SEARCH · PubMed Health

Results for “VASCULAR RESISTANCE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

PubMed1982

Increased pulmonary vascular resistance and permeability due to arachidonate metabolism in isolated rabbit lungs.

Liberation and metabolism of arachidonic acid may be the common final pathway of different stimuli on the pulmonary vascular bed. In a model of isolated, ventilated rabbit lungs, perfused with Krebs Henseleit albumin buffer in a recirculating system, changes of pulmonary vascular resistance and of vascular permeability are monitored continuously. The addition of free arachidonic acid or of the Ca-ionophore A 23187 to the perfusion fluid consistently evokes a biphasic increase in vascular resistance as well as an initially reversible increase in vascular permeability, followed by pulmonary edema. Both phases of increased vascular resistance are completely suppressed by inhibition of the cyclooxygenase, decreased to a large degree by inhibitors of thromboxane synthetase, and markedly augmented by short preincubation of arachidonic acid with ram seminal vesicular microsomes and by sulfhydryl reagents. The increased pulmonary vascular permeability is augmented by inhibition of cyclooxygenase and reduced by simultaneous lipoxygenase inhibition. Antagonists of histamine, serotonin and sympathic or parasympathic activity do not have any influence. PG F2alpha., TxB2, PG E2 and PG I2 alter the pulmonary vascular resistance, but do not increase vascular permeability. In conclusion, increased availability of free arachidonic acid evokes a rise in pulmonary vascular resistance, which can be ascribed to cyclooxygenase products, especially to thromboxane, and causes a rise in vascular permeability which can be ascribed to lipoxygenase products. The findings may be related to acute pulmonary lesions with increase in vascular resistance and with vascular leakage.

Animals↗

PubMed1979

Renal vascular resistance and reactivity in the spontaneously hypertensive rat.

Renal vascular resistance is elevated in spontaneously hypertensive rats (SHR) when compared to normotensive control Wistar-Kyoto rats (WKY). The present study examined possible determinants of this raised vascular resistance in in situ autoperfused kidneys of pentobarbital-anesthetized, 12- to 16-wk-old SHR and WKY. Over a wide range of arterial pressures (30--100 mmHg) renal blood flow was consistently higher in WKY than in SHR. This relative flow difference was unchanged by acute renal denervation, with renal vascular resistance decreasing approximately 20% in both strains. Changes in renal vascular resistance to renal nerve stimulation and the administration of intra-arterial vasoactive hormones also were assessed. Vascular responses to renal nerve stimulation, tyramine, angiotensin II, and acetylcholine were similar in kidneys of the two strains, but reactivity to norepinephrine was significantly less in kidneys of SHR. It was concluded that elevated renal vascular resistance in the SHR does not result from an excessive neurogenic influence on the renal vasculature or from vascular hyperreactivity to norepinephrine or angiotensin II.

Acetylcholine↗

PubMed1980

[Shunt method of determining vascular resistance].

A method is suggested for determining vascular resistance from the blood flow in the test vascular bed and in the shunt tube that is invariable in length and diameter, paralleled to this bed. In conformity with Hagen-Poiselles's equations, the viscosity component dependent on the composition and the temperature of blood should be omitted in the results obtained by the formula (Formula: see text) where Rv -- vascular resistance; Qs and Qv -- blood flow in the shunt tube and in the vascular bed; Rs -- resistance of the shunt tube calculated according to Poiselle's formula from the shunt parameters and the viscosity index equal to 1 centipoise. At the same time the viscous-rheological component of the resistance closely related to the anatomic functional properties of the vascular network should not be replaced. In contradistinction to the general resistance, this index is designated as specific vascular resistance.

Animals↗

PubMed2002

Hemodynamic effects of inhaled aerosolized iloprost and inhaled nitric oxide in heart transplant candidates with elevated pulmonary vascular resistance.

OBJECTIVE: An elevated pulmonary vascular resistance (PVR) is described as a predictor of postoperative right heart failure and increased mortality in patients undergoing orthotopic heart transplantation. The use of intravenous vasodilators is limited by their systemic effects. We evaluated the pulmonary and systemic hemodynamic effects of inhaled nitric oxide (NO) and inhaled aerosolized iloprost (IP) in heart transplant candidates with elevated PVR. METHODS: Fourteen male heart transplant candidates due to dilative or ischemic cardiomyopathia with elevated PVR (> or = 180 dyn s cm(-5)) were included in the study. Increasing concentrations of NO (5, 10 and 30 ppm) and 50 microg aerosolized IP were administered by inhalation. Hemodynamic measurements preceded and followed administration of each agent. RESULTS: Inhalation of IP, 10, and 30 ppm NO reduced PVR and mean pulmonary artery pressure (MPAP), but did not affect blood pressure or systemic vascular resistance. Comparing the effectiveness of 10 ppm NO and IP, we found a significant higher reduction of MPAP in patients treated with IP. An increase of cardiac index and stroke index could only be shown with IP-inhalation. CONCLUSIONS: Inhaled iloprost induces pulmonary vasodilation which is significantly greater than the effects of 10 and 30 ppm NO. The results of our study show, that inhaled iloprost induces a reliable hemodynamic response in the evaluation of heart transplant candidates. Further advantages of iloprost inhalation are the lack of adverse reactions and toxic side effects and an easier administration. Due to this facts we recommend iloprost as a routine screening drug for vascular reactivity in HTx-candidates. Based on our results it would be of great interest to investigate the role of iloprost in management of postoperative right heart insufficiency following cardiac transplantation.

Administration, Inhalation↗

PubMed1980

Increased total and regional vascular resistance produced by propranolol.

Propranolol when administered acutely causes little change in blood pressure and a decrease in cardiac output. Blood pressure is maintained due to increased vascular resistance. The purpose of this investigation was to determine if increased vascular resistance after propranolol occurs uniformly among various tissues and if increased resistance is due to reflex vasoconstriction. Total and regional vascular resistance were determined with the radioactive microsphere technique in dogs anesthetized with chloralose. Intravenous propranolol, 1 mg/kg, caused little change in blood pressure, cardiac rate, cardiac output and total and regional vascular resistance 30 min after administration. These changes were not different than changes after saline injection. In dogs pretreated with the alpha adrenergic receptor antagonist, dibozane, i.v. propranolol did not affect cardiac rate or blood pressure but reduced cardiac output and increased total peripheral resistance. Vascular resistance in brain, heart, lung, duodenum and skin was increased whereas kidney, spleen and muscle vascular resistance was not significantly changed. It is concluded that increased vascular resistance produced by propranolol does not occur uniformly among tissues. Increased vascular resistance after propranolol is not due to reflex activation of alpha adrenergic receptors but may involve alterations in unidentified vasoconstrictor or vasodilator influences in certain vascular beds.

Animals↗

PubMed1994

Intermediate follow-up of pediatric heart transplant recipients with elevated pulmonary vascular resistance index.

OBJECTIVES: This study examined perioperative and intermediate outcomes in pediatric cardiac transplant recipients who had elevated pulmonary vascular resistance indexes preoperatively. BACKGROUND: Elevated pulmonary vascular resistance was associated with poor outcome in previous studies and constitutes a relative contraindication to transplantation. Few studies have evaluated this poor outcome risk factor in pediatric patients. METHODS: To evaluate outcomes of nonneonatal transplant recipients, records were reviewed and divided into Group I (preoperative pulmonary vascular resistance index > or = 6 units.m2) and Group II (pulmonary vascular resistance index < 6 units.m2). Donor/recipient weight ratios, ischemic times, length of intensive care unit stay, posttransplantation infection rates, arrhythmia, response to pretransplantation vasodilator infusions and pulmonary vascular resistance indexes at the first and most recent posttransplantation biopsies were analyzed. RESULTS: Group I (8 patients) had a mean (+/- SEM) pulmonary vascular resistance index of 11.5 +/- 3.5 units,m2; Group II (29 patients) had a mean pulmonary vascular resistance index of 2.3 +/- 0.4 units,m2 (p < 0.002). Pulmonary vascular resistance index decreased from 12.3 +/- 3.9 to 3.9 +/- 0.9 units.m2 (p < 0.05) in 7 Group I patients undergoing vasodilator infusion during pretransplantation catheterization. Thirty-six orthotopic heart transplantations were performed and one heterotopic transplantation. Donor weights exceeded recipient weights by 13% and 31% for Groups I and II, respectively (p > 0.25). Donor ischemic time was 215 min for Group I and 225 min for Group II (p > 0.75). Intensive care unit stay was 11.5 days in Group I and 15.1 days in Group II (p = 0.20). Infection rate was 38% in both groups (p > 0.80). Arrhythmias occurred in 90% of Group I and 42% in Group II (p < 0.03) patients. Pulmonary resistance index in Group I decreased from 11.5 +/- 3.5 to 3.3 +/- 1.2 units.m2 (p < 0.03) by the first posttransplantation biopsy and have not changed subsequently. During 2.3 years (range 0.3 to 8.5) of follow-up, the mortality rate was 25% and 21% for Groups I and II, respectively (p > 0.80). CONCLUSIONS: Group I patients did not require significantly oversized donors, restricted donor locations or longer intensive care unit stays or have higher infection rates; however, arrhythmias were more frequent. Pulmonary resistance index normalized early after transplantation. Pulmonary vascular reactivity may be more important for survival than absolute resistance index.

Adolescent↗

PubMed1990

Umbilical artery flow velocity waveforms and placental vascular resistance during maternal placental outflow obstruction in sheep.

This study was designed to test the hypothesis that the pulsatility index (PI) of the umbilical artery flow velocity waveform varies as a function of placental vascular resistance. Placental vascular resistance was raised by a one-minute occlusion of the maternal inferior vena cava. Occlusion of the maternal inferior vena cava resulted in a decrease in fetal heart rate from 183 +/- 7.8 beats/min to 142 +/- 8.6 beats/min at the end of occlusion (P less than 0.05). Placental vascular resistance increased from 0.113 +/- 0.021 mmHg.ml-1.min during control to 0.151 +/- 0.033 mmHg.ml-1.min (P less than 0.05) during occlusion. The pulsatility index increased from 1.05 +/- 0.05 to 1.85 +/- 0.4 (P less than 0.05) during occlusion. After parasympathetic blockade with atropine fetal heart rate did not change during occlusion. Placental vascular resistance increased from 0.091 +/- 0.014 before to 0.121 +/- 0.021 mmHg.ml-1.min during occlusion (P less than 0.05). The pulsatility index increased from 0.98 +/- 0.1 before to 1.12 +/- 0.12 during occlusion (P less than 0.05). These results support the hypothesis that, in the fetal sheep, placental vascular resistance is one of the determinants of the pulsatility index of the umbilical artery.

Animals↗

PubMed1986

The effect of pregnancy on the changes in hind-limb vascular resistance following haemorrhage in the rabbit.

The change in vascular resistance of the skinned hind limb perfused at constant flow has been measured following rapid removal of 10% of the blood volume in anaesthetized pregnant rabbits (27-29 days gestation) and compared with that of non-pregnant rabbits. 5 s after haemorrhage was completed vascular resistance had risen in all rabbits, but in the pregnant ones this increase was only one-fifth of that in the non-pregnant ones. After section of either the carotid sinus and aortic nerves or the sympathetic innervation to the hind limb the increases of vascular resistance at this time were abolished. It is concluded that the previously described diminution during pregnancy of the protective function of the baroreflexes during haemorrhage results, to some extent, from their diminished role in a vascular bed not associated with the reproductive process. The blood withdrawn was not re-infused for 10 min, throughout which, in all rabbits with sinus, aortic and sympathetic nerves intact, the increase in vascular resistance was sustained. After section of the carotid sinus and aortic nerves and the sympathetic innervation there was, during this 10 min, a slow increase in vascular resistance comparable in final size to that which occurred immediately in the respective innervated preparations, i.e. it was smaller in the pregnant than in the non-pregnant rabbits. A possible difference in action during pregnancy of a vasoconstrictor substance released during haemorrhage is discussed briefly.

Animals↗

PubMed1993

Insulin differentially regulates systemic and skeletal muscle vascular resistance.

To explore the relationships among insulin action, vascular resistance, and insulin sensitivity, we studied three groups of lean (Ln) and one group of obese (Ob) men. Glucose uptake was measured in whole body (WBGU) and in leg muscle (LGU) under basal and hyperinsulinemic euglycemic conditions. Mean arterial pressure (MAP), cardiac output (CO), leg blood flow (LBF), and systemic (SVR) and leg (LVR) vascular resistance were also ascertained. Ln groups were studied during insulin infusion rates of 20, 40, and 600 mU.m-2.min-1 and the Ob group at 40 mU.m-2.min-1. In Ob vs. Ln groups, WBGU and LGU were reduced by 51 (P < 0.01) and 42% (P < 0.05), respectively. In response to insulin, LBF increased > 60% (P < 0.01) in Ln groups but only approximately 20% in the Ob group, P = not significant (NS). CO was unchanged in Ob compared with a 15% increase (P < 0.05) in Ln groups, LBF was highly correlated with CO, r 0.70, P < 0.001. During hyperinsulinemia, MAP and LVR decreased in Ln (P < 0.001) but not in the Ob group (P = NS). In Ln groups, SVR decreased by 26 vs. 9% in the Ob group, P < 0.01. In summary, 1) insulin decreases LVR more than SVR and via this mechanism redistributes CO to insulin-sensitive tissues, 2) this insulin effect is blunted in Ob humans, and 3) insulin decreases MAP and vascular resistance more effectively in insulin-sensitive than in insulin-resistant subjects. In conclusion, insulin resistance to carbohydrate metabolism is associated with resistance to insulin's effect to decrease skeletal muscle vascular resistance and as such could act as a risk factor for the development of hypertension.

Animals↗

PubMed2001

Carotid vascular resistance in long-term estrogen users.

OBJECTIVE: To compare carotid vascular resistance in long-term estrogen users with that of age-matched nonusers. METHODS: Pairwise comparisons between 18 long-term users of 17beta-estradiol (E2) implants (mean age 67.8 years, mean duration of treatment 18.8 years, range 5.8-33.9 years) and 18 age-matched (+/- 2 years) nonusers. We used color Doppler ultrasound to assess pulsatility index (PI) and resistance index (RI) in common, external, and internal carotid arteries. RESULTS: Estrogen users compared with age-matched nonusers had significantly lower mean values for common carotid RI, -4%; -0.04 (95% confidence interval [CI] -0.07, -0.03, P =.036) and marginally significant for PI, -12%; -0.25 (95% CI -0.54, 0.04, P =.087). Differences in external and internal carotids were smaller and insignificant. Age was a determinant of internal carotid vascular resistance in estrogen users and nonusers. Increasing pairwise differences in external carotid vascular resistance with advancing age (r = 0.55; P =.02), with magnitudes of mean group differences indicate a modest but true effect of long-term estrogen therapy on vascular resistance in common carotids, less in external, and negligible in internal carotid arteries. The study had an 80% power to detect a 10% mean difference (0.08 units) in common carotid RI at the 5% level. The standard deviation was considerably lower for estimates of RI than for PI. CONCLUSION: Long-term estrogen therapy was associated with minor reduction of vascular resistance in common carotid, less in external, and negligible in internal carotid arteries. Effects on carotid vascular resistance do not seem to be a major mechanism in the long-term protective effect of estrogen therapy on cardiovascular risk.

Aged↗

PubMed1987

Dose-related effects of pharmacological mediators on tracheal vascular resistance in dogs.

1 Various doses of mediators were tested on tracheal vascular resistance in dogs anaesthetized with pentobarbitone. Tracheal vascular resistance was determined by perfusing the cranial tracheal arteries at constant flows and measuring inflow pressures. 2 All drugs produced dose-related changes in vascular resistance. 3 The peptides bradykinin, substance P and vasoactive intestinal peptide (VIP) each had similar vasodilator potencies and were much more powerful than histamine, methacholine and salbutamol. 4 Platelet activating factor (Paf) was a weaker dilator than the peptides. Prostaglandins D2, E1 and F2 alpha had wide dilator potency ranges, PGE1 being very effective even at low concentrations. 5 Phenylephrine, an alpha-adrenoceptor agonist, was the only drug tested that always increased vascular resistance. 6 All the drugs studied also had effects on the contralateral tracheal vascular resistance.

Animals↗

PubMed1987

Factors influencing coronary vascular resistance during hypothermia.

Factors influencing total coronary vascular resistance (CVR) during hypothermia were studied in 30 mongrel dogs. Complete isolation of the heart in situ was achieved by transection of all cardiac neural and vascular connections in 15 dogs (denervated, Group I). Cardiac innervation was maintained in the other 15 dogs using systemic normothermic cardiopulmonary bypass (innervated, Group II). The aortic root was perfused with heparinized oxygenated blood at a constant flow rate at variable myocardial temperatures. Electromechanical arrest was achieved using potassium chloride (KCl) (25 meq/liter) added to the coronary perfusate. In each group, 5 dogs were maintained at a flow rate of 10 cc/kg/min without KCl and allowed to beat spontaneously, another 5 at a flow rate of 10 cc/kg/min and arrested with KCl, and the remaining 5 at a flow rate of 5 cc/kg/min with KCl. Total coronary vascular resistance was calculated from aortic root pressure, right atrial pressure, and flow rate and expressed in units per 100 grams of cardiac tissue. At 37 degrees C, resistance was lower in the denervated arrested (1.3 +/- 0.2) than in the innervated arrested hearts (2.1 +/- 0.2) (P less than 0.001). Preservation of spontaneous electromechanical activity in the innervated hearts resulted in a lower resistance (0.4 +/- 0.1) (P less than 0.001). A progressive decrease in myocardial temperature to 15 degrees C resulted in a corresponding decrease in coronary vascular resistance to a plateau value (0.5 to 0.7 U) in all arrested groups. The data suggest that at normothermia, innervation increases vascular tone in the coronary vascular bed, while electromechanical activity decreases it.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Doppler echocardiographic evaluation of pulmonary vascular resistance in children with congenital heart disease.

Noninvasive assessment of pulmonary vascular resistance has not been well defined. Cardiac catheterization findings in 33 patients with congenital heart disease (mean age 1.4 years) were compared with Doppler echocardiographic parameters. The right ventricular pre-ejection period (RVPEP), ejection time (RVET), and the ration RVPEP/RVET correlated better with pulmonary vascular resistance than with pulmonary artery pressure. A highly significant correlation with a small standard error of estimate (SEE) was demonstrated between pulmonary vascular resistance and a newly derived parameter RVPEP/velocity time integral (VTI) [r = 0.87, p < 0.0001, SEE = 2]. An RVPEP/VTI value of < 0.4 seconds/meter (M) was able to select patients with pulmonary vascular resistance < 3 Wood Unit.M2, even in the presence of pulmonary artery hypertension caused by increased pulmonary blood flow, with 97% accuracy (100% sensitivity, and 92% specificity). An RVPEP/VTI value of 0.4 to 0.6 seconds/M identified patients with pulmonary vascular resistance between 3 to 7.5 Wood Unit.M2 with 91% accuracy, and a value of > or = 0.6 seconds/ M selected patients with total pulmonary vascular resistance > or = 7.5 Wood Unit.M2 with 94% accuracy.

Adolescent↗

PubMed1987

Effects of bisoprolol on local vascular resistance.

Changes in systolic and diastolic blood pressure, heart rate, arterial blood flow and vascular resistance in the arm and in the leg were investigated in 9 healthy volunteers (22-40 years) after oral dosing with bisoprolol 10 mg, propranolol 40 mg, and placebo in a randomized double-blind cross-over study. Arterial blood flow and vascular resistance were determined in brachial and femoral arteries with unimpeded circulation, after exclusion of the hand or foot by placing a tourniquet on the wrist or ankle, and during post-ischaemic hyperaemia. Distal arterial occlusion allows one to isolate a predominantly muscular circulation in the forearm or, to a lesser extent, in the leg. Both active drugs induced a significant fall in heart rate and systolic blood pressure versus placebo with no significant difference between the drugs. Brachial and femoral flow rates were reduced by both drugs probably due to a fall in cardiac output, but the two beta blockers produced different effects on vascular resistance: propranolol significantly increased brachial vascular resistance compared with placebo and bisoprolol, both during unimpeded circulation and during occlusion of the hand by a wrist tourniquet. Bisoprolol had no influence on brachial vascular resistance. Both drugs induced small increases in femoral vascular resistance. The different action on local vascular resistance in the brachial artery territory could be interpreted as the expression of the high beta 1 selectivity of bisoprolol leaving the vascular beta 2 receptors unopposed, whereas non-selective propranolol acts on both beta-adrenoceptor subtypes.

Adrenergic beta-Antagonists↗

PubMed1999

High and low pulmonary vascular resistance in heart transplant candidates. A 5-year follow-up after heart transplantation shows continuous reduction in resistance and no difference in complication rate.

BACKGROUND: In heart transplantation candidates, high pulmonary vascular resistance has been found to decrease promptly after heart transplantation without any further reduction during follow-up. Pulmonary hypertension has been described as associated with an increased peri- and postoperative complication rate and mortality. This study describes the evolution of pulmonary vascular resistance and the outcome for patients during 5 years following heart transplantation. METHODS AND RESULTS: Haemodynamic data, complication rate and mortality have been analysed during 5-year follow-up in all patients (n = 80) who were heart transplanted at Sahlgrenska University Hospital from 1988 through 1990. We found a significant and continuous reduction in pulmonary vascular resistance both in patients with a pre-operative high (> 3 Wood Units; n = 36), but reversible on nitroprusside, and pre-operative low (< or = 3 Wood Units; n = 44) pulmonary vascular resistance. A multivariate analysis showed that a pre-operative high mean pulmonary artery and low mean pulmonary capillary wedge pressure predicted the decline in pulmonary vascular resistance during 5 years after heart transplantation. The need for a postoperative assist device, complication rate, and early and late mortality were independent of the pre-operative level of pulmonary vascular resistance. CONCLUSIONS: A continuous reduction in pulmonary vascular resistance during 5 years following heart transplantation was found in patients with both high, but reversible, and low pre-operative resistance levels. The outcome and survival were independent of the pre-operative pulmonary vascular resistance level.

Adolescent↗

PubMed1986

Measurement of portal vascular resistance in patients with portal hypertension.

Portal vascular resistance was measured percutaneously in 60 patients with chronic liver disease and in 5 control subjects. The portal vascular resistance (PVR) was calculated, using the following equation, from the portal blood flow (QPV), portal venous pressure (PPV), and hepatic venous pressure (PHV): PVR = (PPV - PHV)/QPV. The portal blood flow was measured using an ultrasonic Doppler duplex system, and the portal venous and hepatic venous pressures were measured using percutaneous transhepatic catheterization and venous catheterization, respectively. The wedged hepatic venous pressure was measured by occluding the hepatic venous branch using a balloon catheter. The portal vascular resistance was 0.25 +/- 0.13 mmHg X ml-1 X min X kg body weight (mean +/- SD, n = 5) in the control group, 0.64 +/- 0.29 mmHg X ml-1 X min X kg body wt (n = 13) in the chronic active hepatitis group, 1.34 +/- 0.79 mmHg X ml-1 X min X kg body wt (n = 30) in the cirrhosis group, and 0.85 +/- 0.69 mmHg X ml-1 X min X kg body wt (n = 13) in the idiopathic portal hypertension group.

Blood Flow Velocity↗

PubMed1990

Effects of normal pregnancy on cellular cation metabolism and peripheral vascular resistance.

Normal pregnancy is associated with a poorly understood loss of vascular responsiveness to the pressor effects of infused angiotensin II. Since cellular cation metabolism appears to be a critical determinant of basal vascular tone and vascular reactivity, we have evaluated platelet ionized calcium, erythrocyte sodium, calcium and magnesium levels, and erythrocyte Ca-ATPase and Na/K ATPase activity in 15 normal black pregnant women (37.5 +/- 0.6 weeks gestation) and 10 normal age-matched nonpregnant black women. Plasma levels of factors potentially affecting vascular reactivity (endoxin, renin activity (PRA), and atrial natriuretic peptide (ANP] were measured by RIA and peripheral vascular resistance by biolectrical impedance. Peripheral vascular resistance was almost twice as high (P less than .003) in the normal group as in the pregnant women. Intracellular calcium concentrations were not significantly different in erythrocytes or platelets of the two groups. Although erythrocyte membrane Ca-ATPase was similar, Na/K ATPase activity was significantly higher in the pregnant subjects than in the nonpregnant controls, and intracellular sodium was lower. All three measured plasma factors, ANP, endoxin and PRA, were significantly elevated in the pregnant women. Our results suggest that the decrease in peripheral vascular resistance seen in normal pregnancy is probably not the result of alterations in cellular cation concentrations and/or cell membrane pump activity. However, the significant correlation between vascular reactivity and circulating ANP indicates this potent vasodilator may play a role in the observed decrease in peripheral vascular resistance associated with pregnancy.

Adult↗

PubMedDate not supplied

Long-term outcome of patients operated for large ventricular septal defects with increased pulmonary vascular resistance.

BACKGROUND: There is a paucity of data regarding the long-term outcome of patients operated for ventricular septal defect with severe pulmonary arterial hypertension and elevated pulmonary vascular resistance. METHODS AND RESULTS: We evaluated the long-term follow-up results of a selected cohort of patients with nonrestrictive ventricular septal defect and elevated pulmonary vascular resistance (>6 Wood units). Thirty-eight patients, median age 7.5 years (range 6 months-27 years), with nonrestrictive ventricular septal defect with severe pulmonary hypertension were operated between 1985 and 1996 at our institute. Preoperative pulmonary vascular resistance, ratio of pulmonary blood flow to systemic blood flow, and ratio of pulmonary vascular resistance to systemic vascular resistance were 7.63+/-1.8 Wood units, 1.9+/-0.48, and 0.41+/-0.12, respectively. The majority (68.4%) had perimembranous ventricular septal defect. Thirty patients (79%) had a good outcome and were asymptomatic at a mean follow-up of 8.7 years, with significant reduction in pulmonary artery pressures. Eight patients (21%) had a poor outcome, which included 5 immediate postoperative deaths, 1 late death and 2 surviving patients with persistent severe pulmonary arterial hypertension. There was no significant difference regarding hemodynamic parameters at baseline between those who had a good outcome and those who did not. Eleven patients with a preoperative pulmonary blood flow to systemic blood flow ratio of <2:1. who had a good outcome following surgery, underwent repeat catheterization at follow-up. There was a significant reduction in their mean pulmonary vascular resistance (8.03+/-1.4 v. 4.16+/-1.6 Wood units, p=0.001) and pulmonary vascular resistance to systemic vascular resistance ratio (0.41+/-0.12 v. 0.19+/-0.06, p=0.05). CONCLUSIONS: The late results of surgery on this selected group of patients with nonrestrictive ventricular septal defect with high pulmonary vascular resistance are encouraging. Operative correction of the ventricular septal defect should be actively considered in all children presenting with nonrestrictive ventricular septal defect with a significant left-to-right shunt, despite moderately elevated pulmonary vascular resistance. Even among older patients with ventricular septal defect and moderately elevated pulmonary vascular resistance, there is a specific group that does well after operation.

Adolescent↗