Changes In Peak Pressure Research Articles

Why vehicle design matters: Exploring the link between line-of-sight, driving posture and risk factors for injury

Load haul dump (LHD) vehicles have been involved in workplace accidents resulting in fatal injuries and LHD operators also report high rates of musculoskeletal injury. Poor line-of-sight (LOS) and awkward postures adopted by the LHD operator increase the risk of driving related accidents and musculoskeletal injury. The purpose of this case study was to simultaneously measure point of regard (POR), driving posture and sitting position during the operation of a LHD in an underground mining environment in order to further understand the link between these variables and the design of the LHD vehicle. A 5.35 m3 bucket LHD vehicle was used and several driving tasks were analysed. The case study results showed that despite the driving task, the operator looked to the left side of the vehicle 65% of the time. Postural implications include extreme neck rotation (> 40 degrees) for 85% of the work cycle and the average peak compression at L4/L5 was 1843N. Despite changes in driving posture the average center of pressure location for the seated operator moved very little; however changes in peak pressure were observed. The design of the LHD vehicle dictated what the operator could see, which had a direct influence on driving postures adopted by the operator and resulted in several risk factors for musculoskeletal injury.

Physics-Based Modeling and Control of Residual-Affected HCCI Engines

Abstract Homogeneous charge compression ignition (HCCI) is a novel combustion strategy for IC engines that exhibits dramatic decreases in fuel consumption and exhaust emissions. Originally conceived in 1979, the HCCI methodology has been revisited several times by industry but has yet to be implemented because the process is difficult to control. To help address these control challenges, the authors here outline the first generalizable, validated, and experimentally implemented physics-based control methodology for residual-affected HCCI engines. Specifically, the paper describes the formulation and validation of a two-input, two-state control-oriented system model of the residual-affected HCCI process occurring in a single engine cylinder. The combustion timing and peak pressure are the model states, while the inducted gas composition and effective compression ratio are the model inputs. The resulting model accurately captures the system dynamics and allows the simultaneous, coordinated control of both in-cylinder pressure and combustion timing. To demonstrate this, an H2 optimal controller is synthesized from a linearized version of the model and used to dictate step changes in both combustion timing and peak pressure within about four to five engine cycles on an experimental test bed. The application of control also results in reductions in the standard deviation for both combustion timing and peak pressure. The approach therefore provides accurate mean tracking, as well as a reduction in cyclic dispersion. Another benefit of the simultaneous coordination of both control inputs is a reduction in the control effort required to elicit the desired response. Instead of using a peak pressure controller that must compensate for the effects of a combustion timing controller, and vice versa, the coordinated approach optimizes the use of both control inputs to regulate both outputs.

The Effects of Rate‐Adaptive Atrial Pacing Versus Ventricular Backup Pacing on Exercise Capacity in Patients with Left Ventricular Dysfunction

Atrial rate-adaptive pacing may improve cardiopulmonary reserve in patients with left ventricular dysfunction. A randomized, blinded, single-crossover design enrolled dual-chamber implantable defibrillator recipients without pacing indications and an ejection fraction < or =40% to undergo cardiopulmonary exercise treadmill stress testing in both atrial rate-adaptive pacing (AAIR) and ventricular demand pacing (VVI) pacing modes. The primary endpoint was change in peak oxygen consumption (VO(2)). Secondary endpoints were changes in anaerobic threshold, perceived exertion, exercise duration, and peak blood pressure. Ten patients, nine males, eight with New York Heart Association class I, mean ejection fraction 24 +/- 7%, were analyzed. Baseline VO(2) was 3.6 +/- 0.5 mL/kg/min. Heart rate at peak exercise was significantly higher during AAIR versus VVI pacing (142 +/- 18 vs 130 +/- 23 bpm; P = 0.05). However, there was no difference in peak VO(2) (AAIR 23.7 +/- 6.1 vs VVI 23.8 +/- 6.3 mL/kg/min; P = 0.8), anaerobic threshold (AAIR 1.3 +/- 0.3 vs VVI 1.2 +/- 0.2 L/min; P = 0.11), rate of perceived exertion (AAIR 7.3 +/- 1.5 vs VVI 7.8 +/- 1.2; P = 0.46), exercise duration (AAIR 15 minutes, 46 seconds +/- 2 minutes, 54 seconds vs VVI 16 minutes, 3 seconds +/- 2 minutes, 48 seconds; P = 0.38), or peak systolic blood pressure (AAIR 155 +/- 22 vs VVI 153 +/- 21; P = 0.61) between the two pacing modes. In this study, AAIR pacing did not improve peak VO(2,) anaerobic threshold, rate of perceived exertion, or exercise duration compared to VVI backup pacing in patients with left ventricular dysfunction and no pacing indications.

Scarf Osteotomy for the Correction of Hallux Valgus: Midterm Clinical Outcome

We prospectively reviewed 22 patients (31 feet) who underwent a scarf osteotomy between January 2001 and March 2002. There were 20 females and 2 males. Ages ranged from 35 to 77 years (mean = 57 years). American Orthopedic Foot and Ankle Society (AOFAS) scores improved from a preoperative mean of 47.94 +/- 13.57 and increased significantly to 96.10 +/- 6.15 (P < .01) after 12 months. The hallux valgus angle improved in all patients from a preop mean of 31.4 +/- 8.0 degrees to 11.0 +/- 10.8 degrees at 12 months. The intermetatarsal angle improved from 13.0 +/- 4.2 degrees to 6.1 +/- 3.2 degrees. All of these changes were significant. Bony union was achieved in all patients. There were no significant changes in peak pressure, pressure/time, or force/time pedobarography noted after 12 months. Significant improvement in pain scores from preoperative mean of 21.29 +/- 11.0 to 32.90 +/- 9.57 at 5 years (P < .01) was noted and 90.9% of patients remained satisfied with the operation and would recommend the procedure. There were 2 complications. One patient experienced a traumatic neuroma and another avascular necrosis of the first metatarsal head. The scarf osteotomy is a safe and effective procedure with reproducible and excellent medium-term results.

Changes in Chopart joint load following tibiotalar arthrodesis: in vitro analysis of 8 cadaver specimen in a dynamic model

BackgroundIn the current discussion of surgical treatment of arthroses in the ankle joint, arthrodesis is in competition with artificial joint replacement. Up until now, no valid biomechanical findings have existed on the changes in intraarticular loads following arthrodesis. One argument against tibiotalar arthrodesis is the frequently associated, long-term degeneration of the talonavicular joint, which can be attributed to changes in biomechanical stresses.MethodsWe used a dynamic model to determine the changes in intraarticular forces and peak-pressure in the talonavicular joint and in the calcaneocuboid joint on 8 cadaver feet under stress in a simulated stance phase following tibiotalar arthrodesis.ResultsThe change seen after arthrodesis was a tendency of relocation of average force and maximum pressure from the lateral onto the medial column of the foot. The average force increased from native 92 N to 100 N upon arthrodesis in the talonavicular joint and decreased in the calcaneocuboid joint from 54 N to 48 N. The peak pressure increased from native 3.9 MPa to 4.4 MPa in the talonavicular joint and in the calcaneocuboid joint from 3.3 MPa to 3.4 MPa. The increase of force and peak pressure on the talonavicular joint and decrease of force on the calcaneocuboid joint is statistically significant.ConclusionThe increase in imparted force and peak pressure on the medial column of the foot following tibiotalar arthrodesis, as was demonstrated in a dynamic model, biomechanically explains the clinically observed phenomenon of cartilage degeneration on the medial dorsum of the foot in the long term. As a clinical conclusion from the measurements, it would be desirable to reduce the force imparted on the medial column with displacement onto the lateral forefoot, say by suitable shoe adjustment, in order to achieve a more favourable long-term clinical result.

Cerebellar fastigial nuclei activity during blood pressure challenges

The cerebellar fastigial nuclei (FN) assist in regulating compensatory responses to large blood pressure changes and show structural injury and functional impairment to cardiovascular challenges in syndromes with sleep-disordered breathing. The patterned time course of FN responses to elevation or lowering of blood pressure and location of responsive regions within the nuclei are unclear. We evaluated FN neural activity in six anesthetized rats using optical imaging procedures during elevation and lowering of arterial pressure by phenylephrine and nitroprusside, respectively. Hypertension diminished optical correlates of FN neural activity, while measures of activity increased to hypotension, with peak neural responses occurring 5-10 s later than peak blood pressure changes. Blood pressure responses were followed by heart rate changes, and peak respiratory rates developed even later, in close temporal proximity to FN activity patterns. Although overall topographical response trends were similar, regional patterns of altered neural activity appeared to both hypertension and hypotension. The extent of neural change was greater during recovery from hypertension than for hypotension at high-dose levels. Blood pressure levels saturated with increasing phenylephrine doses, while FN activity continued to decline. No saturation appeared in heart or respiratory rate trends. The findings suggest that the FN compensate for large blood pressure changes by sympathoexcitatory and inhibitory processes, which accompany late-developing somatic or respiratory adjustments.

Pressure-calcium relationships in perfused mouse hearts

We explored the relationship between left ventricular (LV) pressure and intracellular free calcium concentration ([Ca](i)) in the isolated perfused mouse heart. [Ca](i) (rhod-2) and LV pressure were recorded simultaneously. In response to increases in LV volume (Frank-Starling, FS, protocol), there were increases in developed pressure (up to 250%), with no changes in pressure morphology (rise or relaxation time) or [Ca](i) (magnitude and morphology) for up to 10 min. During transient increases in the stimulus interval at a fixed LV volume (mechanical restitution, MR, protocol), developed pressure increased significantly (31.3 +/- 1.2%), with relatively small changes in peak systolic [Ca](i) (7.4 +/- 1.4%). The relaxation of [Ca](i), however, was prolonged (30.0 +/- 5.5%), resulting in prolonged pressure relaxation (21.2 +/- 1.9%) and increased area under the calcium transient that paralleled the increase in developed pressure (1:1 ratio). A model-based analysis showed that changes in LV pressure during the MR protocol could be completely explained by altered [Ca](i); it was not necessary to invoke any changes in model parameters (i.e., dynamic processes that link calcium to pressure). For the FS data, the model predicted only a change in the gain parameter; however, this change alone cannot reproduce well-established length-dependent changes in the steady-state force-pCa relationship. In summary, the mouse myocardium appears to be unique in that significant changes in peak developed pressure can occur with little or no change in the peak [Ca](i). Additionally, unlike other mammalian species, load-dependent prolongation of pressure relaxation is absent in the mouse heart, and pressure relaxation is primarily governed by intracellular free calcium relaxation.

Changes in Peak Respiratory Flow and Quality of Life during Nebivolol Therapy

Background: Nebivolol is a highly cardioselective β₁-adrenoceptor antagonist with proven efficacy and safety in the treatment of hypertension. This study aimed to specifically address the effects of nebivolol on lung function and quality of life in patients suffering from mild to moderate hypertension. Objectives: The study assessed the effects of nebivolol, taken alone or in combination with other antihypertensives for 12 weeks, on peak respiratory flow, libido, general health, and physical condition. The effects on blood pressure and heart rate were also determined. Methods: A total of 367 patients suffering from mild to moderate hypertension were enrolled in 93 private general practices. Changes in peak respiratory flow, blood pressure, and heart rate were recorded after 4 and 12 weeks. A questionnaire on items of sexual function, physical energy, and general health elicited the patients’ perception of their quality of life. Safety was assessed on the basis of adverse events. Results: After 4 and 12 weeks, peak respiratory flow was significantly increased in patients receiving nebivolol alone (p < 0.01). Diastolic blood pressure (p < 0.01), systolic blood pressure (p < 0.01), and heart rate (p < 0.01) were significantly lowered during treatment. Moreover, nebivolol treatment (alone or in combination with other antihypertensives) statistically significantly improved libido, breathlessness, and energy level (p < 0.05). Conclusion: The favourable effect on peak respiratory flow, coupled with an improved quality of life, renders this cardioselective β₁-blocker useful in the treatment of essential hypertension in the general practice setting.

Reflex vascular responses to independent changes in left ventricular end-diastolic and peak systolic pressures and inotropic state in anaesthetised dogs.

1. Ventricular mechanoreceptors are known to exist and can when stimulated induce reflex vasodilatation, but the nature of the effective stimuli and the physiological role of the reflex remain to be established. 2. Dogs were anaesthetised with chloralose and a cardiopulmonary bypass established. Ventricular pressures were separated from those in the aortic root and coronary arteries by a balloon inflated in the ventricular outflow tract. Ventricular filling was controlled by adjusting the rate of inflow of blood through an apical cannula and peak pressure by regulating the outflow pressure from the same cannula. Carotid and aortic pressures were also controlled and vascular resistance was assessed from changes in perfusion pressure (constant flow conditions) to the descending abdominal aorta. 3. Increased coronary or carotid sinus pressure induced a significant vasodilatation. Changes in ventricular peak systolic pressure, without associated changes in end-diastolic pressure, had no significant effect on vascular resistance. In contrast, changes in end-diastolic pressure did induce vasodilatation that, although small, was proportional to the magnitude of the end-diastolic pressure change. 4. Changes in ventricular inotropic state induced by dobutamine infusion or by stimulation of efferent cardiac sympathetic nerves did not induce significant responses. Furthermore, the combined effects of reduced ventricular filling and increased inotropic state were also ineffective in inducing responses. 5. We conclude that, to induce reflex responses, the only effective stimulus to ventricular mechanoreceptors was an increase in filling. Compared with other mechanoreflexes, however, responses to ventricular distension were small and seem unlikely to be of importance except perhaps during abnormal ventricular distension.

An equation to predict the changes in peak left ventricular pressure in hypertrophic obstructive cardiomyopathy after treatment: application to the administration of disopyramide.

A theoretical equation was derived based on the time-varying elastance model to predict theoretically the relationship between the delay in the onset of left ventricular outflow obstruction and the reduction in peak left ventricular pressure (LVP) caused by treatment in hypertrophic obstructive cardiomyopathy (HOCM). ECG, LVP, and other hemodynamic parameters were measured during catheterization at a constant heart rate with atrial pacing in 16 patients with HOCM before and after intravenous administration of disopyramide (1 mg/kg). After disopyramide administration, the duration between the R wave of the ECG and the onset of obstruction (T1) was prolonged significantly (from 117 +/- 30 to 155 +/- 32 ms, P < 0.0001), and peak LVP was reduced significantly (from 222 +/- 42 to 177 +/- 39 mmHg, P < 0.0001). The relation between the prolongation of T1 and the percent reduction in peak LVP was predicted well by the theoretical equation (coefficient of determination R2 = 0.926). Our model simplifies the therapeutic strategy for reducing the left ventricular outflow pressure gradient in patients with HOCM, which is to delay the time of onset of obstruction by some methods.

Model experiment to study sonic boom propagation through turbulence. Part I: General results

A model experiment to study the effect of atmospheric turbulence on sonic booms is reported. The model sonic booms are N waves produced by electric sparks, and the model turbulence is created by a plane jet. Of particular interest are the changes in waveform, peak pressure, and rise time of the model N waves after they have passed through the model turbulence. A review is first given of previous experiments on the effect of turbulence on both sonic booms and model N waves. This experiment was designed so that the scale factor (approximately 10−4) relating the characteristic length scales of the model turbulence to those of atmospheric turbulence is the same as that relating the model N waves to sonic booms. Most of the results reported are for plane waves. Sets of 100 or 200 pressure waveforms were recorded, for both quiet and turbulent air, and analyzed. Sample waveforms, scatter plots of peak pressure and rise time, histograms, and cumulative probability distributions are given. Results are as follows: (1) The model experiment successfully simulates sonic boom propagation through the atmosphere. The waveform distortion of actual sonic booms is reproduced, both in scale and in character, in the laboratory study. (2) Passage through turbulence almost always causes rise time to increase; decreases are rare. (3) Average rise time is always increased by turbulence, threefold for the particular data reported here. (4) Average peak pressure is always decreased by turbulence, but the change is not as striking as that for average rise time.

Potentiation by aminopeptidase P of blood pressure response to bradykinin.

We examined whether a specific aminopeptidase P (APP) inhibitor, apstatin, increases vasodepressor responses to bradykinin in anaesthetized rats, and whether it would augment blood pressure responses further after treatment with the angiotensin-converting enzyme inhibitor (ACEi), lisinopril. Apstatin doubled the maximum blood pressure response to bradykinin. The area under the curve (AUC), which incorporates both peak blood pressure changes and duration of response, was doubled in apstatin-treated rats vs controls and in the apstatin+lisinopril group vs lisinopril alone. These data demonstrate that APP is an important kinase in vivo.

Dual action of angiotensin II on coronary resistance in the isolated perfused rabbit heart.

We studied the functional role of angiotensin II (AII) receptor subtypes and vasodilatory endothelial autacoid release in response to AII in isolated perfused rabbit hearts. AII infusion induced biphasic changes in coronary perfusion pressure (CPP): an initial increase was followed by a decrease until a plateau was reached. At higher concentrations of AII (> or = 10 nmol/l) this plateau phase was lower than the initial CPP level. AII infusion elicited inverse changes in peak left ventricular pressure (LVP): coronary constriction was associated with a transient decline, and during the plateau phase LVP was clearly increased. AII also moderately augmented prostacyclin (PGI2) release from the coronary vascular bed. The AII-induced changes in CPP, LVP, and PGI2 release were effectively inhibited by the AT1 receptor subtype antagonist ICI D8731 (30 nmol/l), but not by the AT2 receptor antagonist CGP 42112 (30 nmol/l). The adenosine A1 receptor antagonist 8-phenyltheophylline (0.1 mumol/l) attenuated the decline in CPP following the constriction phase without affecting the changes in LVP during AII infusion. The cyclooxygenase inhibitor diclofenac (1 mmol/l) had no effect on the AII-induced changes in CPP, whereas the nitric oxide-synthase inhibitor NG-nitro-L-arginine (30 mumol/l) markedly potentiated the vasoconstriction but was without effect on the plateau phase of the response. In contrast to AII, the thromboxane analogue U46619 elicited sustained increases in CPP which were associated with slight decreases in LVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Fosinopril monotherapy: Relationship between blood pressure reduction and time of administration

The time to peak antihypertensive effect and the trough-to-peak ratio were determined in 64 Caucasian patients (19 men, 45 women) with mild to moderate hypertension [supine diastolic blood pressure (DBP) 95 to 115 mmHg]. They received placebo or fosinopril 10, 20, or 40 mg once daily for 4 weeks. The study consisted of a 4-week placebo lead-in, 4 weeks' double-blind treatment, and a 1-week placebo washout period. Vital signs were determined biweekly before dosing, and blood pressures were measured every 1 to 2 h during two 27-h periods at the beginning and end of treatment. After the first and last doses of all three regimens, the peak effect on blood pressure occurred 5 to 7 h after all three dosages. Neither peak nor trough blood pressure changes showed a clear dose-response relationship. Trough to peak ratios for the first dose, corrected for placebo effects, were 79% for fosinopril 10 mg, 48% for fosinopril 20 mg, and 74% for fosinopril 40 mg, and the trough-to-peak ratios for the last dose were 41% for fosinopril 10 mg, 32% for fosinopril 20 mg, and 44% for fosinopril 40 mg. In the 38 responders among the 48 patients receiving fosinopril (supine DBP decrease of at least 5 mmHg at 24 h postdose), trough-to-peak ratios ranged from 50 to 81%, and the range indicates that fosinopril is efficacious when administered once daily. Adverse effects were mild to moderate, and no patient discontinued treatment. Changes in the laboratory test results, electrocardiograms, or the results of physical examinations were unremarkable.(ABSTRACT TRUNCATED AT 250 WORDS)

No effect of coronary perfusion on regional myocardial function within the autoregulatory range in pigs. Evidence against the Gregg phenomenon.

The hypothesis that increases in coronary perfusion increase ventricular performance independently from providing enhanced oxygen supply ("Gregg phenomenon") remains controversial. To study the physiological significance of changes in coronary perfusion on global and regional myocardial function in situ, the left anterior descending coronary artery of isoflurane-anesthetized swine was cannulated, and perfusion was varied. In one group of swine (n = 5), coronary arterial pressure was increased in four steps from 88 +/- 11 to 186 +/- 11 mm Hg by increasing the speed of the pump circuit providing coronary blood flow. No changes in left ventricular end-diastolic pressure, peak pressure, or maximum left ventricular dP/dt were observed. Subendocardial blood flow (by radiolabeled microspheres) increased from 0.96 +/- 0.27 to 2.04 +/- 0.73 ml/min/g without any increase in systolic wall thickening (by sonomicrometry) or myocardial oxygen consumption of the anterior myocardium. In a second group of swine (n = 8), coronary arterial pressure was kept constant and coronary blood flow was increased stepwise by intracoronary adenosine infusion. End-diastolic pressure, peak pressure, and maximum left ventricular dP/dt remained unchanged when coronary blood flow increased from 21.7 +/- 9.8 to 93.8 +/- 34.1 ml/min. Subendocardial blood flow increased from 0.89 +/- 0.26 to 3.28 +/- 1.02 ml/min/g, again without any increase in systolic wall thickening (45.6 +/- 8.6 versus 42.6 +/- 9.8%) and myocardial oxygen consumption (5.75 +/- 1.18 versus 5.87 +/- 1.67 ml/min/100 g). In a third group of swine (n = 10), coronary arterial pressure was lowered by intracoronary adenosine infusion during constant coronary inflow. Left ventricular hemodynamics remained unchanged. With a decrease in coronary arterial pressure from 130 +/- 25 to 71 +/- 14 mm Hg, no decreases in subendocardial blood flow and systolic wall thickening were observed. Only when coronary arterial pressure was further reduced to 57 +/- 13 mm Hg did systolic wall thickening fall to 25.7 +/- 9.9% (control, 31.1 +/- 11.1%), associated with a decrease in subendocardial blood flow from 1.17 +/- 0.39 to 0.87 +/- 0.52 ml/min/g. Thus, the Gregg phenomenon plays no significant role within or above the autoregulatory pressure-flow range normally seen in anesthetized swine in situ.

Noninvasive determination of age-related changes in the human arterial pulse.

Arterial pressure waves were recorded noninvasively from the carotid, radial, femoral, or all three of these arteries of 1,005 normal subjects, aged 2-91 years, using a new transcutaneous tonometer containing a high fidelity Millar micromanometer. Waves were ensemble-averaged into age-decade groups. Characteristic changes were noted with increasing age. In all sites, pulse amplitude increased with advancing age (carotid, 91.3%; radial 67.5%; femoral, 50.1% from first to eighth decade), diastolic decay steepened, and diastolic waves became less prominent. In the carotid pulse, there was, in youth, a second peak on the downstroke of the waves in late systole. After the third decade, this second peak rose with age to merge with and dominate the initial rise. In the radial pulse, a late systolic wave was also apparent, but this occurred later; with age, this second peak rose but not above the initial rise in early systole, even at the eighth decade. In the femoral artery, there was a single systolic wave at all ages. Aging changes in the arterial pulse are explicable on the basis of both an increase in arterial stiffness with increased pulse-wave velocity and progressively earlier wave reflection. These two factors may be separated and effects of the latter measured from pressure wave-contour analysis using an "augmentation index," determined by a computer algorithm developed from invasive pressure and flow data. Changes in peak pressure in the central (carotid) artery show increasing cardiac afterload with increasing age in a normal population; this can account for the cardiac hypertrophy that occurs with advancing age (even as other organs atrophy) and the predisposition to cardiac failure in the elderly. Identification of mechanisms responsible offers a new approach to reduction of left ventricular afterload.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts.

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

Depressor and pressor actions of purine nucleosides and nucleotides in the anaesthetized rat.

In pentobarbitone-chloralose anaesthetized rats, the effects of aortic administration of various purine compounds on systemic arterial pressure were investigated. All animals were pretreated with atropine and guanethidine to (largely) eliminate reflex neurogenic cardiovascular adjustments, and drugs influencing purine receptors, prostaglandin synthesis, etc. were used for analytical purposes. The compounds used were adenosine (AD) and its slowly degradable analogue, 2-chloroadenosine (2-chloro), adenosine-5'-triphosphate (ATP) and its slowly degradable analogues beta, gamma-methyleneATP (beta,gamma-meATP) and alpha,beta-methyleneATP (alpha,beta-meATP). Control cardiac output measurements before, at and after the peak pressure changes in some experiments revealed that they were at least 80% due to changes in systemic resistance, i.e. dominated by shifts in resistance vascular tone. Adenosine, 2-chloro, ATP and beta,gamma-meATP all elicited depressor (vasodilator) responses. 2-chloro was more potent than AD. Furthermore, the results suggest that the depressor action of ATP involves P1-purinoceptors, following the rapid degradation of ATP to AD, and probably also other mechanisms. The stable ATP analogues caused prompt pressor (vasoconstrictor) responses, where alpha,beta-meATP was more potent than beta,gamma-meATP. The latter compound also produced delayed (probably P1-purinoceptormediated) depressor actions, presumably via slow degradation to AD.

Influence of pacing site on canine left ventricular contraction.

We investigated the influence of pacing site on several aspects of left ventricular (LV) performance to test the hypothesis that "effective ventricular muscle mass" is reduced with direct ventricular pacing. All studies were performed on isolated supported canine hearts that were constrained to contract isovolumically. To determine the influence of pacing site on magnitude and time course of isovolumic LV pressure (P) generation, LVP waves were recorded in eight isolated hearts paced at 130 beats/min. Pacing was epicardially from atrium, LV apex, LV free wall, right ventricular free wall (RVF), and endocardially from right ventricular endocardium. In a given heart, peak LVP was greatest with atrial pacing and smallest with RVF pacing, the difference being on average 26 +/- 10% (mean +/- SD) of the former pressure. The other pacing sites produced intermediate peak LVPs. When instantaneous LVP waves, obtained while pacing from each of the five sites, were normalized by their respective amplitudes, they were virtually superimposable up to the time of peak pressure and only slightly different during the remainder of the cardiac cycle. With changes in pacing site there was a linear negative correlation (r = 0.971) between changes in peak pressure and changes in duration of the QRS complex of a bipolar epicardial electrogram with an average slope of -0.51 mmHg/ms. Compared with atrial pacing, the slope of the end-systolic pressure-volume relation, Ees, was decreased with ventricular pacing, but Vo, the volume axis intercept, was relatively constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of altering P-R interval on the amplitude of the first heart sound in the anesthetized dog.

To determine the effect of changing the P-R interval on the intensity of the mitral component of the first heart sound (M 1 amplitude), fixed-rate sequential atrioventricular pacing was used to vary the P-R interval in a steady hemodynamic state in six anesthetized dogs. Left ventricular sound and pressure events were monitored with a catheter-tip micromanometer, and the rate of rise of left ventricular pressure (dP/dt) was recorded using an R/C differentiator. The P-R interval was varied from the longest interval at which continuous ventricular capture was achieved (indifferent P-R interval) to 0.00 msec in 10-msec increments. The mean increase in M 1 amplitude at the short P-R intervals (30 to 50 msec) was 119% compared to the amplitude at the indifferent P-R interval; there was no significant change in maximum dP/dt. No significant changes in left ventricular ejection time and left ventricular peak pressure occurred over the range of P-R intervals. At the indifferent P-R interval, a norepinephrine infusion increased M 1 amplitude 22% and maximum dP/dt 50%. At short P-R intervals in the new inotropic state, the M 1 amplitude was further augmented. These data indicate that both the timing of atrial and ventricular systoles and the force of left ventricular contraction are major, independent determinants of M 1 amplitude. These findings are consistent with the concept that the abrupt deceleration of blood by the mitral valve shortly after the onset of ventricular systole sets the cardiohemic system into vibration producing the M 1 sound. The intensity of the first heart sound is proportional to the force produced in this manner.