Biomedical subjects

Kenji Sunagawa

Publications and source records attributed to Kenji Sunagawa.

At least 109 records · Page 6Linked to original sources

PubMed2003

Uniformity in dynamic baroreflex regulation of left and right cardiac sympathetic nerve activities.

Functional laterality of cardiac sympathetic nerve stimulation in chronotropic and inotropic effects is well known. Whether left (LSNA) and right (RSNA) cardiac sympathetic nerve activities show laterality during dynamic baroreflex activation remains to be determined. In nine anesthetized, vagotomized, and aortic-denervated rabbits, we randomly perturbed intracarotid sinus pressure (CSP) in both carotid sinus regions while simultaneously recording LSNA and RSNA. The baroreflex neural arc transfer function from CSP to LSNA and from CSP to RSNA revealed derivative characteristics, i.e., the magnitude of LSNA and RSNA responses became greater as the input frequency of CSP perturbation increased. The average slope of increasing gain in the frequencies between 0.03 and 0.3 Hz showed no difference between LSNA and RSNA responses (9.7 +/- 2.9 vs. 9.7 +/- 3.1 dB/decade, means +/- SD). The amplitude ratio and phase difference between LSNA and RSNA approximated unity and zero radians, respectively, in the frequencies from 0.01 to 1 Hz. In addition, the LSNA-RSNA relationship during stepwise CSP perturbation from 40 to 160 mmHg showed a straight line (r(2) ranged from 0.969 to 0.999). These findings indicate no laterality in the dynamic as well as static baroreflex regulation of LSNA and RSNA as far as grouped axonal activity is concerned.

Adrenergic Fibers↗

PubMed2003

Effects of ketamine on exocytotic and non-exocytotic noradrenaline release.

To characterise ketamine-induced sympathomimetic action, we examined the effects of ketamine on in vivo cardiac sympathetic nerve endings function. Using adult cats given anaesthesia with pentobarbital, dialysis probes were implanted in the left ventricular myocardium and dialysate noradrenaline (NA) concentrations were measured as an indicator of NA output at the cardiac sympathetic nerve endings. Ketamine was locally administered through the dialysis probe, and dialysate NA responses were obtained in the following conditions. (1) In the resting state, ketamine (10 mM) increased dialysate NA concentration. This increase in dialysate NA was not altered by addition of omega-conotoxin GVIA (N-type Ca(2+) channel blocker) or desipramine (membrane NA uptake blocker). (2) Sympathetic activation by electrical stimulation of the stellate ganglia (ES-SG; exocytotic NA release): ES-SG caused an increase in dialysate NA, which was further augmented by addition of desipramine. During co-administration of desipramine and ketamine, dialysate NA response to ES-SG was smaller than with desipramine alone. Further, there was no significant difference in the dialysate NA response to ES-SG between ketamine and ketamine + desipramine. These data suggested that both exocytosis and NA uptake function were impaired by ketamine. (3) Non-exocytotic NA release by ouabain: ouabain caused increases in dialysate NA. These increases in dialysate NA were suppressed by ketamine, which impaired the membrane outward NA transport evoked by ouabain. We conclude that ketamine impaired exocytotic and non-exocytotic NA release. However, ketamine spontaneously evoked NA efflux that was independent of exocytosis and insensitive to NA transporter.

Animals↗

PubMed2003

Differential gene expression in the rat skeletal and heart muscle in glucocorticoid-induced myopathy: analysis by microarray.

Administration of glucocorticoids results in hypertension, cardiac hypertrophy, and general myopathy. The present study analyzed the acute effect of dexamethasone (0.5 mg/100 g for 3 days) or dexamethasone plus insulin-like growth factor-1 (0.35 mg/100 g for 3 days) on differential gene expression in the gastrocnemius muscle and the left ventricular myocardium of rats. Dexamethasone induced atrophy of gastrocnemius muscle. Cathepsin L, and not ubiquitin, was the earliest mediator of skeletal muscle proteolysis induced by dexamethasone. Insulin-like growth factor-1 reversed gastrocnemius muscle mass, and deleted a part of downregulated genes by dexamethasone. On the other hand, dexamethasone administration did not result in cardiac hypertrophy or hypertension. Only prostaglandin D synthase gene was upregulated by dexamethasone in myocardium, and genes related to extracellular matrix and proteinase inhibitor were downregulated. Molecular alteration for hypertrophy might have initiated. Dexamethasone-induced proteolysis and reversal with insulin-like growth factor-1 occurred rapidly in skeletal muscle; but was relatively delayed in the myocardium.

Animals↗

PubMed2003

Dynamics of sympathetic baroreflex control of arterial pressure in rats.

By a white noise approach, we characterized the dynamics of the sympathetic baroreflex system in 11 halothane-anesthetized rats. We measured sympathetic nerve activity (SNA) and systemic arterial pressure (SAP), while carotid sinus baroreceptor pressure (BRP) was altered randomly. We estimated the transfer functions from BRP to SNA (mechanoneural arc), from SNA to SAP (neuromechanical arc), and from BRP to SAP (total arc). The gain of the mechanoneural arc gradually increased about threefold as the frequency of BRP change increased from 0.01 to 0.8 Hz. In contrast, the gain of the neuromechanical arc rapidly decreased to 0.4% of the steady-state gain as the frequency increased from 0.01 to 1 Hz. Although the total arc also had low-pass characteristics, the rate of attenuation in its gain was significantly slower than that of the neuromechanical arc, reflecting the compensatory effect of the mechanoneural arc for the sluggish response of the neuromechanical arc. We conclude that the quantitative estimation of the baroreflex dynamics is vital for an integrative understanding of baroreflex function in rats.

Animals↗

PubMed2003

Transmural heterogeneity of the action potential configuration in the feline left ventricle.

There are M cells in the canine, rabbit, guinea pig, and human left ventricle (LV), but it is not known if they are present in the feline LV. Arterially perfused feline LV preparations were used for the recording of transmembrane action potentials from the epicardium (Epi), midmyocardium (M) and endomyocardium (Endo) under control conditions (n=12) and in the presence of I(Ks) blocker (chromanol 293B: 10 micromol/L, n=6) or I(Kr) blocker (E-4031: 2 micromol/L, n=6). The steady-state action potential duration at 90% repolarization and cycle length (APD90/CL) relation was obtained and fitted by the hyperbolic function APD(90) = CL/[(a x CL) + b]. In control, the shortest and longest action potential duration (APD) were observed in Epi and M, respectively, and the APD(90)/CL-relation curve was steeper in the M or Endo than in the Epi. Chromanol 293B prolonged APD in Epi, but not in M or Endo, resulting in no significant difference of the APD(90)/CL-relation curve among the 3 regions. E-4031 markedly, but homogeneously, prolonged APD in all regions, giving rise to decreased transmural dispersion of repolarization. In conclusion, there exists an M cell layer with a longer APD than the Epi and Endo layers and there is transmural electrical heterogeneity in the feline LV; however, the response to I(Kr) blocker is different from that of the canine LV probably because of species differences in the I(Kr) and I(Ks).

Action Potentials↗

PubMed2003

Biphasic response of action potential duration to sudden sympathetic stimulation in anesthetized cats.

Although certain roles of the sympathetic nervous system have been suggested as possible mechanisms of life-threatening arrhythmias and sudden cardiac death, the dynamic electrophysiological response to sympathetic activation remains unclear. The aim of this study was to investigate the dynamic response of action potential duration (APD) to sudden sympathetic stimulation (SYM) using monophasic action potential (MAP) recording. In 10 anesthetized cats, MAPs were continuously recorded from the right ventricular endocardium under constant pacing. The dynamic response of the APD to SYM (3 Hz) were examined before and after the administration of propranolol (0.5 mg/kg i.v.) (n=5) or phentolamine (1.0 mg/kg i.v.) (n=5). In response to SYM, the APD was transiently prolonged by 5.5+/-3.2 ms at 7.0+/-1.3 s, and monotonically shortened toward a steady-state level (-14.5+/-6.9 ms). Propranolol almost abolished both the transient prolongation (6.6+/-4.5 to 0.2+/-0.4 ms, p<0.05) and the steady-state shortening (-13.7+/-3.6 to -1.1+/-2.4 ms, p<0.005), whereas phentolamine did not have a significant effect on the response of APD to SYM. These findings might partly account for the propensity of ventricular arrhythmias to occur immediately after sudden sympathetic activation.

Action Potentials↗

PubMed2003

Intravenous angiotensin II does not affect dynamic baroreflex characteristics of the neural or peripheral arc.

Although the elevation of angiotensin II (Ang II) associated with cardiovascular diseases has been considered to suppress the arterial baroreflex function, how Ang II affects dynamic arterial pressure (AP) regulation remains unknown. The aim of the present study was to elucidate the acute effects of Ang II on dynamic AP regulation by the arterial baroreflex. In seven anesthetized Japanese white rabbits, we randomly perturbed intra-carotid sinus pressure (CSP) according to a binary white noise sequence while recording renal sympathetic nerve activity (RSNA) and AP. We estimated the neural arc transfer function from CSP to RSNA and the peripheral arc transfer function from RSNA to AP before and after 30-min intravenous administration of Ang II (100 ng/kg/min). Ang II increased mean AP from 75.7 +/- 3.1 to 95.5 +/- 5.1 mmHg (p < 0.01), while it did not affect mean RSNA (from 5.9 +/- 1.3 to 5.7 +/- 1.2 a.u.). The neural arc transfer functions did not differ before or after Ang II administration (dynamic gain: -0.94 +/- 0.04 vs. -0.94 +/- 0.13, corner frequency: 0.06 +/- 0.01 vs.0.06 +/- 0.01 Hz, pure delay: 0.16 +/- 0.01 vs. 0.17 +/- 0.02 s). The peripheral arc transfer function did not differ before or after Ang II administration (dynamic gain: 1.18 +/- 0.05 vs. 1.06 +/- 0.11, natural frequency: 0.07 +/- 0.01 vs. 0.08 +/- 0.01 Hz, damping ratio: 1.19 +/- 0.06 vs. 1.24 +/- 0.19, pure delay: 0.83 +/- 0.06 vs. 0.78 +/- 0.05 s). Intravenous Ang II hardly affects the dynamic characteristics of neural and peripheral arc around the physiological operating pressure.

Algorithms↗

PubMed2003

Heat stress modifies human baroreflex function independently of heat-induced hypovolemia.

Since human thermoregulatory heat loss responses, cutaneous vasodilation and sweating, cause hypovolemia, they should resultantly stimulate human baroreflexes. However, it is possible that the thermoregulatory system directly interacts with the baroreflex system through central neural connections independently of the heat-induced hypovolemia. We hypothesized that heat stress modifies the baroreflex control of sympathetic nerve activity independently of heat-induced hypovolemia in humans. We made whole-body heating with tube-lined suits perfused with warm water (46-47 degrees C) on 10 healthy male subjects. The heating increased skin and tympanic temperatures by 10.0 and 0.4 degrees C, respectively. It increased resting total muscle sympathetic nerve activity (MSNA, microneurography) by 94 +/- 9% and decreased central venous pressure (CVP, dependent arm technique) by 2.6 +/- 0.9 mmHg. The heating increased arterial baroreflex gain by 193%, assessed as a response of MSNA to a decrease in diastolic arterial pressure during Valsalva's maneuver, but it did not change threshold arterial pressure for MSNA activation. Although the heating did not change the cardiopulmonary baroreflex gain assessed as a response of MSNA to a change in estimated central venous pressure (CVP) during a 10 degrees head-down and -up tilt test, it upwardly shifted the stimulus-response baroreflex relationship. These changes in baroreflex functions during heating were not restored by an intravenous infusion of warmed isotonic saline (37 degrees C, 15 ml/kg) that restored the heat-induced reduction of CVP. Our results support our hypothesis that heat stress modifies the baroreflex control of MSNA independently of heat-induced hypovolemia in humans. Our results also suggest that the hyperthermal modification of baroreflex results from central neural interaction between thermoregulatory and baroreflex systems.

Adult↗

PubMed2003

Effects of moderate hypothermia on norepinephrine release evoked by ouabain, tyramine and cyanide.

Using the dialysis technique, we examined the effect of moderate hypothermia on the norepinephrine efflux evoked by ouabain, tyramine and cyanide in anesthetized cats. Dialysis probes were implanted in the left ventricular myocardium, and we measured the dialysate norepinephrine levels as an indicator of norepinephrine output at the cardiac sympathetic nerve endings. Through the dialysis probe, locally applied ouabain, tyramine and cyanide induced the norepinephrine efflux. The addition of desipramine (neuronal norepinephrine transport blocker, 100 microM) suppressed the norepinephrine efflux evoked by ouabain, tyramine and cyanide. This finding suggests that pharmacological agent-induced norepinephrine efflux was due to carrier-mediated outward norepinephrine transport. Moderate hypothermia (27.4 +/- 0.2 degrees C) caused suppression of the norepinephrine efflux evoked by ouabain, tyramine and cyanide. We conclude that moderate hypothermia suppresses the non-exocytotic norepinephrine release evoked by ouabain, tyramine and cyanide.

Animals↗

PubMed2002

Input-size dependence of the baroreflex neural arc transfer characteristics.

Static characteristics of the baroreflex neural arc from pressure input to sympathetic nerve activity (SNA) show sigmoidal nonlinearity, whereas its dynamic characteristics approximate a derivative filter where the magnitude of SNA response becomes greater as the input frequency increases. To reconcile the static nonlinear and dynamic linear components, we examined the effects of input amplitude on the apparent linear transfer function of the neural arc. In nine anesthetized rabbits, we perturbed isolated carotid sinus pressure by using binary white noise while varying the input amplitude among 5, 10, 20, and 40 mmHg. With increasing input amplitude, the transfer gain at 0.01 Hz decreased from 1.21 +/- 0.27 to 0.49 +/- 0.28 arbitrary units/mmHg (P < 0.01). Moreover, the slope of the transfer gain between 0.03 and 0.3 Hz decreased from 14.3 +/- 3.7 to 6.5 +/- 2.5 dB/decade (P < 0.01). We conclude that the model consisting of a sigmoidal component following rather than preceding a derivative component explains the observed results and thus can be used as a first approximation of the overall neural arc transfer characteristics.

Acoustic Stimulation↗

PubMed2002

Disruption of vagal efferent axon and nerve terminal function in the postischemic myocardium.

Despite the importance of vagal control over the ventricle, little is known regarding vagal efferent conduction and nerve terminal function in the postischemic myocardium. To elucidate postischemic changes in the cardiac vagal efferent neuronal function, we measured myocardial interstitial acetylcholine (ACh) levels by using in vivo cardiac microdialysis and examined the ACh responses to electrical stimulation of the vagi or local administration of ouabain in anesthetized cats. Sixty-minute occlusions of the left anterior descending coronary artery (LAD) followed by 60-min reperfusion abolished electrical stimulation-induced ACh release (20.4 +/- 3.9 vs. 0.9 +/- 0.4 nmol/l; means +/- SE, P < 0.01). In different groups of animals, 60-min LAD occlusion followed by 60-min reperfusion decreased but did not completely abolish ouabain-induced release of ACh (9.2 +/- 1.8 vs. 3.9 +/- 0.7 nmol/l; P < 0.05). These results indicate that function of the vagal efferent axon was completely interrupted, whereas the local ACh release was partially suppressed in the postischemic myocardium. The postischemic disruption of vagal efferent neuronal function might exert deleterious effects on cardiac regulation.

Acetylcholine↗

PubMed2002

Bionic technology revitalizes native baroreflex function in rats with baroreflex failure.

BACKGROUND: We developed a bionic technology for the treatment of baroreflex failure and tested its efficacy in restoration of arterial pressure against head-up tilt (HUT) in rats with baroreflex failure. METHODS AND RESULTS: The bionic baroreflex system (BBS) was a negative feedback system controlled by a computer, the artificial vasomotor center. It sensed systemic arterial pressure (SAP) through a micromanometer placed in the aortic arch and automatically computed the frequency of a pulse train to stimulate sympathetic efferent nerves. We selected the celiac ganglion as the sympathetic vasomotor interface. To make this system bionic, the operational rule of the artificial vasomotor center (H(BRP-->STM); BRP indicates baroreceptor pressure; STM, electrical stimulation) was actively matched to that of the native center. First, we identified the open-loop transfer functions of the native baroreflex control of SAP (H(Native)) and the response of SAP to electrical stimulation of the celiac ganglion (H(STM-->SAP)). We computed H(BRP-->STM) from H(Native)/H(STM-->SAP) and transplanted the operational rule into the computer. In 10 rats with baroreflex failure, we evaluated the performance of the BBS during rapid hypotension induced by HUT. Abrupt HUT dropped SAP by 34+/-6 mm Hg in 2 seconds and by 52+/-5 mm Hg in 10 seconds. During real-time execution of the BBS, on the other hand, the fall in SAP was 21+/-5 mm Hg at 2 seconds and 15+/-6 mm Hg at 10 seconds after HUT. These arterial responses controlled by the BBS were indistinguishable from those by the native baroreflex. CONCLUSIONS: We concluded that the BBS revitalized the native baroreflex function in rats with baroreflex failure.

Animals↗

PubMed2002

Differential effects of beta-blockade on dispersion of repolarization in the absence and presence of sympathetic stimulation between the LQT1 and LQT2 forms of congenital long QT syndrome.

OBJECTIVES: This study compared the effects of beta-blockade on transmural and spatial dispersion of repolarization (TDR and SDR, respectively) between the LQT1 and LQT2 forms of congenital long QT syndrome (LQTS). BACKGROUND: The LQT1 form is more sensitive to sympathetic stimulation and more responsive to beta-blockers than either the LQT2 or LQT3 forms. METHODS: Eighty-seven-lead, body-surface electrocardiograms (ECGs) were recorded before and after epinephrine infusion (0.1 microg/kg body weight per min) in the absence and presence of oral propranolol (0.5-2.0 mg/kg per day) in 11 LQT1 patients and 11 LQT2 patients. The Q-T(end) interval, the Q-T(peak) interval and the interval between T(peak) and T(end) (T(p-e)), representing TDR, were measured and averaged from 87-lead ECGs and corrected by Bazett's method (corrected Q-T(end) interval [cQT(e)], corrected Q-T(peak) interval [cQT(p)] and corrected interval between T(peak) and T(end) [cT(p-e)]). The dispersion of cQT(e) (cQT(e)-D) was obtained among 87 leads and was defined as the interval between the maximum and minimum values of cQT(e). RESULTS: Propranolol in the absence of epinephrine significantly prolonged the mean cQT(p) value but not the mean cQT(e) value, thus decreasing the mean cT(p-e) value in both LQT1 and LQT2 patients; the differences with propranolol were significantly larger in LQT1 than in LQT2 (p < 0.05). The maximum cQT(e), minimum cQT(e) and cQT(e)-D were not changed with propranolol. Propranolol completely suppressed the influence of epinephrine in prolonging the mean cQT(e), maximum cQT(e) and minimum cQT(e) values, as well as increasing the mean cT(p-e) and cQT(e)-D values in both groups. CONCLUSIONS: Beta-blockade under normal sympathetic tone produces a greater decrease in TDR in the LQT1 form than in the LQT2 form, explaining the superior effectiveness of beta-blockers in LQT1 versus LQT2. Beta-blockers also suppress the influence of sympathetic stimulation in increasing TDR and SDR equally in LQT1 and LQT2 syndrome.

Adolescent↗

PubMed2002

Modulatory effects of ketamine on catecholamine efflux from in vivo cardiac sympathetic nerve endings in cats.

With the use of the microdialysis technique, we examined the modulatory effect of ketamine on catecholamine efflux from in vivo cardiac sympathetic nerve endings. A dialysis probe was implanted in the left ventricular myocardium, and dialysate norepinephrine (NE) levels in anesthetized cats were measured with liquid chromatogram-electrical detection. A 60-min occlusion of the left anterior descending coronary artery caused increases in dialysate NE levels. Through the dialysis probe, locally applied ketamine (10 mM) augmented the dialysate NE responses to coronary occlusion in the presence and absence of desipramine (membrane NE transport blocker). Thus, the ketamine-induced NE increment is not mediated through the neuronal NE transporter. The sympathomimetic action of ketamine may augment the NE efflux evoked by myocardial ischemia.

Adrenergic Uptake Inhibitors↗

PubMed2002

Effects of brief ischaemia on myocardial acetylcholine and noradrenaline levels in anaesthetized cats.

Although brief ischaemic events make the myocardium tolerant to subsequent prolonged ischaemia, known as ischaemic preconditioning, whether brief ischaemia also affects neural regulation at the in vivo heart remains unknown. We examined the effects of brief ischaemia on myocardial interstitial acetylcholine (ACh) and noradrenaline (NA) levels in anaesthetized cats (n = 6). Baseline ACh and NA levels were 0.65 +/- 0.13 and 0.66 +/- 0.17 nmol l(-1) (mean +/- SE), respectively. Two sets of 5-min brief occlusion followed by 20-min reperfusion of the left anterior descending coronary artery (LAD) significantly increased the myocardial interstitial ACh level to 4.6 +/- 0.7 nmol l(-1) (P < 0.01), while not affecting the myocardial interstitial NA level. Subsequent 60-min LAD occlusion significantly increased the ACh and NA levels to 34.9 +/- 6.0 and 96.5 +/- 17.0 nmol l(-1) (P < 0.01), respectively. Vagotomy abolished the myocardial interstitial ACh release during brief ischaemia and attenuated the ACh release during subsequent 60-min ischaemia (n = 6). In contrast, vagotomy did not affect the subsequent ischaemia-induced myocardial interstitial NA release. We conclude that the brief ischaemia affects myocardial interstitial ACh release but not NA release in the ischaemic myocardium in vivo.

Acetylcholine↗

PubMed2002

A novel photocurable insulator material for autonomic nerve activity recording.

The two-component, addition-curing silicone glue is widely used as an insulator for autonomic nerve activity recording. Due to its high fluidity before curing, a sizable mass of the glue is needed to completely cover the electrode tips, which may cause mechanical stress on the nerve. To overcome this problem, we designed a novel photocurable insulator material composed of Vaseline and 1,12-dodecanediol diacrylate (50:50wt%) together with a photoinitiator, camphorquinone, at 0.25wt%. This material had an appropriate viscosity of 0.18 Pa s at 25 degrees C and was converted to a soft solid upon an arbitrary timing of photoirradiation. The compressive force per mm deformation of the resulting solid was 155.5 kPa at 1 min of photoirradiation. The impedance of the solid for 1 mm length and 10 mm2 cross-sectional area was above 1 Mohm. In anesthetized rabbits, a very small mass of the photocurable material was able to cover the electrode tips and the nerve in situ. Changes in both the aortic depressor nerve activity and renal sympathetic nerve activity were stably recorded. These results indicate that the photocurable material developed is useful as an in vivo insulator material for autonomic nerve activity recording.

Animals↗

PubMed2002

Right ventricular dP/dt/P(max), not dP/dt(max), noninvasively derived from tricuspid regurgitation velocity is a useful index of right ventricular contractility.

BACKGROUND: Although right ventricular (RV) contractility is important in determining functional capacity, few quantification methods are clinically available. RV dP/dt(max) can be assessed by Doppler echocardiography by using tricuspid regurgitation (TR) but is not routinely used because of its dependency on a Doppler incident angle and preload. Doppler-derived dP/dt/P(max) is relatively insensitive to preload and theoretically independent of the incident angle. We investigated the clinical feasibility of this index as an RV contractility index. METHODS: We computed RV dP/dt(max) and dP/dt/P(max) from the TR-derived RV pressure in 68 patients with dominant RV failure (13 in New York Heart Association [NYHA] class I, 33 in class II, 17 in class III, and 5 in class IV). Peak oxygen consumption (peak VO(2)) was measured in 20 patients during a maximal bicycle ergometer test. RESULTS: dP/dt(max) did not significantly correlate with NYHA class. In contrast, dP/dt/P(max) decreased monotonically with the functional class (r = -0.49, P <.0001), and correlated with peak VO(2) (r = 0.66, P <.002). CONCLUSION: TR-derived dP/dt/P(max), not dP/dt(max), is a clinically useful index of RV contractility, allowing researchers to account for the functional capacity.

Adolescent↗

PubMed2002

Inelastic vascular prosthesis for proximal aorta increases pulsatile arterial load and causes left ventricular hypertrophy in dogs.

OBJECTIVES: Elastic property of the proximal aorta plays an important role in reducing pulsatile load to the ventricle. When a stiff vascular prosthesis is used for the proximal aorta, the pulsatile load increases. We designed this study to elucidate whether the increase in pulsatile load caused left ventricular hypertrophy. METHODS: We created an ascending aorta-abdominal aorta bypass in 9 dogs with a noncompliant vascular prosthesis. The aortic arch proximal to the left subclavian artery was occluded to direct blood flow into the bypass. Closed chest studies were performed after a median of 139 days (range 45-588) days. We assessed the pulsatile load of the ventricle by calculating characteristic impedance from pressure and flow velocity in the ascending aorta. The left ventricle was weighed, normalized with body weight, and compared with the control group, which had sham operations (7 dogs). RESULTS: Characteristic impedance of the bypassed dogs was 175% higher than the control (0.146 +/- 0.056 vs 0.053 +/- 0.014 mm Hg. s. mL(-1), P =.009), which resulted in wider pulse pressure (57 +/- 11 vs 25 +/- 11 mm Hg, P <.001). No difference was found in arterial resistance, cardiac output, or systolic blood pressure. Left ventricular weight normalized by body weight was significantly heavier in the bypass group (5.61 +/- 0.75 vs 4.15 +/- 0.62 g/kg, P =.001). CONCLUSION: Since there was no increase in arterial resistance, we conclude that the increase in pulsatile load was the cause of left ventricular hypertrophy. A stiff vascular prosthesis used for the proximal aorta may cause left ventricular hypertrophy.

Animals↗