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Biomedical subjects

I Vergroesen

Publications and source records attributed to I Vergroesen.

34 records · Page 2Linked to original sources
PubMed1996

Rate of coronary flow adaptation in response to changes in heart rate before and during anesthesia for coronary artery surgery.

BACKGROUND: The rate of adaptation of coronary blood flow in response to stepwise changes in heart rate (HR) has been extensively studied in dogs and goats to improve our understanding of the dynamics of coronary regulation processes and their pathophysiology and to obtain time constants for mathematical modeling of the coronary regulation. However, little is known about the dynamic characteristics of coronary flow adaptation in humans. In patients undergoing coronary artery surgery, we investigated the rate of coronary adaptation in response to stepwise changes in HR, in the awake and anesthetized states. METHODS: In 11 patients with stable coronary artery disease, arterial blood pressure, right atrial pressure, and coronary sinus blood flow, measured by continuous thermodilution, were calculated per beat. The ratio of beat-averaged arterial blood pressure minus right atrial pressure and coronary sinus blood flow was calculated to obtain an index of coronary resistance. The rate of change of coronary resistance index was quantified by t50, defined as the time required to establish 50% of the total change in coronary resistance index. Responses of coronary resistance index after HR changes, before and after induction of anesthesia, were compared. The anesthesia technique consisted of 100 micrograms.kg-1 fentanyl and 0.1 mg.kg-1 pancuronium bromide in combination with oxygen in air ventilation (FIO2 = 0.5). RESULTS: In the awake situation, t50 values of the dilating and constricting responses, induced by an increase and a decrease in HR were 5.0 +/- 2.1 (SD) s (range 2.6-9.0 s) and 5.7 +/- 1.2 s (range 4.1-7.8 s), respectively. During fentanyl/pancuronium anesthesia, the rate of coronary flow adaptation was significantly slower, with t50 values of 10.2 +/- 2.1 s (range 7.7-13.1 s) after an HR step-up and 9.8 +/- 2.1 s (range 6.6-13.2 s) after an HR step-down. Compared to the awake situation, arterial blood pressure was significantly reduced during anesthesia, but coronary vascular resistance remained unchanged. This implies that the steady-state static regulation of coronary blood flow had not changed. CONCLUSIONS: These preliminary data suggest that, in patients with coronary artery disease, the rate of change in coronary vascular resistance in response to pacing-induced changes in HR is mitigated by fentanyl/pancuronium anesthesia during positive pressure ventilation. A further qualification of our findings in a larger number of patients is warranted.

Adaptation, Physiological↗
PubMed1995

The pressure-flow relation in the canine coronary artery: combined effects of critical stenosis and intracoronary thrombosis.

OBJECTIVE: To characterise the effect of coronary intra-arterial thrombosis upon the downstream vascular bed. BACKGROUND: The vascular response downstream from a coronary intra-arterial thrombus has not previously been characterised. We postulated that downstream vasoconstriction might result from the presence of endothelial damage with consequent growth of platelet-rich thrombus. METHODS: We measured the pressure gradient and flow across, and the pressure/flow ratio distal to, a canine left circumflex artery stenosis with and without endothelial damage causing intracoronary thrombosis. We also observed the effects of transient complete conclusions. RESULTS: At occlusion, the pressure gradient was maximal; relief of occlusion caused a rapid increase flow and distal pressure with a rapid decrease in stenosis pressure gradient and resistance. Subsequently there was a period of stable stenosis resistance with pressure gradient and flow declining; distal pressure therefore increased at this time. Finally in the thrombus group only, stenosis resistance increased again towards re-occlusion. During occlusion, distal pressure averaged 49 +/- 18 mmHg in the presence of thrombus vs. 22 +/- 4 mmHg in its absence (P < 0.001). Following release of occlusion, the flow increased faster than distal pressure, so that the ratio (distal pressure/flow) fell rapidly. Subsequently, distal pressure continued to increase after flow had reached a peak and begun to decline, suggesting vasoconstriction. In the presence of thrombus, the distal pressure/flow ratio was higher than in the absence of thrombus, both at maximal vasodilation (P < 0.005) and at maximum vasoconstriction (P < 0.025). CONCLUSIONS: During cyclic flow variations the stenosis resistance changes are exactly as expected from thrombus growth and embolisation. The distal pressure/flow ratio showed a time-dependent increase which appeared greater when conditions favoured intracoronary thrombosis.

Animals↗
PubMed1994

Cardiac contraction and intramyocardial venous pressure generation in the anaesthetized dog.

1. Two hypotheses relating to the influence of contraction of the heart on coronary venous pressure (Pv) were tested. The first assumes a direct transmission of left ventricular pressure (PLV). According to the alternative hypothesis the Pv is caused by cyclical changes in the elastance of the surrounding tissue. 2. A small epicardial vein was cannulated retrogradely in eight open-chest dogs deeply anaesthetized with fentanyl. The duration of diastoles was varied after induction of a heart block with formaldehyde. Coronary arterial inflow and perfusion pressure were controlled by a perfusion system connected to the left main coronary artery by a Gregg cannula. Stopped-flow Pv was studied with intrinsic coronary tone (IT) and after maximal dilatation with adenosine. 3. The Pv pulse in the first contraction after a long diastole was not significantly correlated to the PLV pulse, with a slope of 0.5, in any dog, either with IT or during adenosine treatment. Comparing the first contraction after the long diastole with the last beat before, systolic Pv pulse decreased significantly in seven out of eight dogs, but systolic PLV pulse increased in five dogs and was unaltered in three dogs in both conditions. In contrast, end-diastolic Pv was significantly correlated to the systolic Pv in each individual animal under either condition. 4. The results indicate that pressure generation in the small coronary veins can be explained on the basis of the time-varying elastance hypothesis and that a direct transmission of PLV to Pv is absent.

Adenosine↗
PubMed1993

Left ventricular pressure transmission to myocardial lymph vessels is different during systole and diastole.

In six open-thorax-anaesthetized dogs with paced hearts and a retrogradely cannulated epicardial lymph vessel, the sensitivity of myocardial lymph pressure to left ventricular pressure during systole and during diastole was determined. The lymph vessels were cannulated using PE-90 tubing, and lymph pressure was measured by connecting the cannula to a microtip pressure transducer. To obtain the systolic sensitivity, left ventricular pressure was changed by clamping the descending aorta, which caused left ventricular pressure to increase. The diastolic sensitivity was obtained from natural variation to left ventricular pressure caused by atrial contractions during induced long diastoles. The mean ratio of the pulse in lymph pressure to the pulse in left ventricular pressure was determined: systole: 0.069 +/- 0.013, n = 213, diastole: 0.76 +/- 0.16, n = 249 and, if possible, linear regression analysis between lymph and left ventricular pressure was performed. The systolic regression coefficients could be determined in six dogs and the diastolic coefficients in three dogs. During long diastoles lymph pressure variations are on average 76 per cent of those in the left ventricle. However, during systole, the sensitivity of lymph pressure to left ventricular pressure is more than ten times lower. It is not unlikely that the structural embedment of lymph vessels within the myocardium is such that volume variations by cardiac contraction are limited.

Animals↗
PubMed1993

Stopped-flow epicardial lymph pressure is affected by left ventricular pressure in anesthetized goats.

We measured epicardial lymph pressure (Plymph) in the anesthetized goat (n = 5 goats). To study the transmission of systolic left ventricular pressure (PLV) to Plymph, the effect of an increase in PLV caused by clamping of the descending aorta on Plymph was evaluated. Peak systolic PLV was 131 +/- 4 (+/- SE) mmHg during control (43 beats) and 188 +/- 4 mmHg when elevated due to aortic clamping (157 beats). Peak systolic Plymph was 24.8 +/- 1.0 and 34.8 +/- 1.1 mmHg during control and elevated PLV, respectively. In the first beat of elevated PLV, peak Plymph did not change, although the pressure waveform did. In the subsequent beats, Plymph increased proportionally with increased PLV. When PLV was decreased back to control, Plymph also decreased but did not reach control level until after three beats. The relationship between normalized Plymph and normalized PLV is given by Plymph = 0.70 x PLV + 0.09. The results show that PLV does affect Plymph in a normal beating heart.

Animals↗
PubMed1992

Dynamic response of coronary regulation to heart rate and perfusion changes in dogs.

The rate of change of coronary adjustment in the anesthetized dog to a step change in heart rate (HR) and in perfusion was analyzed. The left main coronary artery was perfused either at constant pressure (CP) or at constant flow (CF). Coronary arterial pressure and flow were continuously measured and averaged per beat, after which their ratio, being an index of coronary resistance in steady state, was calculated. The rate of change of pressure-to-flow ratio was quantified by t50, the time required to establish half of the completed response. The t50 values for the dilating responses at CP were 5.5 +/- 0.4 (SE) s for an increase in HR and 5.5 +/- 0.1 s for a decrease in perfusion. At CF these values were 9.3 +/- 0.9 and 9.7 +/- 1.6 s, respectively. The t50 values for the constricting responses with CP were 6.6 +/- 0.5 s for a decrease in HR and 6.2 +/- 0.2 s for an increase in perfusion. At CF these values were 12.2 +/- 1.5 and 10.8 +/- 2.2 s. The responses in the dog are faster than in the goat. Furthermore, the directional sensitivity in responses with perfusion changes, observed earlier in goats, is normally absent in dogs.

Animals↗
PubMed1992

Retrograde coronary flow is limited by time-varying elastance.

The study examined the influence of left ventricular pressure (PLV) on coronary arterial flow and pressure. In eight anesthetized open-thorax goats with cannulated and artificially perfused left main coronary artery, the PLV was disturbed by aortic occlusions. In the constant pressure perfusion (CPP) protocol the response of systolic arterial inflow on a change in PLV was studied with fixed perfusion pressure and at several perfusion pressure levels. Similarly, in the constant flow perfusion (CFP) protocol the response of systolic perfusion pressure was examined with fixed levels of perfusion flow and repeated for several flow levels. The results show an early systolic response determined by PLV for both protocols. Midsystolic responses were almost absent in the CPP protocol but present in the CFP protocol. At CPP, the effect of a change of PLV on arterial flow in mid systole was only 20% of that on early systolic flow with intact coronary tone and 33% with adenosine-induced vasodilation. At CFP the pulsations in perfusion pressure were 30% of PLV pulsations, both with intact tone and vasodilation; in contrast with the CPP results, no difference for this value was found in different stages of systole. We suggest that stiffness of cardiac muscle determines the influence of PLV on coronary flow. The difference in mid systolic relations between the CPP and CFP protocols is explained by the difference in time constants induced by the perfusion system. The results are best explained by a synthesis between the intramyocardial pump model and the elastance concept.

Animals↗
PubMed1989

Antihypertensive and anti-ischemic effects of nicardipine and nitroprusside in patients undergoing coronary artery bypass grafting.

The efficacy of nicardipine vs nitroprusside in controlling hypertension after sternotomy was compared in 120 patients undergoing coronary artery bypass grafting and anesthetized with fentanyl (100 micrograms/kg). All had good left ventricular function and had been receiving long term oral beta-blocking therapy. Patients were randomly allocated to 1 of 3 groups: group C, the control (n = 40), received no vasodilator; group N (n = 40) received intravenous nicardipine at an initial rate of 3 micrograms/kg/min; and group S (n = 40) received intravenous nitroprusside at an initial rate of 1 microgram/kg/min. Vasodilator infusion was begun before surgery and infusion rates were adjusted to maintain systolic blood pressure between 80 and 120% of postintubation (baseline) values. Additional measurements were obtained before incision and after sternotomy. In groups N and S, arterial blood pressure was effectively controlled in all patients. Before the incision, pulmonary artery pressure decreased in group S and systemic vascular resistance decreased in groups N and S. After sternotomy, mean arterial pressure, heart rate, pulmonary artery pressure, pulmonary capillary wedge pressure, cardiac index and rate-pressure product increased in group C. At this time, pulmonary artery pressure returned to baseline values in group S. In groups N and S, heart rate, cardiac index and rate-pressure product increased, but, compared with baseline values, systemic vascular resistance remained low after sternotomy. Ischemic changes were seen in the electrocardiogram in 11 patients (28%) in group C, 10 patients (25%) in group S and 4 patients (10%) in group N. The concentration of creatine phosphokinase MB was not significantly different in the first 24 postoperative hours in any group.

Aged↗
PubMed1989

The efficacy of nicardipine and nitroprusside in preventing poststernotomy hypertension.

The efficacy of nicardipine and nitroprusside in preventing poststernotomy hypertension was compared in two groups of 45 patients undergoing coronary artery surgery. Patients were anesthetized with fentanyl, 100 micrograms/kg, and oxygen. Group N received nicardipine at an initial rate of 3 micrograms/kg/min. Group S received sodium nitroprusside at an initial rate of 1 microgram/kg/min. The vasodilators were started before surgery, and infusion rates were adjusted to maintain systolic blood pressure between 80% and 120% of postintubation (baseline) values. Additional measurements were obtained before incision and after sternotomy. In both groups, arterial blood pressure could be controlled effectively in all patients. In group S, pulmonary artery pressure (PAP) decreased before incision. At this time, systemic vascular resistance (SVR) decreased in both groups. After sternotomy, PAP returned to baseline values in group S. In both groups, heart rate, rate-pressure product, and cardiac index increased, while SVR remained decreased. In the period from induction of anesthesia to the start of cardiopulmonary bypass, the incidence of myocardial ischemia was greater (P less than 0.01) in group S (24%) than in group N (9%). Between the groups, the concentration of creatine phosphokinase MB was not significantly different in the first 24 hours postoperatively. In conclusion, it was shown that nicardipine may be a suitable alternative to nitroprusside for the prevention of poststernotomy hypertension and myocardial ischemia in patients undergoing coronary artery surgery.

Blood Pressure↗
PubMed1989

Dynamics of coronary adjustment to a change in heart rate in the anaesthetized goat.

1. We have previously shown that steady-state coronary flow during auto-regulation and metabolic rate changes is predicted by a mathematically expressed theory which assigns control of coronary vascular resistance to tissue PO2. Our present purpose was to test the applicability of this theory to the non-steady state as exemplified by a sudden step change in heart rate. 2. The theory predicted that the response time of change of resistance in these circumstances would be slower with constant-flow perfusion of the coronary bed than with constant-pressure perfusion, and that with constant-pressure perfusion only, the rate of adaption of resistance would be dependent on the level of pressure used. 3. These predictions were tested in open-chest goats with cannulation of the left main coronary artery and perfusion with alternately constant pressure or constant flow. Sudden step changes in heart rate were induced by pacing to induce rapid transients in myocardial metabolic rate. 4. The half-time of subsequent change in perfusion pressure-flow ratio, which in the dynamical state is not equal to resistance, was 15.7 +/- 0.4 s (mean +/- S.E.M.), which was statistically shorter than for constant flow (22.2 +/- 0.5 s, P less than 0.001). 5. The half-time of subsequent change in perfusion pressure-flow ratio with constant-pressure perfusion was 14.4 +/- 0.6 s at low pressure and 17.0 +/- 0.6 s at high pressure (P less than 0.001). 6. The results differed from those predicted by the theory, in that the changes described above were preceded by a rapid (5 s) step change in pressure-flow ratio, up with an increase in heart rate and down with a decrease in heart rate. We postulated that this was a mechanical effect due to greater compression of the coronary microvasculature with more frequent contractions. 7. To test this hypothesis, we measured changes in coronary blood volume by integrating the difference between arterial inflow and venous outflow. These experiments showed a decrease in coronary blood volume with heart rate increase and vice versa. 8. Abolition of autoregulation and metabolic regulation was achieved with maximum vasodilatation of the coronary bed with adenosine. A sudden switch in heart rate then produced the initial step change in pressure-flow ratio, but not the subsequent adaptation over 13-25 s. This confirmed that the former effect is attributable to a passive mechanical mechanism.

Animals↗
PubMed1989

Dynamic response of the coronary circulation to a rapid change in its perfusion in the anaesthetized goat.

1. We tested predictions of a mathematical formulation of a hypothesis of dynamic control of coronary blood flow by tissue oxygen tension. 2. The rate of change of adjustment of the coronary circulation to a step change in arterial perfusion was analysed in the cannulated main stem preparation of the anaesthetized goat. The variable studied was the ratio between driving pressure and coronary flow, each averaged per heart beat. The response of this ratio was measured following a sudden change in perfusion pressure with constant-pressure perfusion and a sudden change in flow with constant-flow perfusion. 3. The rate of change of the pressure-flow ratio was quantified by t50, the time required to establish half of the completed response. For a pressure decrease t50 was 4.9 +/- 0.2 s (n = 35) (mean +/- S.E.M., n = number of individual measurements), 11.3 +/- 1.2 s (n = 25) for a flow decrease, 14.5 +/- 1.6 (n = 34) for a pressure increase and 25.1 +/- 2.3 (n = 19) for a flow increase. 4. No effect of the level of flow or pressure on t50 was found for a decrease in perfusion. Furthermore, with a flow increase, the t50 value did not depend on the level of flow, which is in agreement with the outcome of earlier experiments where the response to a change in heart rate was measured. With a pressure increase, the mean t50 value of the pressure-flow ratio was lower at high perfusion pressure but the difference with low perfusion pressure was not significant (P = 0.11). 5. The t50 value in the cases of an increase in pressure and flow are similar to those found for a change of heart rate in an earlier study. 6. Unlike step changes of metabolic rate, some of the measured responses to mechanical step changes were not predicted by the oxygen hypothesis. It is suggested that the increased rate of coronary adjustment induced by the reduction of coronary perfusion is due to arteriolar smooth muscle mechanics which apparently differ in strength depending on the direction of change of the arteriolar dimensions. 7. This suggestion is strengthened by the results of experiments in which smooth muscle responses were abolished with adenosine.

Animals↗
PubMed1988

Rate of decrease of myocardial O2 consumption due to cardiac arrest in anesthetized goats.

The rate of change of myocardial O2 consumption, MVO2, has been measured during the transition from beating to cardiac arrest. Cardiac arrest was achieved by destruction of the bundle of His by injection of formalin and induced by 25 s interruption of pacing. The left main coronary artery was perfused under constant pressure and the great cardiac vein was drained under controlled pressure. The arterio-venous O2 content difference, [O2](a-v), and coronary arterial and venous flows, CAF resp CVF, were continuously measured. The MVO2 transient was calculated using the following equation based on a 3 compartment model: MVO2 = CAF . [O2](a-v) - (Vc + Vv) . d[O2]v/dt - (Vc . Vv/CVF) . d2[O2]v/dt2 where Vc and Vv are the capillary and the venous blood volume as function of time and [O2]v is the venous oxygen content. A 7th order polynoma was fit to the [O2]v-data and the fitted equation was differentiated analytically to obtain the first and second order derivatives. The MVO2 decreased from 94 +/- 5 microliters O2/s/100 g (mean +/- SE) before cardiac arrest to 15.4 +/- 5 microliters O2/s/100 g after 15 s of cardiac arrest. The change in MVO2 (50% in 3.8 +/- 0.3 s) preceded the change in venous oxygen content (50% in 12.7 +/- 0.5 s) and the change in coronary resistance (50% in 14.9 +/- 0.9). These results are in accordance with the hypothesis that interstitial O2 concentration is a major determinant of coronary resistance.

Animals↗
PubMed1987

Quantification of O2 consumption and arterial pressure as independent determinants of coronary flow.

The steady-state relationship between coronary arterial blood flow (CBF) and both myocardial O2 consumption (MVO2) and coronary arterial pressure (P) was explored in anesthetized dogs and goats. Both species were subjected to constant pressure perfusion of the left main coronary artery by an external pressure-controlling circuit. In addition a group of goats was studied with normal aortic perfusion using an occluder around the left main coronary artery to vary coronary arterial pressure. The statistical analysis revealed that despite the direct effect of P on MVO2 (the Gregg effect) the effects of both variables on CBF were independent and linear over a wide range of P and MVO2 so that multiple regression analysis with a linear equation (CBF = a X P + b X MVO2 + c) gave an excellent fit which was not improved by the introduction of an addition interactive term b3MVO2 X P. The mean correlation coefficient for all animals was greater than 0.9. From these data we conclude that any factor regulating coronary arterial flow would be influenced by both MVO2 and perfusion pressure in an independent way. This study characterizes the stationary behavior of local coronary flow control. Hence, it specifies quantitatively the relations to be predicted by hypotheses aiming to explain this control mechanism.

Analysis of Variance↗
PubMed1987

Intramyocardial blood volume change in first moments of cardiac arrest in anesthetized goats.

The effect of cardiac relaxation on the intramyocardial blood volume was studied by measuring the integrated difference between arterial inflow and great cardiac venous outflow. In nine anesthetized goats, the left main coronary artery was perfused under constant pressure. The great cardiac vein was drained under pressure control. The venous flow signal was amplified so that the integrated intramyocardial blood volume was constant in the beating heart. With normal vasomotor tone, the mean change in vascular volume was 3.01 +/- 0.18 (SE) ml/100 g left ventricle (LV); 67% of the volume change was achieved in 1.60 +/- 0.09 s. For the fully dilated bed (adenosine infusion), the values were 4.13 +/- 0.33 ml/100 g and 0.96 +/- 0.06 s, respectively. The volume change could be correlated with the venous pressure during cardiac arrest (Pvd) and the change in mean left ventricular pressure after cardiac arrest (r = 0.95). The correlation improved when data were selected for Pvd less than 6 mmHg to r = 0.98. We assumed that the change in vascular transmural pressure can be approximated as half the mean left ventricular pressure change. The intramyocardial vascular compliance was then estimated as 0.104 +/- 0.012 and 0.146 +/- 0.028 ml X mmHg-1 X 100 g-1 for control and adenosine conditions, respectively. The long time constants excluded the large epicardial veins as the site of volume change; they were much longer than the duration of diastole in the beating heart. We conclude that the intramyocardial vascular compartment is capable of volume expansion on the order of 20% of its normal volume when myocardial compression by ventricular systole is suspended.

Anesthesia↗
PubMed1984

Oxygen and coronary vascular resistance during autoregulation and metabolic vasodilation in the dog.

The hypothesis that tissue oxygen tension controls coronary vascular resistance during changes in perfusion pressure and oxygen consumption was expressed in a simplified mathematical form capable of making quantitative predictions. The predictive value of this formulation of the hypothesis was tested in experiments on anaesthetized mongrel dogs subjected to constant-pressure perfusion of the left main coronary artery, with measurements of coronary blood flow and arterio-venous oxygen content differences. Coronary venous oxygen content was used as an index of tissue oxygenation. The responses of coronary blood flow and arterio-venous oxygen content difference, made over a range of perfusion pressures (which caused autoregulation) and heart rates (which caused metabolic regulation) were predicted qualitatively by the model. Coronary vascular conductance was positively related to metabolic rate only during metabolic regulation (heart rate changes); during autoregulation the relationship between these two variables was inverse. Coronary vascular conductance and resistance values taken from both interventions (both perfusion pressure and heart rate variations) were closely related to coronary venous oxygen content and calculated PO2. These findings suggest that further examination of oxygen tension, as the controller of the coronary vascular bed under physiological conditions should be considered.

Animals↗