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PubMed1993

Haemodynamics and tissue specificity with isradipine.

The significant effects of isradipine in producing arterial vasodilation and mild negative chronotropic effects without significant negative inotropic effects suggests that this agent should provide excellent antihypertensive efficacy in the treatment of perioperative hypertension. Isradipine may prove to be a safe antihypertensive treatment in patients with impaired ventricular function (cardiac failure), impaired myocardial perfusion (ischaemia), and in cases of selected conduction abnormalities or arrhythmias. The demonstration that its effects are limited to vascular resistance rather than vascular capacitance is an important distinguishing feature of isradipine compared with other antihypertensive agents. Finally, the potential application of this dihydropyridine calcium antagonist for cytoprotection and its effects on atherosclerosis remain exciting therapeutic prospects.

Hemodynamics↗
PubMed1995

Effects of pinacidil on arterial and venous resistances and mean circulatory filling pressure in rats.

1. The effects of the potassium channel opener, pinacidil, on mean arterial pressure (MAP), mean circulatory filling pressure (MCFP), total peripheral resistance (TPR), cardiac output (CO) and resistance to venous return (Rv) were studied in rats. 2. In pentobarbitone-anaesthetized rats given mecamylamine (ganglionic blocker, 3.7 micrograms kg-1) and noradrenaline (1.5 micrograms kg-1 min-1) to suppress autonomic reflexes, pinacidil (60 and 180 micrograms kg-1 min-1), relative to the vehicle, reduced MAP and TPR in a dose-dependent manner but did not significantly alter CO, MCFP or RV. 3. Pinacidil (10-300 micrograms kg-1 min-1) caused similar increases in MCFP, an inverse index of venous compliance, and similar dose-dependent reductions in mean arterial pressure (MAP) in conscious, intact rats and rats infused with the ganglionic blocker, hexamethonium (150 micrograms kg-1 min-1). In rats with vasomotor tone elevated by the infusion of noradrenaline (1.5 micrograms kg-1 min-1), pinacidil caused markedly greater depressor responses but did not significantly alter MCFP. 4. Our results show that pinacidil is an efficacious vasodilator of arterial resistance blood vessels but has little venodilator activity.

Anesthesia↗
PubMed1991

The effect of discrete stimulation of carotid body chemoreceptors on atrial natriuretic peptide in anaesthetized dogs.

1. In seven chloralose-anaesthetized and artificially ventilated beagles, the carotid sinus regions were vascularly isolated and perfused with either arterial or mixed (arterial and venous) blood (PO2 46.4 +/- 1.5 mmHg, mean +/- S.E.M.) to stimulate the chemoreceptors at constant flow and pressure. Cervical vagosympathetic trunks were ligated in all dogs, and gallamine triethiodide (2.0 mg kg-1 h-1, I.V.) was given in five dogs. Right atrial pressure was measured in all dogs, and left atrial pressure in four dogs. Mean aortic pressure was held constant (91.0 +/- 3.0 mmHg) by means of a reservoir connected to the animal via the common carotid and femoral arteries. Plasma atrial natriuretic peptide (ANP) was measured by radioimmunoassay and urinary sodium by flame photometry. 2. In seven dogs with mean carotid sinus pressure maintained at 96.0 +/- 4.3 mmHg, stimulation of the carotid chemoreceptors for 25 min produced significant increases in left atrial pressure of 41.2 +/- 3.3% (n = 4; P less than 0.005) from 5.4 +/- 0.6 cmH2O and of 30.9 +/- 4.5% (n = 7; P less than 0.002) in ANP from 31.6 +/- 2.1 pg ml-1. However, chemoreceptor stimulation produced significant decreases in urine flow rate of 26.1 +/- 1.9% (n = 9; P less than 0.001) from 0.29 +/- 0.03 ml min-1 (100 g kidney weight)-1 and sodium excretion of 29.0 +/- 2.3% (P less than 0.001) from 8.5 +/- 1.7 mumol min-1 (100 g kidney weight)-1 but right atrial pressure and heart rate did not change significantly. In three of the dogs, beta-adrenoceptor blockade by atenolol (2 mg kg-1, I.V.) greatly reduced the effects of chemoreceptor stimulation on plasma levels of ANP. 3. The results show, for the first time, that discrete stimulation of the carotid chemoreceptors caused an increase in plasma ANP levels, probably due to the reflex increase in atrial pressure that results from an inhibition of the cardiac sympathetic nerves, and an increase in venous return from a reduction of peripheral vascular capacitance.

Anesthesia↗
PubMed2002

An analysis of turbulent shear stresses in leakage flow through a bileaflet mechanical prostheses.

In this work, estimates of turbulence were made from pulsatile flow laser Doppler velocimetry measurements using traditional phase averaging and averaging after the removal of cyclic variation. These estimates were compared with estimates obtained from steady leakage flow LDV measurements and an analytical method. The results of these studies indicate that leakage jets which are free and planar in shape may be more unstable than other leakage jets, and that cyclic variation does not cause a gross overestimation of the Reynolds stresses at large distances from the leakage jet orifice.

Blood Flow Velocity↗
PubMed2004

An in vivo method for measuring turbulence in mechanical prosthesis leakage jets.

This work introduces a method for the in vivo measurement and analysis of turbulence within the leakage of a mechanical heart valve. Several analysis techniques were applied to ultrasound measurements acquired within the atrium of a pig, and error associated with these techniques was analyzed. The technique chosen applies cyclic averaging to mean and maximum velocity measurements within small, normalized phase windows to calculate Reynolds normal stresses in the direction of the ultrasound beam. Maximum shear stresses are estimated from these normal stresses using an analytical technique. The stresses observed were smaller than those reported from previous in vitro simulations.

Animals↗
PubMed1997

Acquired aortic regurgitation following occlusion of the persistent arterial duct: an echocardiographic assessment.

OBJECTIVE: To document the development of aortic regurgitation following occlusion of a patent arterial duct. DESIGN: Case series involving nine children referred for surgical ligation of an isolated patent arterial duct. SETTING: Academic referral centre. METHODS: A preoperative transthoracic and transoesophageal echocardiogram was performed in theatre to look for aortic regurgitation. Thereafter, aortic flow was monitored throughout the operation by colour flow mapping with the transoesophageal probe in situ. Onset of aortic regurgitation was documented. An immediate postoperative transthoracic echocardiogram was performed on all patients and then daily until discharge on day 5. A follow up clinical and echocardiographic assessment was performed six weeks postoperatively. RESULTS: With ligation of the patient arterial duct, transoesophageal echocardiography showed immediate regurgitation in seven of the nine patients, seen as a small central jet on colour flow mapping. Six of the seven patients continued to have aortic regurgitation on transthoracic echocardiography before leaving theatre. In none was aortic regurgitation audible clinically. At discharge, five patients still had evidence of aortic regurgitation; of four seen at follow up six weeks later, only one had residual regurgitation. CONCLUSIONS: Ligation of the patient arterial duct results in the acute termination of the "run off" in a volume overloaded situation. This, together with a rise in the peripheral vascular resistance and the persistence of increased proximal vascular capacitance, is considered to be the underlying aetiology of the acquired aortic regurgitation.

Aortic Valve Insufficiency↗
PubMed1986

Vasodilator therapy of dilated cardiomyopathy.

Vasoconstriction increases impedance to ventricular ejection and impairs the performance of the dilated myopathic heart. Vasodilator drug therapy by reducing vascular resistance, increasing vascular compliance and increasing vascular capacitance improves cardiac function and relieves the signs and symptoms of congestive heart failure. Earlier intervention in an attempt to alter the natural history of cardiomyopathy should be studied.

Blood Pressure↗
PubMed1983

A new method for estimating intestinal capillary pressure.

The purpose of this study was to compare the venous occlusion method for measuring capillary pressure with the stop-flow isovolumetric method in the cat small intestine. Venous occlusion pressures were determined from the inflection point of the venous pressure tracing after sudden occlusion of the venous outflow cannula. Venous occlusion pressure was highly correlated (r = 0.98, P less than 0.01) with stop-flow capillary pressure. This finding indicates that the major sites of fluid filtration and vascular capacitance reside at the same segment of the intestinal microcirculation. The venous occlusion method is a relatively simple technique for measuring whole-organ capillary pressure that is not constrained by the technical difficulties associated with volumetric/gravimetric techniques.

Animals↗
PubMed1992

Ultrasonic crystal measurement of blood volume changes in liver and spleen.

Two methods of measurement of splenic and hepatic vascular capacitance responses were compared in cats anesthetized with pentobarbital. For the spleen, measurements using ultrasonic crystals were compared with recordings of splenic weight. The cube of the relative change in thickness at one point on the longitudinal axis of the spleen was closely correlated with the overall change in spleen weight. For the liver, measurements by ultrasonic crystals were compared with plethysmographic recordings of liver volume. Individual measurements of cubed relative thickness did not correlate well with plethysmographic volume, and two sets of crystals on the same liver lobe gave different estimates of relative liver volume. However, averaged measurements for a group of animals showed similar means by the two methods. We conclude that ultrasonic crystals, when appropriately attached, can reliably monitor changes in splenic volume, but that for the liver, the variability in thickness responses at different sites on different livers is high. Unless a large number of observations are made, the results will be unreliable.

Animals↗
PubMed1997

Cardiac function in a rat model of chronic aortic stiffness.

Cardiac function was investigated in conscious normotensive rats in which increased aortic stiffness was produced as a result of vascular calcium overload after treatment with vitamin D3 plus nicotine (VDN rats, n = 16; controls, n = 17). Baseline stroke volume, cardiac output, and cardiac response to a venous volume overload were unchanged after 1 mo of exposure to increased aortic stiffness, as were baseline venous return and total vascular capacitance. The latter was estimated from the change in mean circulatory filling pressure after modification of circulatory volume. Cardiovascular reflexes were modified in VDN rats. Bradycardia evoked by an increase in arterial PCO2 (PaCO2) or hypotensive hemorrhage was more pronounced. The PaCO2-induced bradycardia was accompanied by a fall in cardiac output in VDN rats but not in controls. In VDN rats, the attenuation of sympathetic reflexes may explain the slower recovery of blood pressure after hypotensive hemorrhage. In conclusion, a chronic increase in aortic stiffness does not compromise cardiac performance, but cardiovascular reflexes are impaired in VDN rats. Whether this is because of the increase in aortic stiffness or the effect of VDN treatment on the baroreceptors or other components of the reflex arc remains to be elucidated.

Animals↗
PubMed1991

Elevated central venous pressure: a consequence of exercise training-induced hypervolemia?

Resting blood volumes and arterial and central venous pressures (CVP) were measured in 14 men before and after exercise training to determine whether training-induced hypervolemia is accompanied by a change in total vascular capacitance. In addition, resting levels of plasma arginine vasopressin (AVP), atrial natriuretic peptide (ANP), aldosterone (Ald), and norepinephrine (NE) were measured. The same measurements were conducted in seven subjects who did not undergo exercise and acted as controls. Exercise training consisted of 10 wk of controlled cycle exercise for 30 min/day, 4 days/wk at 75-80% of maximal O2 uptake (VO2max). A training effect was verified by a 20% increase in VO2max, a resting bradycardia, and a 9% increase in blood volume. Mean arterial blood pressure was unaltered by exercise training, but resting CVP increased by 16% (P less than 0.05). The percent change in blood volume from before to after training was linearly related to the percent change in CVP (r = 0.903, P less than 0.05). As a consequence of elevations in both blood volume and CVP, the volume-to-pressure ratio was unchanged after exercise training. Plasma AVP, ANP, Ald, and NE were unaltered. Our results indicate that elevated CVP is a consequence of training-induced hypervolemia without alteration in total effective venous capacitance.

Adult↗
PubMed1998

Effect of hypoxia on pulmonary blood flow-segmental vascular resistance relationship in perfused cat lungs.

To investigate the effect of alveolar hypoxia on the pulmonary blood flow-segmental vascular resistance relationship, we determined the longitudinal distribution of vascular resistance while increasing blood flow during hyperoxia or hypoxia in perfused cat lungs. We measured microvascular pressures by the micropipette servo-null method, partitioned the pulmonary vessels into three segments [i.e., arterial (from main pulmonary artery to 30- to 50-micron arterioles), venous (from 30- to 50-micron venules to left atrium), and microvascular (between arterioles and venules) segments] and calculated segmental vascular resistance. During hyperoxia, total resistance decreased with increased blood flow because of a reduction of microvascular resistance. In contrast, during hypoxia, not only microvascular resistance but also arterial resistance decreased with increase of blood flow while venous resistance remained unchanged. The reduction of arterial resistance was presumably caused by arterial distension induced by an elevated arterial pressure during hypoxia. We conclude that, during hypoxia, both microvessels and arteries >50 micron in diameter play a role in preventing further increases in total pulmonary vascular resistance with increased blood flow.

Animals↗
PubMedDate not supplied

Isolated systolic hypertension from a vascular point of view.

Due to the results of antihypertensive intervention studies, isolated systolic hypertension (ISH) has gained new interest lately. Yet, apart from increased aortic stiffness, the specific pathophysiological features of ISH have remained largely undetermined. Therefore, we investigated the elastic properties of the vascular bed of an upper arm segment in uncomplicated ISH patients and matched normotensive controls using an electrical bioimpedance technique. Compared with the controls, the compliance of the arterial bed as a whole at normotensive blood pressure level was on the average 108.0% higher (p < 0.005) in the hypertensive patients. The blood volume of the arterial bed as a whole at operating blood pressure level and that of the larger arteries were significantly higher (40.5%, p < 0.05, and 40.5%, p < 0.01, respectively). The same held true for the venous blood volume (64.4%, p < 0.05), and for the width of the arterial compliance-pressure relation (34.6%, p < 0.01). We concluded that ISH is a separate pathophysiological entity in which all parts of a peripheral vascular bed are changed and the decreased buffering function of the aorta and large arteries is partly compensated for by an increase in small artery compliance.

Aged↗
PubMed2003

Microvascular filtration is increased in postural tachycardia syndrome.

BACKGROUND: Postural tachycardia syndrome (POTS) is related to defective peripheral vasoconstriction of dependent extremities with redistributive hypovolemia. METHODS AND RESULTS: To test whether enhanced microvascular filtration produces leg enlargement, we studied 12 patients 13 to 19 years of age with POTS and defective leg vasoconstriction and 13 age-matched healthy control subjects, with strain-gauge plethysmography used to measure venous pressure (Pv), forearm and calf blood flow, vascular capacitance, and the microvascular filtration coefficient (Kf). Measurements were made while the patient was supine and at steady state during upright tilt to 35 degrees. Supine Pv was not different in POTS, but upright leg Pv tended to be increased above control. Arm and leg peripheral arterial resistance was decreased in the supine and upright positions in patients with POTS compared with control subjects (P=0.01, upright legs). Supine Kf was not significantly increased in the forearm in patients with POTS but was increased in the calf (9.3+/-2.2 versus 5.7+/-2.4 [10(-3)] mL/100 mL per minute per mm Hg, P=0.04), correlating with calf blood flow (rs=0.84, P=0.002). Kf was invariant with orthostasis. The hydraulic contribution to upright filtered flow at 35 degrees tilt, the product of Kf and Pv, was approximately twice that of control (0.41+/-0.09 versus 0.19+/-0.04 mL/100 mL per minute, P=0.04). CONCLUSIONS: Increased microvascular filtration accounts for enhanced leg swelling in patients with POTS with increased arterial blood flow.

Adolescent↗
PubMed1989

Analysis of the characteristics of the flow velocity waveforms in left atrial small arteries and veins in the dog.

To clarify the characteristics of the phasic blood velocity pattern in small arteries and veins on the left atrial surface, we used our newly developed fiber-optic laser Doppler velocimeter. We intended particularly to examine the influence of atrial contraction and relaxation on velocity waveforms to obtain some insight into the nature of the mechanical force acting on the atrial intramyocardial vascular beds. In 14 anesthetized open-chest dogs, the left atrial appendage was gently displaced to expose small branches of the artery and vein. Vessels with an outer diameter of about 150-500 microns were chosen for the measurements because their walls are transparent to laser light. The fiber tip (velocity sensor) was fixed on the vessel surface with a drop of cyanoacrylate when good-quality Doppler signals were consistently observed. Additional experiments with three dogs were performed to observe the blood velocities in the atrial artery and vein during arrhythmia. The blood velocity waveform in the artery was similar to the pattern of aortic pressure during ventricular ejection (peak velocity, 18.8 +/- 7.8 cm/sec) but was characterized by a pronounced dip during atrial contraction. The temporal coincidence between the dip formation and atrial contraction was confirmed during atrial flutter with an atrioventricular block. After isoproterenol administration (2 micrograms i.v.), the acceleration rate of the forward flow velocity increased by 176% (p less than 0.05), and reverse flow appeared during atrial contraction in five cases out of eight (p = 0.013). The blood flow velocity in atrial small veins, on the other hand, was predominant during atrial contraction (peak velocity, 15.6 +/- 5.8 cm/sec). Isoproterenol increased the acceleration rate of this forward flow velocity by 121% (p less than 0.01). Nitroglycerin did not change the blood velocity waveform significantly in atrial arteries or in veins. The phase opposition between arterial inflow into and venous outflow from the atrial myocardium indicates that a large portion of the coronary inflow to the atrial myocardium may be stored due to the presence of atrial myocardial vascular capacitance. We conclude that atrial myocardial contraction impedes atrial inflow and promotes venous outflow from atrial capacitance vessels.

Animals↗
PubMed1999

Impaired response of the forearm resistance but not conductance vessels to reactive hyperemia in hypertrophic cardiomyopathy.

It has been suggested that in hypertrophic cardiomyopathy (HC), vascular abnormalities are not restricted to the heart. Flow-mediated dilation of peripheral conductance arteries (reflecting their endothelial function) has not yet been studied in HC. Our aim was to assess both flow-dependent dilation of the brachial artery and flow responses (dependent on resistance vessels) during forearm reactive hyperemia (RH) in nontreated HC patients. The authors studied 13 HC patients and 14 age- and sex-matched healthy controls. None of them exhibited any factors known to be associated with endothelial dysfunction. Using 7 MHz ultrasound, brachial artery diameter and Doppler flow velocity were measured continuously at baseline and throughout 1 min of RH following 5 min of forearm ischemia induced by inflation of a blood pressure cuff. Arterial diameter and RH flow are expressed as percent changes with respect to the baseline. Flow-dependent dilation was similar in the HC patients and control subjects (7.2 +/- 9.5% vs 9.9 +/- 10.4%, p>0.05). Compared to the control group, RH flow in HC was decreased; however, differences did not reach statistical significance until 60 sec of RH (112 +/- 102% vs 261 +/- 217%, p<0.05; HC vs controls). In HC patients, endothelial function of peripheral conductance arteries is preserved. Hence, a defect in the forearm arterial bed in HC seems to be limited to mechanisms maintaining the dilation of resistance vessels during decreasing RH flow.

Adult↗
PubMedDate not supplied

Hemodynamic consequences of heart-lung interactions.

The management of critically ill patients requires a fundamental understanding of cardiopulmonary interactions associated with mechanical ventilation. The hemodynamic changes due to ventilation are a result of changes in lung volume and intrathoracic pressure (ITP) and can occur during spontaneous or positive pressure ventilation despite constant tidal volumes. Pulmonary vascular resistance (PVR) and mechanical heart-lung interactions play prominent roles in determining the hemodynamic response to mechanical ventilation. Lung inflation alters PVR and right ventricular wall tension and, at high lung volume, mechanically limits cardiac volumes. The authors will consider the mechanisms of the effects of ITP on the pulmonary arterial and venous branches. These effects will aid in understanding the complex interactions between ventilation and right and left ventricular pressures and volumes, as well as the influence of lung inflation pressure on ventricular interdependence.

Cardiac Volume↗
PubMed2003

Angiotensin-converting enzyme inhibitors: mechanisms of action and implications in anesthesia practice.

This review summarizes physiology of circulating and local renin-angiotensin system (RAS), enzymatic properties and mechanism of action of angiotensin I converting enzyme inhibitors (ACEIs) on RAS, and implications of ACEIs in anesthetic management of patients treated with these drugs. ACEIs, through their effect on RAS, may improve cardiovascular functions, pulmonary dynamics, and body fluid homeostasis. Thus, ACEIs have become an integral part of management of patients with hypertension, congestive heart failure (CHF) and chronic renal disease. ACEIs, due to differences in their chemical structure, exert different pharmacological actions and can have protective or occasional damaging effects on different organs. The anesthesiologists are commonly involved in the management of patients treated with ACEIs. Thus, the role of ACEIs and their possible interaction with anesthetic agents must be an integral part of clinical decision-making during anesthesia Hemodynamic variation during anesthesia is mainly related to specific effects of anesthetic agents on sympathetic nervous system. Those with preoperative fasting, volume depletion and extended sympathetic blockade can have reduced vascular capacitance resulting in decreased venous return, reduced cardiac output and severe arterial hypotension. Angiotensin II (ANG2) a potent vasoconstrictor may counterbalance such hypotensive effect. During ACE inhibition ANG2 cannot counterbalance this hypotension. Thus, induction of anesthesia may cause severe hypotension in hypovolemic patients specifically in those receiving diuretics as a complement to ACEIs. Recent advances in RAS and the pharmacology of ACEIs have identified some predisposing factors and risks associated with anesthesia in patients treated with ACEIs. Practitioners should be vigilant, and readily have vasopressors, necessary fluids and other resuscitative measures for treatment of unexpected hemodynamic instability during anesthesia and surgery.

Anesthesia↗