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PubMed1992

[Clinical significance of peripheral vascular resistance for early bypass occlusion rate. Errors and dangers in measuring vascular resistance].

An estimation of the peripheral resistance was performed during 264 peripheral bypasses. After completion of the distal anastomosis, saline was infused via the proximal graft end in constant flow rates. The mean distal pressure was used for calculation of peripheral resistance. There was a close correlation between the peripheral resistance (based on flow rates of 100 ml/min) and the 30 day graft failure rates. Below the level of 450 mPRU the failure rate was 4%, above 750 mPRU, however, this rate was more than 20%. It is concluded, that the estimation of the peripheral vascular resistance during the operation is a valuable tool to estimate the prognosis of graft patency.

Aged↗
PubMed2005

Doppler sonographic analysis of synovial vascularization in knee joints of patients with rheumatoid arthritis: increased color flow signals and reduced vascular resistance.

Synovial vascularization was analyzed by power Doppler and spectral Doppler sonography in 42 knee joints of 28 patients with rheumatoid arthritis. The synovial vessels with greater intensity of color flow signals demonstrated significantly lower indicators of vascular resistance - resistive index (P < 0.01) and pulsatility index (P < 0.01) - than those with lesser intensity. Consequently, an inverse correlation was observed between intensity of color flow signals and both resistive index (P < 0.01) and pulsatility index (P < 0.01).

Journal Article↗
PubMedDate not supplied

Acetylcholine causes dose dependent increase in pulmonary flow in patients with chronic heart failure and elevated pulmonary vascular resistance.

Elevated pulmonary vascular resistances occur to a variable degree in patients with chronic congestive heart failure (CHF). These might be caused by increased levels of endogenous vasoconstrictors, defective endothelial vasodilatory mechanisms or structural vascular abnormalities. To determine the contribution of defective endothelial mediated vasodilation, we tested 10 patients with CHF due to coronary artery disease (n = 4) or dilated cardiomyopathy (n = 5), and congenital corrected transposition of the great arteries (n = 1) (median pulmonary artery pressure 36 mmHg, range of pulmonary vascular resistance 0.94-10.7 WE). Patients were in median functional class NYHA III, median left ventricular ejection fraction was 21%, median oxygen uptake at the anaerobic threshhold was 8.25 ml/kg/min. Flow was measured by a flow wire (0.018 inch) positioned in a pulmonary artery branch with a diameter of 3-8 mm determined by intravascular ultrasound before. Acetylcholine infusion was adjusted to 10(-6), 10(-5) and 10(-4) molar concentrations in the pulmonary artery branch. A dose dependent increase in flow between 64 to 140% was seen in 8 out of 10 patients. We conclude: Acetylcholine mediated vasodilation is found in patients with CHF and elevated pulmonary vascular resistances.

Acetylcholine↗
PubMed1982

Pulmonary vascular responses to nitrous oxide in patients with normal and high pulmonary vascular resistance.

The pulmonary vascular responses to 50 per cent nitrous oxide were studied in 32 anesthetized patients ventilated to maintain normal PaCO2. One group consisted of sixteen patients with coronary artery disease (CAD) and normal pulmonary vascular resistance (PVR) about to undergo coronary artery bypass surgery. A second group consisted of 16 patients with markedly elevated PVR values due to chronic mitral valve stenosis (MVS). CAD patients showed a significant increase in PVR irrespective of whether halothane or fentanyl was used as background anesthetic. Individual changes, however, did not exceed the upper limit of normal and therefore are not considered to be of clinical importance in these patients. In patients with MVS subjected to fentanyl anesthesia, N2O caused a marked increase in PVR from 357 to 530 dyn . s. cm-5. Halothane anesthesia did not significantly attenuate the effect of nitrous oxide on the pulmonary vasculature as mean PVR increased from 351 to 451 dyn . s. cm-5. These results suggest that the preexisting PVR value is of more importance for the pulmonary vascular response to N2O than the influence of background anesthesia. We conclude that nitrous oxide should be used with caution in patients with elevated pulmonary vascular resistance, particularly in the presence of right ventricular dysfunction and/or right coronary artery disease.

Coronary Disease↗
PubMed1990

Heart transplantation in patients with severe pulmonary hypertension and increased pulmonary vascular resistance.

Irreversibly increased pulmonary vascular resistance is a contraindication for cardiac transplantation. At our hospital patients referred for recipient evaluation with systolic pulmonary artery pressure greater than 50 mmHg and pulmonary vascular resistance greater than 2 Wood units (Wu) are tested with intravenous sodium nitroprusside for reversibility. In 23 patients whose increased systolic pulmonary artery pressure (67.4 +/- 10.4 mmHg) and resistance (4.8 +/- 2.4 Wu) were reduced by nitroprusside, orthotopic heart transplantation was performed without early mortality. Right heart catheterization after transplantation revealed a significant and persistent fall of the elevated pulmonary artery pressure and pulmonary vascular resistance. We conclude that if severe pulmonary hypertension and elevated pulmonary vascular resistance are reversible with nitroprusside, the patient can safely undergo heart transplantation.

Adult↗
PubMed1999

Effect of antenatal betamethasone administration on placental vascular resistance.

BACKGROUND: High placental vascular resistance is an important cause of fetal growth restriction and subsequent perinatal mortality. Identification of affected pregnancies allows appropriate fetal surveillance and delivery, but there are no known therapeutic strategies to decrease resistance and improve blood flow. However, placental corticotropin-releasing hormone (CRH) is thought to be a potent fetoplacental vasodilator, and exogenous corticosteroids can increase placental CRH secretion. Therefore, we examined whether corticosteroids could improve fetoplacental blood flow in pregnancies with increased vascular resistance. METHODS: A retrospective review of umbilical-artery flow-velocity waveforms (FVWs) before and after betamethasone administration was undertaken in pregnancies with increased placental vascular resistance, as shown by umbilical-artery absent end-diastolic flow (AEDF). FVWs were obtained by pulsed-wave doppler ultrasonography. We studied all 28 pregnancies monitored at the maternal-fetal medicine unit of a university teaching hospital since 1995. FINDINGS: The median duration of gestation at presentation with AEDF was 27 weeks (range 23-33). In 19 (68% [95% CI 49-86]) pregnancies, umbilical-artery diastolic flow returned within 24 h after betamethasone administration, consistent with decreased resistance. The median duration of this effect was 3 days (range 2-7). There were no differences in duration of gestation at diagnosis or delivery, or in birthweight between fetuses showing a return of flow after betamethasone and those not showing a return of flow. INTERPRETATION: In pregnancies with umbilical-artery AEDF, betamethasone treatment is associated with decreased placental vascular resistance, possibly induced via increased placental CRH secretion. This study does not provide insights into whether this effect would be beneficial or harmful to the fetus.

Anti-Inflammatory Agents↗
PubMed1997

Resting hemodynamics after total versus standard orthotopic heart transplantation in patients with high preoperative pulmonary vascular resistance.

OBJECTIVE: Pretransplant pulmonary vascular resistance > or = 4 Wood-units predisposes to right ventricular failure after heart transplantation. Total orthotopic heart transplantation with bicaval and pulmonary venous anastomoses offers synchronous contractions of the atria and a normal ventricular filling pattern, but requires longer ischemic time than standard orthotopic heart transplantation. To test if total orthotopic heart transplantation improves resting hemodynamics in pts with high preoperative pulmonary vascular resistance, we analyzed 65 pts with standard and 65 with total orthotopic heart transplantation transplanted between 12/88 and 7/94. Of these, 18 with total and 15 with standard orthotopic heart transplantation had a preoperative pulmonary vascular resistance > or = 4 Wood-units. METHODS: Right heart catheterization data were obtained at each endomyocardial biopsy. All data from biopsies at both 2 weeks and 1 year posttransplant that were free from humoral or greater than 1A cellular rejection (9 versus 13 pts) were included in a two way ANOVA. Pts with postop pacemakers, atrial fib or beta-blocker therapy at the time of biopsy were excluded. RESULTS: Ischemic time was different (172 +/- 44 versus 142 +/- 28 min, P = 0.03). Demographics, NYHA class, pre-TX hemodynamics, donor age and inotropes were similar. Cardiac output and index were higher in the total orthotopic group at 2 weeks (6.5 +/- 1.7 versus 5.1 +/- 1.0 l/min; 3.4 +/- 0.9 versus 2.8 +/- 0.6 l/min per m2) and 1 year (7.1 +/- 2.0 versus 4.9 +/- 1.1 l/min, P = 0.002; 3.6 +/- 1.1 versus 2.6 +/- 0.5 l/min per m2, P = 0.009). Right atrial and pulmonary arterial mean pressure (mmHg) were lower with total orthotopic heart transplantation at 2 weeks (6 +/- 4 versus 9 +/- 5, P = 0.04; 22 +/- 3 versus 25 +/- 7, P = 0.1) and 1 year (5 +/- 2 versus 7 +/- 3, P = 0.02; 19 +/- 4 versus 25 +/- 7, P = 0.03). Pulmonary capillary wedge pressure (mmHg) was borderline nonsignificant (11 +/- 4 versus 13 +/- 7 at 2 weeks, 8 +/- 3 versus 14 +/- 5 at 1 year, P = 0.055), as well as pulmonary vascular resistance (1.9 +/- 1 versus 2.5 +/- 1 at 2 weeks, 1.5 +/- 0.6 versus 2.7 +/- 1.7 WU at 1 year, P = 0.051). CONCLUSIONS: Total orthotopic heart transplantation improves cardiac output and index in pts with high preoperative pulmonary vacular resistance. There is a lower mean RA and PA pressure perhaps due to less tricuspid and mitral regurgitation. In view of the frequently observed restrictive filling pattern after cardiac transplantation, total orthotopic heart transplantation can be beneficial until this pattern has subsided by preserving atrioventricular synchrony and offering better atrial transport.

Aged↗
PubMed1991

Analysis and predictors of pulmonary vascular resistance after cardiac transplantation.

Elevated pulmonary vascular resistance is a known risk factor for early death from acute right ventricular failure after orthotopic cardiac transplantation. Patients in whom the elevated pulmonary vascular resistance is due primarily to increased left atrial pressure ("reactive") frequently have normalization of resistance after transplantation, but few studies have detailed the time course and magnitude of these changes. To analyze the response of pulmonary vascular resistance to cardiac transplantation, we analyzed data from 4353 right heart catheterizations on all 182 patients undergoing cardiac transplantation between 1981 and Jan. 1, 1990. Before transplantation 18% of patients had a pulmonary vascular resistance greater than 4 WU, 16% had a pulmonary artery systolic pressure greater than 60 mm Hg, and 16% had a transpulmonary gradient greater than 14 mm Hg. In the overall group of patients, pulmonary vascular resistance (mean value 2.63 WU), transpulmonary gradient (mean value 9.9 mm Hg), and pulmonary artery systolic pressure (mean value 48.0 mm Hg) were normalized within 1 week of cardiac transplantation. In patients with a high preoperative pulmonary vascular resistance (greater than or equal to 4 WU), the resistance fell promptly within 1 week of transplantation but continued to be slightly elevated throughout the period of follow-up. By multiple regression analysis, pulmonary vascular resistance at 1 week and 1 year after transplantation was significantly correlated with the pretransplantation resistance. Pulmonary vascular resistance anytime after transplantation was related to preoperative resistance, body surface area, and pulmonary artery diastolic pressure. Inferences: (1) As a group, cardiac transplant recipients have a normal pulmonary vascular resistance, transpulmonary gradient, and pulmonary artery systolic pressure within 1 week after transplantation with little change thereafter for at least several years. (2) Patients with reversible elevation of pulmonary vascular resistance before cardiac transplantation typically have a reactive and a fixed component. Cardiac transplantation relieves the reactive but not the fixed component. As a result, pulmonary vascular resistance early (within 1 week) and late after transplantation will have fallen but not completely normalized.

Cardiac Catheterization↗
PubMed1991

Discordant effects of nisoldipine on coronary vascular resistance and permeability changes during reflow after ischemia in isolated rabbit hearts.

Effects of a low dose (5 nM) of nisoldipine on vascular and ventricular function were assessed in isolated rabbit hearts during 2 h of reperfusion after 40 min of global, zero-flow ischemia. External detection of bolus injections of 125I-BSA and pressure data generated during the experiment provided repeated estimates of albumin permeation and vascular hemodynamics (resistance, vascular volume, and fractional rate of intravascular washout of 125I-BSA (k01]. In control hearts perfused continuously for 3.5 h, vascular resistance, vascular volume, LVEDP, and k01 remained constant, while maximum +dP/dt and -dP/dt increased 25% above baseline values, and estimates of albumin permeation increased 1.7 x baseline. Addition of 5 nM nisoldipine to the perfusate after the baseline period produced sustained decreases in vascular resistance (16% vs mean baseline value) without significantly affecting any other parameter. Postischemic perfusion of hearts increased vascular resistance and vascular volume approximately 50% above baseline, decreased k01 by 25% (intravascular washout of 125I-BSA was prolonged), and increased albumin permeation approximately 5 x baseline. While LVEDP remained elevated 3 x baseline, maximum +dP/dt and -dP/dt recovered 100% of baseline values (75-80% of untreated control values at comparable time points). Addition of 5 nM nisoldipine to the perfusate prior to ischemia prevented the increased vascular resistance during reflow, prevented the decrease in k01 and the increase in vascular volume, but did not affect the increased albumin permeation and, in general, did not affect the rate of recovery of left ventricle function. These results indicate that a low dose of nisoldipine preserves postischemic coronary vascular hemodynamics, but has little or no effect on the increased vascular leakage of albumin.

Animals↗
PubMed1979

Vertical gradient in regional vascular resistance and pre to post capillary resistance ratios in the dog lung.

The ratios of pre-capillary (Ra) and post-capillary (Rv) resistances to total vascular resistance (RT) were measured at different vertical distances in the lungs of supine dogs. Capillary pressures were estimated as the algebraic sum of the alveolar absorption pressure for Tyrode's solution and the plasma colloid osmotic pressure. Segmental resistance fractions (Ra/RT, Rv/RT) were calculated using the pressure drops between arterial, capillary, and venous pressures at each vertical distance within the lung. In a second group of animals, total vascular resistance was calculated at each lung level using regional blood flow as measured by radiolabelled microspheres and the corresponding regional vascular pressures. The total vascular resistance was lowest in Zone III portions of the lung, but Ra/RT and Rv/RT were constant throughout this zone (n = 22) averaging .63 +/- .02 (SEM) and .37 +/- .02 (SEM, respectively, resulting in Ra/Rv of 1.70). Total vascular resistance increased markedly in Zone II portions of the lung, but the relative contribution of Ra/RT decreased from .62 +/- .07 (SEM) to .45 +/- .05 (SEM). Thus Ra/Rv decreased from 1.70 to .82 in Zone II. The absolute values of pre- and post-capillary resistances were lowest in Zone III but post-capillary resistance increased to a greater degree than pre-capillary resistance up Zone II.

Animals↗
PubMed1998

Effect of K+ATP channel inhibition on total and regional vascular resistance in guinea pig pregnancy.

Decreased vascular resistance and vasoconstrictor response during pregnancy enables an increase in cardiac output and regional blood flow to the uterine circulation. We sought to determine whether inhibition of vascular smooth muscle ATP-sensitive potassium (K+ATP) channel activity during pregnancy increased systemic and/or regional vascular resistance and resistance response to ANG II. A total of 32 catheterized, awake, pregnant or nonpregnant guinea pigs were treated with either the K+ATP channel inhibitor glibenclamide (3.5 mg/kg) or vehicle (DMSO) (n = 8/group). In nonpregnant and pregnant animals, glibenclamide raised blood pressure and systemic, uterine, and coronary vascular resistance, diminishing cardiac output and organ blood flow. Glibenclamide produced a greater rise in coronary vascular resistance in the pregnant than nonpregnant groups and increased renal and cerebral vascular resistance in the pregnant animals only. ANG II infusion raised blood pressure and systemic and renal vascular resistance and lowered cardiac output and renal blood flow in vehicle-treated animals. Glibenclamide augmented ANG II-induced systemic vasoconstriction in the nonpregnant and pregnant groups and the rise in uteroplacental vascular resistance in the pregnant animals. We concluded that K+ATP channel activity likely modulates systemic, uterine, and coronary vascular resistance and opposes ANG II-induced systemic vasoconstriction in nonpregnant and pregnant guinea pigs. Pregnancy augments K+ATP channel activity in the uterine, coronary, renal, and cerebral vascular beds and the uteroplacental circulation during ANG II infusion. Thus increased K+ATP channel activity appears to influence regional control of vascular resistance during guinea pig pregnancy but cannot account for the characteristic decrease in systemic vascular resistance and ANG II-induced systemic vasoconstrictor response.

Angiotensin II↗
PubMed1995

Media: lumen ratio in human small resistance arteries is related to forearm minimal vascular resistance.

BACKGROUND: For the evaluation in humans of structural alterations in resistance arteries, most studies have used an indirect index, the measurement of minimal vascular resistance (mean blood pressure divided by maximal postischaemic blood flow) in suitable vascular beds. A sensitive and specific micromyographic technique was recently made available for the study of human small resistance arteries. Whether a correlation really exists between results obtained with the two techniques has not yet been investigated. OBJECTIVE: To evaluate both forearm minimal vascular resistance and media:lumen ratio of omental or subcutaneous small arteries in normotensive subjects and hypertensive patients. DESIGN AND METHODS: Thirty-four individuals were included in the study (age range 35-74 years; 24 hypertensive, 10 normotensive). Twenty-five had elective abdominal surgery and nine hypertensive patients had a gluteal biopsy. Omental and subcutaneous small arteries were dissected and mounted on a wire micromyograph (Mulvany's technique), and media:lumen ratio and media thickness were measured. The dose-response curve to noradrenaline was constructed at cumulative concentrations from 3 x 10(-9) to 3 x 10(-5) mol/l. Venous occlusion plethysmography was used to measure blood flow in the forearm, and minimal vascular resistance was calculated from mean blood pressure and postischaemic maximal blood flow (13 min ischaemia plus exercise). RESULTS: A statistically significant correlation was found between media:lumen ratio and minimal vascular resistance (r = 0.74, P < 0.001) as well as between media:lumen ratio and systolic (r = 0.44, P < 0.01) and diastolic (r = 0.38, P < 0.05) blood pressures. Similar correlations were observed between media thickness and systolic and diastolic blood pressures. Small arteries from hypertensive patients had a significantly increased reactivity to noradrenaline (by analysis of variance) compared with those from normotensive subjects, in terms of wall tension but not of active media stress. CONCLUSIONS: The present study demonstrated that the media:lumen ratio of small resistance vessels is significantly related to forearm minimal vascular resistance, suggesting that direct and indirect evaluations of vascular morphology will give similar results.

Adult↗
PubMedDate not supplied

Inhaled nitric oxide in the evaluation of heart transplant candidates with elevated pulmonary vascular resistance.

The reversibility of elevated pulmonary vascular resistance in heart transplant candidates is currently evaluated with intravenous vasodilators. The aim of this study was to evaluate the effects of increased concentrations of inhaled nitric oxide (20, 40, and 80 ppm) on central hemodynamics and right ventricular function in heart transplant candidates with elevated pulmonary vascular resistance (> 2.5 Wood units). Comparison was made with intravenous vasodilators, sodium nitroprusside, and prostacyclin in doses that lowered the mean arterial pressure by about 15%. Inhalation of nitric oxide did not change systemic or pulmonary arterial pressure, cardiac output, right ventricular function, or systemic vascular resistance. Pulmonary capillary wedge pressure increased and transpulmonary pressure gradient and pulmonary vascular resistance decreased (-34% +/- 4% and -36% +/- 4%, respectively; p < 0.01) during 20 ppm nitric oxide, with no further effects at higher doses. Prostacyclin and sodium nitroprusside decreased pulmonary vascular resistance (-50% +/- 6% and -33% +/- 5%; p < 0.01). Prostacyclin reduced to some extent (p = 0.08) transpulmonary pressure gradient, which was not seen during sodium nitroprusside infusion. Systemic vascular resistance decreased during both sodium nitroprusside (-37% +/- 5%) and prostacyclin (-44% +/- 4%) infusion. The pulmonary vascular resistance/systemic vascular resistance ratio, used as an index of pulmonary selectivity, was decreased by nitric oxide (p < 0.01) but not by the intravenous vasodilators. Metabolic data indicate that inhaled nitric oxide is metabolized in the same way as that formed endogenously. In conclusion, inhaled nitric oxide is a selective pulmonary vasodilator that can be used safely in the hemodynamic evaluation of heart transplant candidates with elevated pulmonary vascular resistance.

Administration, Inhalation↗
PubMed1994

Determinants of low systemic vascular resistance during cardiopulmonary bypass.

Although low systemic vascular resistance occurs during normothermic and hypothermic cardiopulmonary bypass, the determinants of depressed systemic vascular resistance and its effect on outcomes are unknown. To assess the predictors and clinical effects of low systemic vascular resistance, 555 patients undergoing isolated coronary artery bypass grafting were evaluated prospectively. The extent of low systemic vascular resistance during bypass was estimated by the amount of the vasoconstrictor phenylephrine administered: group 1, 0 to 160 micrograms; group 2, 161 to 800 micrograms; group 3, more than 800 micrograms. Multivariate analysis identified bypass temperature, bypass time, and ventricular function as determinants of low systemic vascular resistance. Patients on normothermic bypass accounted for 65% of the patients in group 3 and only 34% of the patients in group 1 (p < 0.0001). The bypass time was longer in the patients in group 3 (97 +/- 28 minutes) than in the patients in group 1 (89 +/- 24 minutes; p < 0.006). Patients with a preoperative left ventricular ejection fraction of 0.40 or less required less phenylephrine during cardiopulmonary bypass (498 +/- 68 micrograms) than did patients with a fraction exceeding 0.40 (1,087 +/- 88 micrograms; p < 0.001). By multivariate analysis, advanced age and the presence of peripheral vascular disease were found to decrease the likelihood of low systemic vascular resistance during normothermic bypass. Diabetes, the left ventricular ejection fraction, the bypass time, and the total cardioplegia infused were found to influence the likelihood of low systemic vascular resistance during hypothermic bypass. Patients in group 3 had a higher cardiac index and lower-mean arterial pressure and systemic vascular resistance postoperatively. In those patients who received a left internal mammary artery graft, the incidences of the low-output syndrome (group 1, 4.9%; group 3, 2.7%; p = not significant) and myocardial infarction (group 1, 1.4%; group 3, 1.8%; p = not significant) were not influenced by the amount of phenylephrine infused during cardiopulmonary bypass. In those patients who were at high risk of suffering a stroke preoperatively, the hypotension induced by the low systemic vascular resistance and its treatment with phenylephrine was not associated with an increased incidence of stroke (group 1, 5.8%; group 3, 2.8%; p = not significant).

Aged↗
PubMed1998

Nitric oxide synthase inhibition increases vascular resistance in sodium and water loaded rats.

The aim of this study was to investigate whether nitric oxide might be involved in the adaptation of the cardiovascular system in sodium and water loaded organisms. The effects of a semi-chronic (4 day) inhibition of nitric oxide production were studied in normovolemic and per os sodium and water loaded rats. Nitric oxide synthase was inhibited by L-NAME (10 mg/kg in normovolemic and 14 mg/kg in sodium loaded rats) dissolved in the drinking solution. Blood pressure, cardiac output (Stewart-Hamilton's principle) and its regional fractions (Sapirstein's technique using 86Rb isotope as indicator), total peripheral resistance and regional vascular resistances were determined on the 5th day in sodium pentobarbital anaesthesia. The increase in blood pressure following L-NAME pretreatment in both groups was similar, but the elevation of total peripheral resistance was 106% in normovolemic and only 30% in sodium loaded animals. The cardiac output decreased by 44% in normovolemic and 14% in sodium loaded groups after nitric oxide synthase inhibition. The organ vascular resistances increased and organ blood flows decreased after L-NAME administration. These changes were less pronounced in sodium and water load, especially those in the skeletal muscle and intestine. Nitric oxide-induced changes in vascular resistance are more pronounced in normovolemia than in sodium load; sodium load might influence the nitric oxide production. The share of nitric oxide in the setting of vascular tone is different in the various organs.

Analysis of Variance↗