PubMed Health⌕ Search

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 127 records · Page 7Linked to original sources
PubMed2000

Role of nitric oxide in a temperature dependent regulation of systemic vascular resistance in cardiopulmonary bypass.

OBJECTIVES: Nitric oxide is the most potent vasodilator among inflammation-mediated vasoactive substances. Tepid cardiopulmonary bypass has been known to maintain low vascular resistance and nitric oxide may also be involved. There has been no previous clinical study elucidating a role of nitric oxide in a temperature dependent regulation of systemic vascular resistance in cardiopulmonary bypass. METHODS: Thirty-one patients who underwent valvular surgery were randomly divided into two comparable groups; consisting of the hypothermic cardiopulmonary bypass (28 degrees C:14 patients) and the tepid cardiopulmonary bypass group (34 degrees C:17 patients). The serum levels of nitric oxide (NO(2)(-)+NO(3)(-)), prostaglandin E(2), bradykinin, 6-keto PGF1alpha, thromboxane B(2), endothelin-1, systemic vascular resistance index were measured before, 0, 12 and 24 h after cardiopulmonary bypass. RESULTS: The pattern of change in systemic vascular resistance index and nitric oxide during and after cardiopulmonary bypass were significantly different between the two groups (P=0.0008, P=0.02). The tepid group showed significantly lower levels of systemic vascular resistance index after cardiopulmonary bypass than the hypothermic group (0 h: 2278+/-735 vs. 4387+/-1289, 12 h: 1827+/-817 vs. 2817+/-1146 and 24 h: 1690+/-548 vs. 2761+/-641 dyne s cm(-5) m(2), P=0.0001, P=0.03, P=0. 0006). The nitric oxide levels were significantly higher at 0, 12 and 24 h after cardiopulmonary bypass in the tepid group than those in the hypothermic group (84.7+/-33.3 vs. 46.3+/-18.1, 69.8+/-31.1 vs. 40.1+/-17.5 and 80.1+/-38.5 vs. 39.1+/-15.6 micromol/l, P=0.008, P=0.03, P=0.01). The prostaglandin E(2) levels in the tepid group was significantly higher just after cardiopulmonary bypass than that in the hypothermic group (37.3+/-20.0 vs. 15.8+/-8.6 pg/ml, P=0.02). The bradykinin level in the hypothermic group was significantly higher just after cardiopulmonary bypass than that in the tepid group (2.40+/-0.32 vs. 1.85+/-0.21 log(10) (pg/ml), P=0.005). Only nitric oxide showed a significant negative correlation with the systemic vascular resistance index both during and after cardiopulmonary bypass (r=-0.60, P<0.0001) as compared with prostaglandin E(2) and bradykinin. CONCLUSIONS: These findings demonstrated that serum nitric oxide levels in tepid cardiopulmonary bypass were significantly higher than those in hypothermic cardiopulmonary bypass. Nitric oxide correlated with systemic vascular resistance. Thus, nitric oxide may play a pivotal role in a temperature dependent regulation of systemic vascular resistance in cardiopulmonary bypass.

Biomarkers↗
PubMed1994

Effect of NG-monomethyl-L-arginine on regional vascular resistance in rats.

This study investigated the effects of intravenous injection of the specific inhibitor of nitric oxide (NO) formation, NG-monomethyl-L-arginine (L-NMMA), on mean arterial pressure and regional vascular resistance in rats (n = 7). Regional vascular resistances of brain, heart, left kidney, intestine (jejunum), left testis and right testis were measured using radiolabelled microspheres before and after injection of 12.5 mg/kg of L-NMMA. Injection of L-NMMA raised mean arterial pressure significantly (p < 0.05) from 119 +/- 4 (mean +/- SEM) mmHg to 139 +/- 7 mmHg, accompanied by a significant (p < 0.05) decrease in both heart rate and cardiac index and an increase in total peripheral resistance. Regional vascular resistances in brain, heart, kidney and intestine increased significantly (p < 0.05) with L-NMMA, but no change was observed in the testes. The results indicate that the resistance of vascular beds is affected by NO synthesis, while the extent of regulation may differ among the various vascular beds.

Animals↗
PubMedDate not supplied

Plasma thromboxane B2 concentrations and pulmonary vascular resistance during lung reperfusion.

The purpose of this study was to measure the behavior of plasmatic thromboxane B2 (pITxB2) after reperfusion of a glucose-insulin-potassium preserved lung. Seven adult mongrel dogs underwent a left lung allotransplantation. Hemodynamic changes including pulmonary artery pressure and cardiac output were measured. Pulmonary artery vascular resistance, systemic resistance, arterio-venous oxygen difference, and shunt were calculated. Immunoreactive arterial and venous plasma thromboxane B2 concentrations were measured at 0 (basal), 60, 120, and 180 min after reperfusion. Hemodynamic measurements were made after 5 min of occlusion of the right pulmonary artery and ventilation with 100% oxygen. Prepreservation, pre-reperfusion, and posttransplant lung weights were obtained. All animals survived the procedure. Ischemic time was 14.72 (+/-0.31) h. Cardiac output, systemic arterial pressure, and arterio-venous oxygen difference decreased while systemic vascular resistance, pulmonary vascular resistance, and shunt increased during the study. Mean pulmonary artery pressure correlated with pulmonary vascular resistance (p < .01). Oxygen tension diminished significantly at 180 min after reperfusion. Mean basal pulmonary arterial TxB2 was 3589 (+/-424) pg/ml; mean plasma pulmonary venous TxB2 was 6578 (+/-1571) pg/ml. Pulmonary arterial to venous TxB2 ratio (a/vTxB2) increased from 0.70 at basal measurement to 0.83 at 60 min, and 0.99 at 120 and 180 min after reperfusion (p < .05). Pulmonary arterial TxB2 had a positive correlation with mean pulmonary artery pressure (p < .05); also, a/v pITxB2 correlated with pulmonary vascular resistance (r = .616, p < .01). Mean post-reperfusion lung weight increase was 74.88% (45.37 g). In conclusion, pITxB2 a/v ratio ratio increases after reperfusion of a 14-h preserved lung; pulmonary vascular resistance significantly increases after 180 min of reperfusion and correlates with the increase in pITxB2 a/v ratio.

Animals↗
PubMed1990

Effects of haemorrhage and volume expansion on portal-systemic collateral vascular resistance in conscious portal hypertensive rats.

1. In order to study the acute effects of blood volume changes on the vascular resistance of portal-systemic collaterals (collateral vascular resistance), a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the rat. In this model, we determined the haemodynamic effects of haemorrhage (1.8 ml/100 g body weight) or intravenous infusion of a volume expander (1.8 ml/100 g body weight). Cardiac output and regional blood flows were measured by the radioactive microsphere method. 2. Haemorrhage significantly reduced arterial pressure from 108 +/- 4 to 92 +/- 4 mmHg (mean +/- SEM), cardiac output from 56 +/- 4 to 24 +/- 2 ml min-1 100 g-1 body weight, portal pressure from 15.1 +/- 1.5 to 10.0 +/- 1.4 mmHg and portal tributary blood flow from 19.9 +/- 2.3 to 8.3 +/- 1.4 ml/min. Consequently, collateral vascular resistance significantly increased from 6.6 +/- 0.9 x 10(3) to 11.1 +/- 2.0 x 10(3) kPa 1(-1) s. 3. Volume expansion reduced arterial pressure from 98 +/- 3 to 90 +/- 3 mmHg, and significantly increased cardiac output from 43 +/- 3 to 55 +/- 3 ml min-1 100 g-1 body weight, portal pressure from 13.9 +/- 0.7 to 16.5 +/- 0.8 mmHg and portal tributary blood flow from 16.4 +/- 1.3 to 28.2 +/- 3.2 ml/min. Consequently, collateral vascular resistance significantly decreased from 7.0 +/- 0.5 x 10(3) to 4.9 +/- 0.4 x 10(3) kPa l-1 s. 4. This study shows that in rats with portal hypertension, portal-systemic collateral vascular resistance is modified by alterations in blood volume.

Animals↗
PubMedDate not supplied

Pulmonary vascular resistance and the risk of heart transplantation.

Elevated pulmonary vascular resistance was an incremental risk factor for premature death after heart transplantation (p = 0.0002). Its effect was continuously variable and not dichotomous (yes or no). The rate of rise in risk of death corresponded quite evenly to the progressive increase in pulmonary vascular resistance from low to high values, rather than abruptly increasing at a certain point. This effect was incremental to the risk imposed by congenital heart disease (in contrast to idiopathic or ischemic cardiomyopathy). Expression of the pulmonary vascular resistance in units times square meters provides more accurate predictions than expression in Wood units (p for difference = 0.03).

Heart Transplantation↗
PubMed1989

Vascular resistance of arterioles with nonuniform diameters.

Arterioles in various vascular beds have been often observed to have nonuniform diameters along the vessel axis. The effect of nonuniformity of arteriolar diameter on vascular resistance was investigated using a theoretical model of blood flow in arterioles. Viscous flow of a Newtonian fluid in tubes with periodically changing diameters along the tube axis was analyzed by a finite element method based on the Stokes equations. Vascular resistance for the nonuniform tube was computed over a spatial period of the variation in diameter and was compared to resistance for a uniform tube with a constant diameter equal to the mean diameter of the nonuniform tube. In all cases, resistance for a tube with a nonuniform diameter was larger than resistance for a uniform tube with a diameter equal to the mean diameter of the nonuniform tube. Increases in the amplitude of the variation in diameter resulted in a rapid increase in resistance when the period of the variation remained constant. On the other hand, as the period of the diameter variation increased when amplitude remained constant, resistance decreased and approached the values obtained under the assumption of a Poiseuille flow at each cross section of the tube in the limit of an infinite period. Our theoretical model was applied to our previous in vivo studies of vessel diameter nonuniformity for rabbit mesentery arterioles in a contracted state. It was shown that vascular resistance calculated by our model was 2 to 11% higher than resistance obtained for a uniform tube with a diameter equal to the mean diameter of the arteriole.

Animals↗
PubMed1994

Nitric oxide regulates basal systemic and pulmonary vascular resistance in healthy humans.

BACKGROUND: The endothelium synthesizes and releases a relaxing factor with the physiochemical properties of nitric oxide (NO). However, the role of endothelium-derived NO in the basal regulation of systemic and pulmonary vascular resistance in humans is not known. Our primary objectives were to determine the effects of inhibiting NO synthesis on blood pressure and systemic vascular resistance and to establish the role of endothelium-derived NO in the regulation of normoxic pulmonary vascular tone. METHODS AND RESULTS: We studied the systemic and pulmonary hemodynamic effects of NG-monomethyl-L-arginine (L-NMMA, 0.03 to 1.0 mg.kg-1.min-1 IV), an NO synthase inhibitor, in 11 healthy volunteers, aged 33 +/- 2 years. An arterial cannula and a pulmonary artery catheter were placed in each subject to measure blood pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure. Cardiac output was determined by the Fick technique, and systemic and pulmonary vascular resistances were calculated. Serum NO levels (free and protein bound) were measured by chemiluminescence in 5 subjects. Six of the subjects also received phenylephrine (25 to 100 micrograms/min IV) to compare the cardiac hemodynamic effects of L-NMMA with those of a direct-acting vasoconstrictor. L-NMMA caused dose-dependent increases in both blood pressure and systemic vascular resistance. At the highest dose of L-NMMA, there was a 15.5 +/- 1.3% increase in mean blood pressure and a 63.4 +/- 8.2% increase in systemic vascular resistance (each P < .01). Pulmonary vascular resistance increased 39.8 +/- 9.4% (P < .01), whereas mean pulmonary artery pressure did not change. Administration of L-NMMA also reduced cardiac output by 27.8 +/- 2.9% and stroke volume by 15.4 +/- 3.5% (each P < .01). Serum NO levels decreased 65 +/- 10% from basal values (P < .05), confirming inhibition of endogenous NO production. Phenylephrine increased blood pressure to a level comparable to that observed with L-NMMA. The decline in stroke volume was greater with L-NMMA than with phenylephrine (P < .01). CONCLUSIONS: This study demonstrates that basal release of endothelium-derived NO is directly involved in the determination of systemic vascular resistance and, therefore, blood pressure in healthy humans. In addition, NO regulates basal normoxic pulmonary vascular tone. The complex hemodynamic effects of NO are composite properties of its actions on systemic and pulmonary vascular resistance and cardiac function.

Adult↗
PubMedDate not supplied

Increased coronary vascular resistance cannot be reduced by inhibiting sympathetic overactivity in hypertension.

The aim of this study was to test whether increased coronary vascular resistance in hypertensive subjects can be reduced by centrally inhibiting sympathetic overactivity with dexamethasone. Coronary vascular resistance was quantitated in 11 men with untreated mild essential hypertension (RR 149 +/- 13/98 +/- 10 mm Hg) and 23 healthy, normotensive, otherwise matched men using positron emission tomography and [(15)O]H(2)O. The measurements were performed at baseline and during adenosine stimulation. Each subject was studied twice, with and without previous dexamethasone treatment for two days (0.5 mg x 4 per day). Before dexamethasone treatment, cardiac index and plasma norepinephrine concentration (1.9 +/- 0.6 vs. 1.3 +/- 0.5 nmol/l, p < 0.01) were significantly higher in hypertensive than in normotensive subjects. Additionally, both baseline and hyperemic coronary vascular resistances were higher in hypertensive than normotensive subjects (147 +/- 31 vs. 113 +/- 24 and 36 +/- 9 vs. 25 +/- 10 mm Hg.min.g.ml(-1); p < 0.05). Dexamethasone treatment significantly decreased plasma norepinephrine concentrations in hypertensive subjects, leading to comparable plasma norepinephrine concentrations in hypertensive and normotensive subjects (1.4 +/- 0.5 vs. 1.2 +/- 0.4 nmol/l; NS). However, coronary vascular resistances remained increased in hypertensive subjects. In conclusion, hypertensive subjects are characterized by sympathetic overactivity, which can be normalized by dexamethasone. However, coronary vascular resistances remained increased in hypertensive subjects after dexamethasone treatment, suggesting that other mechanisms than sympathetic overactivity-induced vasoconstriction explain the increased coronary vascular resistance in hypertension.

Adult↗
PubMed1993

Effects of high salt intake on control of hindlimb vascular resistance by arterial baroreflex and vagal afferents in spontaneously hypertensive rats.

1. This study aimed to examine whether a high salt diet alters control of vascular resistance by arterial baroreflex and vagal afferents in spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). 2. SHR and WKY aged 8 weeks were fed either high (8%) or normal salt (0.4%) diet for 4 weeks. Arterial baroreflex control of hindlimb vascular resistance was assessed by examining reflex-induced vasodilation and vasoconstriction in response to phenylephrine and nitroprusside, respectively, in the constant-flow perfused hindlimb of urethane-anesthetized rats. 3. Tonic influence of the cardiopulmonary vagal afferents was evaluated by examining the effects of vagotomy on hindlimb vascular resistance and on the gain of arterial baroreflex control of hindlimb vascular resistance. 4. The gain of the arterial baroreflex control of hindlimb vascular resistance in response to both phenylephrine and nitroprusside were not significantly different between SHR receiving high and normal salt diets, and between WKY receiving high and normal salt diets. 5. Vagotomy increased hindlimb vascular resistance in all four groups of rats. However the high salt diet than those in SHR on a normal salt diet but similar between the two groups of WKY. Vagotomy increased the slope of arterial baroreflex control of hindlimb vascular resistance in SHR receiving a normal salt diet and the two groups of WKY but not in SHR receiving a high salt diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1997

Effects of desflurane and isoflurane on systemic vascular resistance during hypothermic cardiopulmonary bypass.

OBJECTIVE: The objective of this study was to examine the dose-related effects of desflurane and isoflurane on systemic vascular resistance during hypothermic cardiopulmonary bypass. DESIGN: Randomized, prospective trial. SETTING: University hospital. PARTICIPANTS: Sixty consenting patients, 65 years of age or older, scheduled for elective coronary artery surgery. INTERVENTIONS: Patients were randomly allocated to one of five groups to receive 0.5 or 1.0 minimum alveolar concentration (MAC) (exhaust gas concentration) desflurane or 0.5 or 1.0 MAC isoflurane during hypothermic (32 degrees to 33 degrees C) nonpulsatile cardiopulmonary bypass or to a control group that did not receive any anesthetic agent. Systemic vascular resistance index was recorded at baseline, every 2 minutes for the first 10 minutes during initial administration and every 5 minutes for another 15 minutes during maintenance of anesthesia. MEASUREMENTS AND MAIN RESULTS: In patients receiving 0.5 MAC desflurane and isoflurane, there were significant differences in systemic vascular resistance index only at 20 and 25 minutes compared with control values. In the desflurane 1.0 MAC group, significant decreases were observed at 15, 20, and 25 minutes compared with controls. In the 1 MAC isoflurane group, the 10-, 15-, 20-, and 25-minute value differed significantly from the control. There were significant decreases in systemic vascular resistance index in the 1.0 MAC groups at 20 and 25 minutes compared with 0.5 MAC values, as well. CONCLUSIONS: Equi-MAC concentrations of desflurane and isoflurane had similar effects on systemic vascular resistance; 0.5 MAC maintained systemic vascular resistance; 1.0 MAC decreased systemic vascular resistance during hypothermic cardiopulmonary bypass.

Aged↗
PubMed1986

Effect of T-2 toxin on regional blood flow and vascular resistance in the conscious rat.

The acute effect of T-2 toxemia on local blood flow and vascular resistance in hindquarter, mesenteric, and renal vascular beds was continuously measured by the directional pulsed Doppler technique in conscious, male Sprague-Dawley rats. Intravenous injection of T-2 toxin (1 mg/kg) in the conscious rat reduced blood flow and increased vascular resistance in all blood vessels studied but had no significant effect on mean arterial pressure or heart rate. The blood flow in hindquarters gradually decreased to a minimum of -77 +/- 9% (mean +/- SE) 6 hr after the toxin injection. The hindquarter vascular resistance concomitantly increased to a maximum value of +323 +/- 69% above the resistance before toxin administration. Mesenteric and renal blood flow initially increased (slightly) and then gradually decreased. The maximum drop of blood flow, -90 +/- 13% and -76 +/- 13% for the mesenteric and renal vascular beds, respectively, was achieved 4 hr after T-2 toxin injection and the blood flow values remained low for up to 6 hr. Simultaneously with the impairment of blood flow the mesenteric and renal vascular resistance increased to reach the maximal values of +404 +/- 99% and +556 +/- 15%, respectively. In addition, plasma renin activity was markedly elevated (+653 +/- 160%) at the time of reduced renal blood flow. Intravenous injection of the same value of vehicle (10% ethanol in saline) had no significant effect on any of the cardiovascular variables studied. Two of five rats in the T-2 toxin-treated group died within 5 hr after the T-2 toxin injection and only one animal survived 24 hr while all the control animals survived over 24 hr. The results suggest that strong vasoconstriction in skeletal muscle, mesenteric, and renal vascular beds leads to impairment of local blood flow. The ischemia in vital organs together with the earlier reported decrease in cardiac output by T-2 toxin might then be the cause of rapid death in acute T-2 toxemia.

Animals↗
PubMed1996

Reduced decrease of peripheral vascular resistance during exercise in young type I diabetic patients.

OBJECTIVE: In normal subjects, peripheral vascular resistance decreases during dynamic exercise. We studied blood pressure and peripheral vascular resistance responses to dynamic exercise in young normotensive type I diabetic patients. RESEARCH DESIGN AND METHODS: Thirty adolescent diabetic patients (9-19 years of age) underwent a maximal exercise test on a cycle ergometer. In a subset of 14 patients, cardiac output was measured by a CO2 rebreathing method and peripheral vascular resistance was calculated. Twenty-four normal individuals, age and sex matched, served as control subjects. RESULTS: Diastolic blood pressure was significantly higher in diabetic patients at intermediate workload (77 +/- 2 vs. 71 +/- 1 mmHg) and peak exercise (86 +/- 2 vs. 73 +/- 2 mmHg). Peripheral vascular resistance was significantly higher in diabetic patients at intermediate workload (17.0 +/- 1.1 vs. 12.6 +/- 0.5 mmHg.l-1.min-1.m-2) and peak exercise (16.3 +/- 1.3 vs. 11.4 +/- 0.5 mmHg.l-1.min-1.m-2). There were no significant correlations with the patient's age, diabetes duration, or diabetes control. CONCLUSIONS: We observed the decrease of vasodilator response during dynamic exercise in normotensive young type I diabetic patients.

Adolescent↗
PubMed1989

Relation of sinusoidal stenoses following hepatocyte swelling to hepatic vascular resistance in experimental liver cirrhosis.

To investigate the significance of sinusoidal stenoses and a decrease in the sinusoidal bed due to hepatic cell swelling as a factor increasing hepatic vascular resistance in liver cirrhosis, hepatic vascular resistance in choline-deficient diet-induced cirrhotic rats was measured by an isolated liver perfusion method. In the cirrhotic rats, the swollen hepatic cells resulting from accumulation of fat droplets narrowed the sinusoids and decreased the sinusoidal bed. Consequently, the hepatic vascular resistance was increased by 2.7 times normal (8.60 +/- 2.32 mm H2O.ml-1.min; controls, 3.13 +/- 0.67 mm H2O.ml-1.min), and portal hypertension was also recognized (188.1 +/- 26.3 mm H2O; controls, 114.2 +/- 12.8 mm H2O). In the cirrhotic rats fed with ordinary rat pellets for 2 months, however, the sinusoidal stenoses and the decreased sinusoidal bed recovered to nearly normal as a result of disappearance of the fat droplets in the hepatic cells. The increased hepatic vascular resistance was decreased to 1.5 times normal (4.68 +/- 0.82 mm H2O.ml-1.min), and the elevated portal vein pressure was reduced (141.5 +/- 17.4 mm H2O). These findings clearly demonstrate that an important factor leading to an increase in hepatic vascular resistance is sinusoidal stenoses and a decrease in the sinusoidal bed resulting from swollen hepatic cells.

Animals↗
PubMed2004

Splanchnic and peripheral vascular resistance during lower body negative pressure (LBNP) and tilt.

We tested the hypothesis that vasoconstriction in response to LBNP or head up tilt would be reflected in a reduction in splanchnic (portal vein) blood flow (PVF) and increases in forearm and total peripheral vascular resistance (TPR). Changes in vascular resistance indicators were obtained from measurement of PVF from portal vein cross-sectional area and blood velocity by Doppler ultrasound, from forearm vascular resistance (FVR, by Doppler) and total peripheral resistance (TPR, by impedance cardiography). 21 subjects were tested during LBNP (0, -10, -20 and -30 mmHg) and 9 subjects during tilt (0, 45 and 70 degrees). During progressive LBNP, PVF decreased approximately linearly with LBNP (-30, -48 and -64% at -10, -20 and -30 mmHg) and with tilt angle (-39 and -58% at 45 and 70 degrees). The increase in FVR approximately mirrored these changes during LBNP (20.1, 44.7 and 55.3%) and tilt (45.6 and 63.6%). However, the changes in TPR during LBNP (12.0, 16.9 and 26.4%) and tilt (25.2 and 29.2%) were markedly less. This observation of different percent changes in forearm versus total peripheral resistance might reflect true physiological differences in the forearm (and splanchnic) circulations compared with the whole body, or the data might suggest that impedance cardiography did not provide a reliable indicator of cardiac output and therefore TPR under these conditions. The primary observation in this study was that Doppler ultrasound measurement of portal vein blood flow provided a non-invasive estimate of splanchnic vascular resistance during postural or LBNP challenge and that using the reduction in portal vein flow as an index of increased vasoconstriction paralleled the change in forearm vascular resistance.

Arm↗
PubMed1992

The effect of calcium on pulmonary vascular resistance and right ventricular function.

Calcium chloride is frequently administered to patients immediately after separation from cardiopulmonary bypass to improve the contractile state of the myocardium. Animal studies suggest that calcium chloride may produce increases in pulmonary vascular resistance, which can precipitate right ventricular failure. In an attempt to determine the effect of calcium chloride administration after cardiopulmonary bypass on right ventricular function, this study was designed to evaluate patients with normal and elevated pulmonary vascular resistance. Fifty patients scheduled for elective cardiac surgery were prospectively studied for changes in ionized calcium levels before and after bypass. The impact of calcium administration on right ventricular function was assessed by a pulmonary artery catheter modified for the measurement of right ventricular ejection fraction. In all patients the level of ionized calcium decreased during bypass from a mean of 4.91 to 4.29 mg.dl-1. However, the infusion of calcium chloride (10 mg.kg-1) after bypass resulted in increasing the ionized calcium levels to prebypass levels. Administration of calcium chloride after bypass to patients with normal right ventricular function resulted in a transient increase in both cardiac output and right ventricular ejection fraction without any change in pulmonary vascular resistance. Eight patients with both elevated pulmonary vascular resistance and depressed right ventricular function were evaluated to determine the effect of calcium chloride after bypass on pulmonary vascular resistance and right ventricular ejection fraction. Administration of calcium chloride (10 mg.dl-1) to these patients did not result in any significant increase in pulmonary vascular resistance or depression of right ventricular performance. More important, in these patients, right ventricular ejection fraction and cardiac output were significantly increased after calcium chloride administration. In summary, the results of this study fail to demonstrate any increase in pulmonary vascular resistance or deterioration of right ventricular function with the administration of calcium chloride (10 mg.kg-1) after bypass in patients with elevated pulmonary vascular resistance.

Aged↗
PubMedDate not supplied

Effects of alpha 1 and beta-adrenergic antagonists and 5-hydroxytryptamine receptor antagonist on portal-systemic collateral vascular resistance in conscious rats with portal hypertension.

In order to study the acute effects of pharmacological agents on the vascular resistance of portal-systemic collaterals, a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the conscious rat. The haemodynamic effects of several vaso-active substances were evaluated in this model and compared with those obtained after saline administration. Prazosin (0.5 mg), an alpha 1-adrenergic antagonist, significantly reduced mean arterial pressure by 29%, portal pressure from 13.8 +/- 1.0(mean +/- s.e.m.) to 10.1 +/- 0.4 mmHg and portal tributary blood flow (radioactive microspheres) from 13.6 +/- 2.1 to 11.7 +/- 1.2 mL/min. It also decreased portal-systemic vascular resistance from 95 +/- 16 to 73 +/- 9 dyn s/cm5 x 10(3). Propranolol (4 mg), a beta-adrenergic antagonist, significantly reduced mean arterial pressure by 12% and portal pressure from 15.5 +/- 1.2 to 13.3 +/- 0.9 mmHg while reducing portal tributary blood flow from 14.6 +/- 1.5 to 11.0 +/- 1.7 mL/min and increasing portal systemic collateral vascular resistance from 88 +/- 7 to 103 +/- 8 dyn s/cm5 x 10(3). Ketanserin (0.25 mg/kg), a 5-hydroxytryptamine receptor antagonist, reduced portal pressure from 15.8 +/- 1.0 to 13.3 +/- 0.7 mmHg at a dose that did not alter mean arterial pressure or portal tributary blood flow. It achieved this by reducing portal-systemic collateral vascular resistance from 90 +/- 14 to 74 +/- 13 dyn s/cm5 x 10(3). Saline had no significant effect on systemic and splanchnic haemodynamics. This study shows that ketanserin decreases vascular resistance of portal-systemic collaterals while propranolol increases it. Thus, it is suggested that collateral vascular resistance is accessible to pharmacological manipulation.

Animals↗
PubMedDate not supplied

Evaluation of portal vascular resistance using an intraoperative Doppler ultrasound.

BACKGROUND/AIMS: To evaluate portal vascular resistance using Doppler ultrasound intraoperatively. METHODOLOGY: We measured maximum flow velocities and pressures of umbilical portion of the left portal branch before and after clamping of the right main branch of the Glisson's sheath. We proposed a new index, simplified portal resistive index, that was the ratio of the difference of the portal venous pressure to the difference of maximum portal flow velocity. RESULTS: There were good correlations between portal vascular resistance and simplified portal resistive index. Simplified portal resistive index was found to become higher as fibrotic changes progressed, and there were significant differences between normal liver, chronic hepatitis, and liver cirrhosis. CONCLUSIONS: Simplified portal resistive index evaluated using intraoperative Doppler ultrasound is an easy and reliable index for assessing portal vascular resistance during liver surgery.

Adult↗
PubMed1985

The effects of sublingually administered nitroglycerin on forearm vascular resistance in patients with heart failure and in normal subjects.

This study examined the effects of sublingually administered nitroglycerin on forearm resistance vessels in normal subjects (n = 9) and in patients with congestive heart failure (n = 8). Forearm blood flow was measured with a strain-gauge plethysmograph and forearm vascular resistance was calculated. To assess the magnitude of reflex forearm vasoconstriction triggered by decreased central venous pressure after sublingual nitroglycerin, lower body negative pressure (LBNP) was applied to produce a comparable decrease in central venous pressure to that after nitroglycerin. The change in forearm vascular resistance during LBNP was compared with that after nitroglycerin. In normal subjects, LBNP increased but nitroglycerin did not change forearm vascular resistance. In patients with congestive heart failure neither nitroglycerin nor LBNP changed forearm vascular resistance. The direct vasodilator effect of nitroglycerin on forearm resistance vessels assessed by the difference between the change in forearm vascular resistance produced by nitroglycerin and that during LBNP tended to be less in patients with congestive heart failure than in normal subjects, which might have resulted from decreased vasodilator capacity of resistance vessels in patients with congestive heart failure. Changes in forearm vascular resistance with a cold pressor test were not different between normal subjects and patients with congestive heart failure. These data suggest that in normal subjects, nitroglycerin does not alter forearm vascular resistance because its dilator effect is offset by reflex vasoconstriction. In patients with congestive heart failure, reflex vasoconstriction is impaired but the direct vasodilator effect of nitroglycerin also tends to be reduced, so that as a net effect forearm vascular resistance is not altered.

Adult↗