slope had a tendency to increase with dobutamine, but the increase was statistically insignificant. We conclude that PVA and Emax obtained by the aortic-occlusion method can account for changes in VO2 with changes in loading conditions and contractility in an in situ dog heart.

Animals↗