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PubMed1994

Intraocular pressure measurement after penetrating keratoplasty: minified Goldmann applanation tonometer, pneumatonometer, and Tono-Pen versus manometry.

The accuracy of intraocular pressure measurement with the minified Goldmann applanation tonometer, the pneumatonometer, and the Tono-Pen tonometer were compared in post-mortem human eyes which had undergone penetrating keratoplasty. Enucleated post-mortem human eyes underwent same sized (7.75 mm) or 0.5 mm oversized (8.25 mm) autologous penetrating keratoplasty. Intraocular pressure was then set and measured manometrically while being determined successively with each tonometer over the range of 0-65 mm Hg. Linear regression analysis comparing tonometric and manometric readings showed: (1) minified Goldmann applanation tonometer-slope 0.985 and 0.944, intercept 1.64 and 2.55 mm Hg, correlation coefficient 0.99 and 0.99 in same sized and oversized grafted eyes respectively; (2) pneumatonometer-slope 1.008 and 0.990, intercept 3.37 and 3.69 mm Hg, correlation coefficient 0.99 and 0.98; (3) Tono-Pen-slope 1.061 and 1.002, intercept 5.01 and 4.06 mm Hg, correlation coefficient 0.97 and 0.98. We concluded that the minified Goldmann applanation tonometer is as accurate or more accurate than the pneumatonometer and the Tono-Pen in post-mortem post-keratoplasty human eyes, and may be an economical, convenient alternative to the latter two instruments in clinical practice.

Aged↗

PubMed1976

Heart rate--left ventricular ejection time relations. Variations during postural change and cardiovascular challenges.

Regression equations for heart rate (HR)--ejection time (LVET) relations provide the appropriate factors for predicting or correcting left ventricular ejection time at any HR. We investigated HR-LVET regressions under different conditions common to both physiological and clinical studies of LVET which had been selected because of predictably different physiological responses. Ten normal subjects were studied during both supine and sitting rest and during isometric handgrip (IHG) in both supine and sitting postures and 10 during head-up tilt. Unexpectedly, as compared with pre-exercise rest on a bicycle ergometer, the slope for the resting state on a chair was slightly flatter, and LVET values were uniformly higher throughout the range of HRs measured. Differences among HR-LVET slopes and intercepts appeared to reflect the established behaviour of stroke volume and ejection rate under the conditions studied. Differences observed among intercepts, especially in supine vs. upright postures, are substantial and require that the appropriate intercept be applied in predicting LVET at a given HR. differences among slopes, while not statistically significant, may, under practical conditions, lead to unacceptable error if the appropriate slope factor is not used in correcting LVET for HR.

Adult↗

PubMed1999

A new physiological method for heart rate correction of the QT interval.

AIM: To reassess QT interval rate correction. BACKGROUND: The QT interval is strongly and inversely related to heart rate. To compare QT intervals between different subjects with different heart rates requires the application of a QT interval rate correction formula. To date these formulae have inappropriately assumed a fixed relation between QT interval and heart rate. An alternative method of QT interval rate correction that makes no assumptions about the QT interval-heart rate relation is needed. PROPOSAL: A QT heart rate correction method should maintain or accentuate biological QT interval variability, should totally remove the dependence of the rate corrected QT interval on heart rate, and should be applicable over a wide range of conditions with a wide range of differing autonomic states. METHODS: QT intervals were obtained at rest and during exercise from subjects expected to have different QT intervals and different QT interval-heart rate relations. A linear regression line was obtained from the exercise test data, and the QT interval at a notional heart rate of 60 and 0 beats/min, termed the QT(60) interval, and the QT y intercept obtained by back calculation. RESULTS: QT(60) and QT y intercept values were prolonged in heart failure compared with either left ventricular hypertrophy or controls. There was no relation between heart rate and either QT(60) or QT y intercept CONCLUSIONS: This new physiologically based method of correcting QT interval for heart rate removes the dependence of the corrected QT interval on heart rate, and maintains biological differences.

Cardiac Output, Low↗

PubMed1979

Quantitative study of intramyocardial compression in the fibrillating heart.

Extravascular compression inhibits coronary blood flow in fibrillating hearts. Pressure-flow curves from spontaneously fibrillating hearts whose coronary arteries were maximally dilated were examined to see whether this inhibition involves a vascular waterfall mechanism as has been found in the beating heart. Waterfall behavior is indicated when pressure-flow curves are linear and experience a zero-flow intercept at pressures greater than venous pressure. Regional pressure-flow curves revealed a zero flow intercept of 28.4 mmHg for the inner quarter of the left ventricle, indicating that compression is quite high in that region. A zero-pressure intercept of only 15.1 was found at the outer quarter, which was not significantly different from venous pressure. We conclude that the spontaneously fibrillating heart experiences a gradient of compression falling from 28 mmHg at the subendocardium to near zero at the subepicardium.

Animals↗

PubMed1981

Respiratory sinus arrhythmia in humans: how breathing pattern modulates heart rate.

The relationship of respiratory sinus arrhythmia amplitude (RSA) to tidal volume and breathing frequency was quantified during voluntarily controlled tidal volume and breathing frequency and spontaneous quiet breathing. Seventeen seated subjects breathed via mouthpiece and nose-clip, maintaining constant tidal volumes at each of several breathing frequencies. Inspiratory breath hold was zero frequency. Log RSA was plotted vs. log frequency for each tidal volume. The large stable RSA for frequencies less than 6 cycles/min was called low-frequency intercept (LFI, 20 +/- 5 beats/min). Low-frequency intercept was inversely proportional to a subject's age only to 35 yr. At higher breathing frequencies above a characteristic corner frequency (fC, 7.2 +/- 1.5 cycles/min) RSA decreased with constant slope (roll-off; 21 +/- 3.4 dB/decade). The RSA-volume relationship was linear permitting normalization of RSA-frequency curves for tidal volume to yield one curve. Spontaneous breathing data points fell on this curve. Voluntarily coupling of heart rate to breathing frequency in integer ratios reduced breath-by-breath variability of RSA without changing mean RSA. In conclusion, low-frequency intercept, corner frequency, and roll-off characterize an individual's RSA-frequency relationship during both voluntarily controlled and spontaneous breathing.

Adult↗

PubMed1986

Studies of functional site of origin of native coronary collaterals.

Studies were performed to determine the pressure at the origin of the native coronary collaterals (Pstem) and thus assess the contribution of collaterals arising from proximal conduit coronary vessels vs. those arising from distal microvessels. Nine isolated blood-perfused dog hearts were studied. Aortic pressure was maintained at 80 mmHg. Collateral flow to the circumflex perfusion field was measured (radioactive microspheres) repeatedly before and after successive 25-micron nonradioactive microsphere embolization of the circumflex vasculature. After each microembolization, collateral flow decreased and peripheral coronary pressure (PCP) increased. After all embolizations collateral flow decreased from an initial value of 17 +/- 4 to 2 +/- 0.4 ml X min-1 X 100 g-1 and PCP increased from an initial value of 15 +/- 3 to 65 +/- 3 mmHg. The relationship between decreasing collateral flow and increasing PCP was linear with a pressure intercept of 74 +/- 3 mmHg. This pressure intercept predicts the PCP that would be observed if microembolization produced complete cessation of collateral flow. Accordingly, this pressure intercept allowed an accurate estimate of Pstem. This estimate of Pstem was similar to left anterior descending pressure (75 +/- 2 mmHg). These studies show that Pstem may be accurately estimated by measuring pressure in a nonoccluded large epicardial vessel. The contribution of microvascular anastomoses to total collateral flow is likely small.

Animals↗

PubMed1987

Effects of regional ischemia and ventricular pacing on LV dP/dtmax-end-diastolic volume relation.

We investigated the effects of coronary artery occlusion and pacing from ventricular sites on the relation of the maximum rate of rise of left ventricular pressure (dP/dtmax) to the end-diastolic volume (VED) in dogs previously instrumented to measure left ventricular pressure and to determine left ventricular volume from three ultrasonically measured dimensions. The dP/dtmax-VED relation was generated by vena caval occlusion and compared with the simultaneously produced end-systolic pressure-end-systolic volume (PES-VES) relation. The dP/dtmax-VED relation was described by a straight line during all conditions. Occlusion of the left circumflex coronary artery produced a rightward shift of the dP/dtmax-VED relation, increasing the volume intercept by 11.3 +/- 5.3 (SD) ml (P less than 0.05). Compared with atrial pacing, the dP/dtmax-VED relation was shifted to the right with the volume intercept increasing by 4.8 +/- 4.4 ml (P less than 0.05) during pacing from the right ventricular free wall, 3.7 +/- 5.0 ml (P less than 0.05) during pacing from the right ventricular apex, and 3.7 +/- 2.4 ml (P less than 0.05) during pacing from the left ventricular free wall. Similar increases were observed in the volume intercepts of the PES-VES relations during coronary occlusion or ventricular pacing. These results are consistent with the predictions of the time-varying elastance model and support its use as a conceptual framework to understand left ventricular performance during isovolumic contraction and at end systole, both in the normal ventricle and the ventricle with regional abnormalities of contraction.

Animals↗

PubMed1989

Pressure-flow characteristics of coronary collaterals in dogs.

In this study we utilized two methods to investigate the pressure-flow, P-F, relationship of the coronary collateral vessels in a beating, blood-perfused, isolated heart preparation. In the first method (free-flow method), 12 dog hearts were perfused at pressures ranging from 100 to 0 mmHg, whereas the retrograde flow (index of collateral flow) was measured on the circumflex coronary artery, LCA, against atmospheric pressure, first during autoregulation and then after maximum vasodilation. In the second method (back-pressure method), the back pressure to retrograde flow was varied from 0 to 100 mmHg, whereas the perfusion pressure to the remaining vessels was maintained constant at 100 mmHg. This procedure was performed on four hearts with and without embolization of the LCA by 25-microns spheres. The free-flow method demonstrated a linear P-F relationship with an average correlation coefficient, r, of 0.98. The pressure intercept was 1.7 +/- 1.2 mmHg. The back-pressure method yielded a relationship that was more curvilinear with an average pressure intercept of 13 mmHg without embolization and 38 mmHg with embolization. An analog of the coronary and collateral circulation was used to illustrate that, in the back-pressure method, changes in the coronary resistance at low pressures contributed to the nonlinearity of the collateral P-F characteristics and that the network formed between the collateral and coronary resistances was responsible for the higher pressure intercept value.

Animals↗

PubMed1992

Effects of amrinone and isoproterenol on mechanoenergetics of blood-perfused rabbit heart.

To compare the effects of amrinone (AMR) and isoproterenol (Iso) on left ventricular contractility and energetics, we assessed Emax (ventricular contractility index) and the relation between oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA, a measure of left ventricular total mechanical energy) in isolated cross-circulated (blood-perfused) rabbit hearts during infusion of AMR or Iso in either a constant-flow (CF) or constant-pressure (CP) perfusion mode. Both Emax and the VO2 intercept of the linear VO2-PVA relation increased significantly during AMRCP (increase in Emax 15% and increase in VO2 intercept 11%), ISOCF (49 and 43%), and ISOCP (55 and 54%) but not during AMRCF. However, neither drug changed the slope of the VO2-PVA relation (reciprocal of contractile efficiency) in either perfusion mode. Furthermore, with both drugs the relation between increases in Emax and the VO2 intercept fell on a single regression line (r = 0.92). We conclude that 1) although the mechanism of action and inotropic potency of the two drugs differ, their effects on cardiac energetic cost are essentially the same, i.e., both drugs increase the nonmechanical oxygen cost in proportion to the increase in contractility without changing contractile efficiency, and 2) a significant portion of the inotropic effect of AMR in the whole ventricle is likely due to increased coronary blood flow, i.e., Gregg's phenomenon.

Amrinone↗

PubMed1992

End-systolic pressure-volume and MVO2-pressure-volume area relations of isolated rat hearts.

We tested the utility of a standard isolated, crystalloid-perfused, isovolumic rat heart preparation for studying ventricular metabolism in terms of the myocardial oxygen consumption-pressure-volume area (MVO2-PVA) relations. The end-systolic pressure-volume relations (ESPVRs) determined between volumes of 0.15 and 0.65 ml were fit equally well by linear and nonlinear regression analysis within the data range but predicted widely differing volume-intercept (Vo) values. Linear regression analysis of the ESPVRs provided a mean slope (Ees) of 419 +/- 186 mmHg.g.ml-1 and Vo of 0 +/- 0.12 ml, respectively (n = 6). The MVO2-PVA relations were linear with a slope and MVO2 intercept of 1.30 +/- 0.31 x 10(-5) ml O2.mmHg-1.ml-1 and 0.38 +/- 0.09 x 10(-3) ml O2-beat-1.g-1, respectively. These MVO2-PVA parameters were not significantly different from those obtained when nonlinear regression analysis was applied to the ESPVR. Decreasing perfusate calcium concentration ([Ca2+]) (n = 7) resulted in a downward shift in the ESPVR, a decrease in the MVO2-PVA intercept (0.52 +/- 0.26 vs. 0.34 +/- 0.20 x 10(-3) ml O2.beat-1.g-1, P less than 0.01), and no significant change in the MVO2-PVA slope (1.33 +/- 0.47 vs. 1.57 +/- 0.69 x 10(-5) ml O2.mmHg-1.ml-1, NS). We conclude that this preparation may be a useful alternative to more expensive preparations for selected experiments in cardiac energetics.

Animals↗

PubMed1994

Loss of elastic recoil in postischemic myocardium induces rightward shift of the systolic pressure-volume relationship.

Ischemia-induced systolic dysfunction has been ascribed to changes in cellular excitation-contraction coupling and diastolic dysfunction because of disruption of the extracellular collagen matrix. Therefore, systolic and diastolic pressure-volume relationships and O2 consumption were determined before and after 5 min of global ischemia in isolated blood-perfused porcine hearts. The slope of the systolic pressure-volume relationship was 7.2 +/- 0.6 (SE) mmHg.ml-1.100 g-1 (n = 18) at baseline and did not change during reperfusion, but the systolic volume intercept shifted from 1.0 +/- 0.4 ml/100 g at baseline to 3.7 +/- 1.4, 4.1 +/- 1.1, and 4.2 +/- 0.9 ml/100 g at 15, 30, and 60 min of reperfusion, respectively (all P < 0.05). The diastolic volume intercept was 8.2 +/- 0.7 ml/100 g at baseline and remained unchanged during reperfusion. Therefore, the difference of the systolic-diastolic volume intercepts, an index of elastic recoil forces, was decreased to 57 +/- 8, 49 +/- 7, and 47 +/- 9% of baseline values (P < 0.05). The shift of the systolic pressure-volume relationship was accompanied by a transient decrease of contractile efficiency (slope of O2 consumption-pressure-volume-area relationship) at 15 min of reperfusion (from 43 +/- 6 to 27 +/- 7%). We hypothesize that the rightward shift of the systolic pressure-volume relationship was compatible with a decrease of elastic-restoring forces, probably induced by alterations in the extracellular collagen matrix and/or the cytoskeleton, and thereby our data imply that left ventricular dysfunction of postischemic myocardium does not result solely from disturbances in excitation-contraction coupling.

Animals↗

PubMed1997

In vivo determination of left ventricular wall stress-shortening relationship in normal mice.

Although targeted alterations of the mouse genome are used increasingly to identify the mechanisms underlying cardiac function, the methods used to study the phenotypic expression of these alterations in vivo are limited. To derive a relatively noninvasive, load-independent measure of left ventricular (LV) contractility in mice, we cannulated the femoral artery and performed two-dimensional directed M-mode echo studies in 28 anesthetized FVB/N mice, using a 9-MHz transducer. Loading conditions were altered by intraarterial methoxamine (3-12 microg/g), and LV shortening fraction was determined at several steady states, both before and after myocardial contractility was altered by either 4 microg/g intraperitoneal dobutamine (n = 16) or 1-2 microg/g verapamil (n = 12). The relation between LV systolic meridional stress and fractional shortening derived from pooled baseline data was inverse and linear [r = 0.80, slope = -0.19, intercept = 48%, standard error of estimate (SEE) = 5.5%, P < 0.001]. Dobutamine produced a parallel upward shift of the relation (r = 0.87, slope = -0.21, intercept = 61%, SEE = 4.5%, P < 0.001), and verapamil produced a downward shift of the relation (r = 0.48, slope = -0.05, intercept = 24%, SEE = 3.7%, P < 0.05). At matched levels of end-systolic stress, dobutamine increased and verapamil decreased the LV shortening fraction. We conclude that 1) inverse stress-shortening relations can be assessed noninvasively in mice; and 2) these relations are sensitive to alterations in inotropic state, independent of loading conditions.

Animals↗

PubMed1997

Spectral characteristics of ventricular response to atrial fibrillation.

To investigate the spectral characteristics of the fluctuation in ventricular response during atrial fibrillation (AF), R-R interval time series obtained from ambulatory electrocardiograms were analyzed in 45 patients with chronic AF and in 30 age-matched healthy subjects with normal sinus rhythm (SR). Although the 24-h R-R interval spectrum during SR showed a 1/f noise-like downsloping linear pattern when plotted as log power against log frequency, the spectrum during AF showed an angular shape with a breakpoint at a frequency of 0.005 +/- 0.002 Hz, by which the spectrum was separated into long-term and short-term components with different spectral characteristics. The short-term component showed a white noise-like flat spectrum with a spectral exponent (absolute value of the regression slope) of 0.05 +/- 0.08 and an intercept at 10(-2) Hz of 4.9 +/- 0.3 log(ms2/Hz). The long-term component had a 1/f noise-like spectrum with a spectral exponent of 1.26 +/- 0.40 and an intercept at 10(-4) Hz of 7.0 +/- 0.3 log(ms2/Hz), which did not differ significantly from those for the spectrum during SR in the same frequency range [spectral exponent, 1.36 +/- 0.06; intercept at 10(-4) Hz, 7.1 +/- 0.3 log(ms2/Hz)]. The R-R intervals during AF may be a sequence of uncorrelated values over the short term (within several minutes). Over the longer term, however, the R-R interval fluctuation shows the long-range negative correlation suggestive of underlying regulatory processes, and spectral characteristics indistinguishable from those for SR suggest that the long-term fluctuations during AF and SR may originate from similar dynamics of the cardiovascular regulatory systems.

Adult↗

PubMed1998

Mechanoenergetic studies in isolated mouse hearts.

We tested the feasibility of an isolated, balloon-in-ventricle, isovolumically contracting, crystalloid-perfused mouse heart preparation (n = 10) for studies of cardiac mechanoenergetics using the end-systolic pressure-volume relation (ESPVR) and myocardial oxygen consumption (VO2)-pressure-volume area (PVA) framework employed in larger species. The intraventricular balloon method was shown to be accurate for measurement of left ventricular volume, especially at relatively higher volumes. The ESPVR demonstrated contractility-dependent curvilinearity. Average slope of the ESPVR was 1,299 +/- 369 (SD) mmHg.g.ml-1, with a volume intercept of 0.018 +/- 0.006 ml. The VO2-PVA relation was well fitted by a straight line, with average slope and VO2 intercept of 3.57 +/- 1.31 x 10(-5) ml O2.mmHg-1.ml-1 and 0.92 +/- 0.21 x 10(-3) ml O2.beat-1.g-1, respectively. Decreasing perfusate Ca2+ concentration resulted in a decrease in the slope of the ESPVR, a decrease in the VO2 intercept of the VO2-PVA relation, but no significant change in its slope. Hearts from hypothyroid (n = 8) mice demonstrated similar mechanoenergetic changes. We conclude that delineation of the ESPVR and the VO2-PVA relation is feasible in the mouse heart. Our method should allow an assessment of cardiac mechanoenergetics as sophisticated as that previously possible only in larger hearts.

Animals↗

PubMed1991

Reproducibility of osmotic and nonosmotic tests of vasopressin secretion in men.

We have studied the reproducibility of the thirst and arginine vasopressin (AVP) responses to osmotic and hypoglycemic stimulation in healthy volunteers undergoing repeat hypertonic (855 mmol/l) saline infusion and insulin tolerance tests (ITTs). Hypertonic saline infusion caused similar mean rises in plasma osmolality, AVP, and thirst on each occasion. Linear-regression analysis defined close relationships between the slopes (r = +0.72, P less than 0.05) and the abscissal intercepts (r = +0.89, P less than 0.001) of the regression lines relating plasma osmolality (Posmol) and plasma AVP (PAVP), and the group intraindividual component of the variance for the slopes and intercepts was 7 and 0.6%, respectively. There were close correlations between the slopes (r = +0.79, P less than 0.02) and the intercepts (r = +0.84, P less than 0.01) of the regression lines relating Posmol and thirst, and group intraindividual component of the variance was 14 and 0.7%, respectively. Hypertonic saline infusion was infused on four occasions in four subjects, and the results showed that the linear regression lines relating PAVP and Posmol and thirst and Posmol were reproducible within an individual. There were similar falls in blood glucose and elevations in PAVP in both ITTs. No relationship was defined between the fall in blood glucose and either the rise in PAVP or the area under the AVP curve (AUC). The intraindividual component of the variance for the rise in AVP and the AUC was 77 and 22.5%, respectively. The AVP and thirst responses to osmotic stimulation are highly reproducible, but there is considerable intraindividual variation in the AVP response to hypoglycemia.

Adult↗

PubMed1984

Comparison of subjects' perception of inspiratory and expiratory resistance.

Six healthy male adults were studied at five levels of suprathreshold added resistance (delta R) applied thrice to either inspiration (I) or expiration (E) in a random sequence. Subjects squeezed on isometric handgrip dynamometer to express the perceived magnitude of the load. Peak mouth pressure (Pm), flow, grip (G), and delta R were analyzed to derive the exponent for Steven's power law. We observed that the slope for log G vs. log delta R was significantly greater for I loads than for E loads (P less than 0.05), but the intercepts for E loads were significantly elevated. However, the slopes and intercepts for log G vs. log Pm during the same I and E loads were not significantly different. When subjects were instructed to target I or E flow to a preset level, we observed no difference between the slopes and intercepts for log G vs. log delta R during I and E loading. These results suggest that 1) the sensory information utilized in judging the magnitude of added resistance is more likely related to the force generated by the respiratory muscles (Pm) rather than delta R per se; and 2) similar muscle receptors and neural processing systems are utilized in the estimation of added loads involving either inspiratory or expiratory muscle groups.

Adult↗

PubMed1984

Hypoxic pulmonary vasoconstriction during steady and pulsatile flow in ferrets.

We examined the effects of hypoxia and pulsatile flow on the pressure-flow relationships in the isolated perfused lungs of Fitch ferrets. When perfused by autologous blood from a pump providing a steady flow of 60 ml/min, the mean pulmonary arterial pressure rose from 14.6 to 31.3 Torr when alveolar PO2 was reduced from 122 to 46 Torr. This hypoxic pressor response was characterized by a 10.1-Torr increase in the pressure-axis intercept of the extrapolated pressure-flow curves and an increase in the slope of these curves from 130 to 240 Torr X l-1 X min. With pulsatile perfusion from a piston-type pump, mean pulmonary arterial pressure increased from 17.5 to 36.3 Torr at the same mean flow. This hypoxic pressor response was also characterized by increases in the intercept pressure and slope of the pressure-flow curves. When airway pressure was raised during hypoxia, the intercept pressure increased further to 25 +/- 1 Torr with a further increase in vascular resistance to 360 Torr X l-1 X min. Thus, in contrast to the dog lung, in the ferret lung pulsatile perfusion does not result in lower perfusion pressures during hypoxia when compared with similar mean levels of steady flow. Since the effects of high airway pressure and hypoxia are additive, they appear to act at or near the same site in elevating perfusion pressure.

Animals↗

PubMed1985

Segmental pulmonary vascular resistance in progressive hydrostatic and permeability edema.

We used the in situ blood-perfused left lower lobe preparation of the dog to examine the effect of hydrostatic and permeability edema on the slope and intercept of the vascular pressure-flow (P/Q) relationship and on the longitudinal distribution of vascular resistance with the arterial and venous occlusion technique. Hydrostatic edema (HE) was induced by raising the venous pressure, and permeability edema (PE) was induced with alpha-naphthylthiourea. When the hematocrit (Hct) of the perfusate was kept normal (approximately 40%), HE had no significant effect on either the slope or the intercept of the P/Q relationship or on the distribution of vascular resistance. PE caused a small increase in the intercept of the P/Q relationship and a small rise in the resistance of the vessels in the middle segment. In another series of HE experiments in which Hct was allowed to increase during edema formation, there was a marked increase in vascular resistance. We conclude that edema per se does not increase vascular resistance significantly and that the increases in vascular resistance which were observed previously by other investigators in the isolated lungs may be due to increases in blood hematocrit.

Animals↗