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Results for “VASCULAR RESISTANCE”

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At least 325 records · Page 18Linked to original sources

PubMed1998

[Diagnostic and prognostic value of vascular resistance in breast tumors].

AIM AND METHOD: In a prospective study of 113 patients with breast tumours, we measured the vascular resistance index (mean RI) of physiologic tissue and the tumour by using pulsed colour coded Doppler sonography. RESULTS: The group of carcinomas showed a significantly higher mean RI (0.71 +/- 0.09 SD) compared to the group of benign tumours (0.66 +/- 0.09 SD) (p = 0.003). After dividing the groups according to menopausal status, this difference disappeared. In general the mean RI was higher in postmenopausal women. Only premenopausal women showed a significantly higher mean RI within the carcinoma (0.69 +/- 0.1 SD) compared to physiological tissue (0.65 +/- 0.07 SD, p = 0.02). The mean RI measured in the tumour area from carcinomas correlated with the S-phase fraction: r = -0.53 (p = 0.003). CONCLUSION: Mean RI reflects vascular resistance but does not allow discrimination between benign or malignant and is significantly influenced by menopausal status. The dynamics of proliferation and low vascular resistance seem to depend on each other. All these facts should be considered when doing Doppler sonographic examination of the breast.

Adult↗

PubMed1986

Estimation of pulmonary vascular resistance by MRI in patients with congenital cardiovascular shunt lesions.

The intensity of the magnetic resonance signal in the pulmonary arteries was assessed in 15 patients with congenital left to right shunts and in 10 normal volunteers, using an ECG-gated multislice spin-echo technique. In normal subjects, magnetic resonance signal was only observed in great vessels of the thorax on images acquired near end-diastole; they disappeared in systole. Among the group of 15 patients, 10 had severe pulmonary hypertension (systolic pressures greater than 80 mm Hg) with severe elevation of pulmonary vascular resistances (greater than 787 dynes cm sec-1). The magnetic resonance signal persisted in systole in all 10 patients, and its intensity could be quantitatively assessed. On the other hand, in one other patient with high pulmonary artery pressure but only moderate elevation of pulmonary vascular resistance, and in patients with moderate pulmonary hypertension and normal pulmonary vascular resistance, the intravascular signal was minimal and no different from the signal recorded in normal subjects. A direct linear relationship was found between the pulmonary vascular resistance and the intensity of the magnetic resonance signal in the right pulmonary artery during systole (r = 0.84). An even closer correlation was found for the linear relationship between the ratio pulmonary vascular resistance/systemic resistance and the magnetic resonance signal in the right pulmonary artery (r = 0.93). Thus, magnetic resonance, with its sensitivity to slow-flow conditions, can potentially provide physiological information in congenital cardiovascular disease.

Adolescent↗

PubMed1985

Pulmonary vascular resistance during unilateral pulmonary arterial occlusion in ducks.

We measured mean pulmonary arterial pressure (Ppa) during temporary unilateral pulmonary arterial occlusion (TUPAO) in 10 ducks. Ppa increased from 11.4 +/- 0.8 mmHg during control conditions to 18.8 +/- 1.8 during TUPAO. In 5 of the 10 ducks we also measured mean left atrial pressure (Pla) and cardiac output (Q). In these ducks Ppa significantly increased with TUPAO from 13.9 +/- 0.4 to 22.0 +/- 1.2 mmHg, whereas Pla and Q did not change significantly. Pulmonary vascular resistance (PVR) increased from 10.6 +/- 1.3 to 24.1 +/- 5.3 mmHg X min X 1(-1) on TUPAO. By assuming equal vascular resistance in either lung it can be calculated that the vascular resistance in only one lung was 22.5 +/- 3.5 mmHg X min X 1(-1) during control conditions. Thus doubling flow resulted in no significant change in one lung's vascular resistance. A morphometric study of both lungs of a domestic goose that were rapidly frozen during TUPAO indicated very little compliance in pulmonary blood capillaries. The relative volume of exchange tissue occupied by blood capillaries was 0.28 in the occluded lung and 0.36 in the perfused lung. Surface-to-volume ratios of blood capillaries were 12,524 cm-1 in the occluded lung and 11,056 cm-1 in the perfused lung. We conclude that PVR in birds is relatively insensitive to changes in Q, in contrast to mammals.

Animals↗

PubMed1981

Improved right ventricular function and reduced pulmonary vascular resistance during prazosin therapy of congestive heart failure.

Although the effect of systemic vasodilator therapy on left ventricular function in congestive heart failure has been extensively evaluated, little is known about its effect on pulmonary vascular resistance and right ventricular function. Since pulmonary vascular resistance is mediated in part by alpha-adrenergic receptors, we studied the effects of the alpha-adrenergic antagonist prazosin on right ventricular function as determined by a radionuclide ventriculographic technique which assessed right and left ventricular ejection fractions simultaneously. In 11 patients treated for two months with prazosin, right ventricular ejection fraction increased from 0.28 +/- 0.04 to 0.44 +/- 0.07 (p less than 0.01). In 10 patients who received a single dose of prazosin 48 hours after withdrawal of prior prazosin therapy, right ventricular ejection fraction increased from 0.29 to 0.05 to 0.38 +/- 0.06 (p less than 0.02). In nine patients who received a single dose of prazosin during right sided heart catheterization, pulmonary vascular resistance decreased from 358 +/- 70 to 236 +/- 60 dyne-sec-cm -5 (p less than 0.01). These studies suggest that prazosin has beneficial effects on right ventricular function both immediately and long-term in patients with severe congestive heart failure. Although the mechanism of this effect is not known, possibilities include a direct effect of prazosin on the pulmonary vasculature, a secondary reduction in right ventricular afterload due to improved left ventricular performance and a withdrawal of reflex-mediated pulmonary vasoconstriction due to improved left ventricular performance.

Adrenergic alpha-Antagonists↗

PubMed1985

Studies on the effects of felodipine on the vascular resistance and reactivity in pentobarbital anesthetized dogs.

Bilateral perfused hindlimb preparations in pentobarbital anesthetized dogs were utilized in the present study to evaluate vasodilator effects of felodipine, in the presence and in the absence of sympathetic neurogenic tone. Vascular resistance was evaluated by establishing pressure-flow characteristics. A lower dose of this agent (0.01 mumol/kg i.v.) produced significant reductions in the systemic arterial blood pressure and vascular resistance only in the innervated but not in the denervated limb. This effect was shown to be due to interference with noradrenaline induced vasoconstriction. However, a tenfold higher dose of felodipine (0.1 mumol/kg i.v.) was indeed effective in attenuating resistance in the denervated vascular bed; this ability of the higher dose (0.1 mumol/kg) to inhibit vascular resistance may be due to an additional intracellular action of this drug affecting myogenic tone and/or due to inhibition of the vascular effects of the endogenous renin-angiotensin system. In the present experimental model, felodipine, a dihydropyridine calcium antagonist, was equally effective in inhibiting either alpha 1- or alpha 2-mediated vasoconstriction. These data suggest that the ability of felodipine to interfere with sympathetic vasoconstrictor mechanisms primarily contributes to its hypotensive effects in the barbiturate-anesthetized dogs.

Angiotensin II↗

PubMed1999

Effects of dipyridamole, nitroglycerin, and nitroprusside on coronary vascular resistance in rabbits: measurement with pulsed Doppler velocimetry.

Dipyridamole, nitroglycerin, and nitroprusside are all effective vasodilators. However, few studies have compared their in vivo coronary vasodilatation effects. The purpose of this study was to compare the effects of these agents on coronary blood flow velocity and vascular resistance in anesthetized, open-chest rabbits. Male New Zealand white rabbits were anesthetized, and a 3-mm, suction-type, pulsed Doppler velocimeter probe was applied to the proximal part of the left anterior descending coronary artery after median sternotomy. The rabbits received infusion of various doses of dipyridamole (0.1 mg/kg, n = 5; 1 mg/kg, n = 5; 10 mg/kg, n = 9), nitroglycerin (0.01 mg/kg, n = 8; 0.1 mg/kg, n = 5; 1 mg/kg, n = 5; 10 mg/kg, n = 7), or nitroprusside (0.01 mg/kg, n = 5; 0.1 mg/kg, n = 5; 1 mg/kg, n = 5). The percent changes in coronary blood flow velocity and coronary vascular resistance were measured. All three vasodilators increased coronary blood flow velocity significantly and decreased coronary vascular resistance dose-dependently. The dose-response curves of dipyridamole, nitroglycerin, and nitroprusside were significantly different from one another (p < 0.01). Dipyridamole at a dose of 10 mg/kg produced the greatest increase in coronary blood flow velocity and the greatest reduction in coronary vascular resistance in anesthetized, open-chest rabbits.

Analysis of Variance↗

PubMed1977

Influence of coronary occlusion on pulmonary vascular resistance in anesthetized dogs.

The effects of occlusion of the left anterior descending coronary artery on pulmonary hemodynamics and calculated pulmonary vascular resistance were measured in 17 open chest dogs anesthetized with chloralose. Coronary occlusion was associated with a slight but insignificant increase in mean pulmonary arterial pressure together with a significant elevation in mean left atrial pressure (P less than 0.01) and a significant reduction in mean pulmonary flow (P less than 0.01). Calculated pulmonary vascular resistance was significantly reduced during occlusion (P less than 0.01). The reduction in resistance was associated with elevated mean left atrial pressure and therefore reflected passive distension of pulmonary vessels secondary to suppressed left ventricular function. In contrast, coronary occlusion after vagotomy was not associated with a significant reduction in pulmonary vascular resistance, and in six experiments the decrease in resistance was converted to an increase. It is concluded that, before vagotomy, pulmonary hemodynamics during coronary occlusion are primarily affected through passive vessel distension whereas, after vagotomy tonic suppression of sympathetic activity is interrupted, thereby allowing enhancement of sympathetic vasoconstrictor activity to the pulmonary vascular bed and producing an increase in calculated resistance.

Animals↗

PubMed1991

The effect of selective umbilical embolization on the common umbilical artery pulsatility index and umbilical vascular resistance in fetal sheep.

In eight anaesthesized fetal sheep (gestational age 112-127 days; term 147 days), embolization of the umbilical placental circulation was performed in order to evaluate the response of the umbilical artery pulsatility index to an exclusive increase in umbilical vascular resistance. Measurements were performed using a 20 MHz pulsed Doppler transducer and an electromagnetic flow meter mounted on the common umbilical artery and catheters at the aortic trifurcation and in one of the umbilical veins. Umbilical vascular resistance was calculated according the Poiseuille equation as the ratio of aortic to umbilical venous pressure gradient and umbilical blood flow. Microspheres were administered at 15-min intervals through a catheter in one of the cotyledonary arteries, until fetal heart rate had decreased beneath 100 beats/min or had become arrhythmic. The period of examination per fetus varied between 60 and 120 min, after which cardiac decompensation occurred. During this period, umbilical perfusion pressure increased from 20.3 +/- 4.9 to 28.1 +/- 4.7 mmHg (SD; P less than 0.01), umbilical blood flow (ml/min) decreased from 342 +/- 127 to 115 +/- 99 mmHg (SD; P less than 0.01), umbilical vascular resistance increased from 0.065 +/- 0.022 to 0.342 +/- 0.150 mmHg.min/ml (P less than 0.01) and common umbilical artery pulsatility index increased from 0.97 +/- 0.23 to 4.03 +/- 1.69 (P less than 0.01). Fetal heart rate did not change significantly (168 +/- 33 prior to cardiac decompensation versus 178 +/- 19 beats/min at baseline condition). The linear correlation between common umbilical artery pulsatility index and umbilical vascular resistance varied between 0.83 and 0.99 and the average correlation was 0.93 (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Local angiotensin-converting enzyme inhibition blunts endothelin-1-induced increase in forearm vascular resistance.

OBJECTIVE: The physiologic role of endothelin-1 is not well established; however, it may have a role in modulation of peripheral vascular tone complimentary to angiotensin II. In vitro and animal studies suggested an interrelationship between angiotensin II and endothelin-1 vasoconstriction. We hypothesized that local vascular or systemic renin-angiotensin II systems must be intact for endothelin-1-mediated vasoconstriction in humans. METHODS: To test this hypothesis, responses to brachial artery infusion of endothelin-1 alone and endothelin-1 plus local low-dose infusion of enaliprilat were studied in seven healthy male and seven healthy female volunteers. RESULTS: In these subjects, baseline forearm vascular resistance (mean +/- SEM; 24 +/- 3.5 mm Hg.ml/dl forearm vol/min) increased with a 38.2 ng/min endothelin-1 infusion (61.8 +/- 6.8 mm Hg.ml/dl forearm vol/min; p < 0.01). Forearm vascular resistance decreased when 38.2 ng/min endothelin-1 was infused concomitantly with a local 5 micrograms/min infusion of enaliprilat (45.5 +/- 5.9 mm Hg.ml/dl forearm vol/min; p < 0.01 compared with endothelin-1 alone). CONCLUSIONS: These data indicate that an endothelin-1-induced increase in forearm vascular resistance is inhibited by local forearm angiotensin-converting enzyme inhibition.

Adult↗

PubMed1975

Endotoxin, prekallikrein, complement and systemic vascular resistance. Sequential measurements in man.

Eighteen patients were studied prior to and again within 6 hours after transurethral resection or cystoscopy. In addition to hemodynamic measurements, detection of endotoxin by limulus assay and bacteriologic sampling; prekallikrein, C3, C3 proactivator and lysosomal enzyme levels were measured. In five patients limulus assays were positive, and in one, gram-positive bacteremia developed but limulus assay remained negative. All six had significant decreases in prekallikrein, C3 or C3 proactivator. Systemic vascular resistance fell in all six. Four additional patients who had a decrease in systemic vascular resistance were not endotoxemic or bacteremic; one of these had a decrease in prekallikrein only. In the remaining eight patients with neither bacteremia nor endotoxemia, systemic vascular resistance did not change or increase after instrumentation. One had a decrease in C3 proactivator, another in prekallikrein. There was no significant difference in age, disease, antibiotic therapy or bactermia in the two groups of patients. Four of the five resectional procedures were performed in the group that showed decreases in systemic vascular resistance. The data suggest that acute endotoxemia or gram-positive bacteremia in man is associated with depletion of prekallikrein, decreased peripheral resistance and, in some instances, activation of the complement system.

Aged↗

PubMed1987

On-line recording of vascular resistance in isolated canine renal artery by use of a differential pressure transducer.

For the assessment of the validity of the perfusion system of vascular segments, both isolated canine renal artery in cylindrical form and artificial tubing were perfused intra- and extraluminally, and vascular resistance was continuously recorded by use of a differential pressure transducer. The model experiments using artificial tubing showed that the vascular resistance, inversely related to outflow and differential pressure, enormously increased when the lumen was occluded more than 85% of the control. Various agonistic stimuli such as norepinephrine, phenylephrine, methoxamine, prostaglandin F2 alpha and 5-hydroxytryptamine, when administered intraluminally, increased the vascular resistance, while verapamil and papaverine decreased it. Transmural electrical stimulation also increased the resistance which was susceptible to tetrodotoxin. The removal of endothelium by infusion of saponin augmented the contractile responses to agonistic stimuli such as norepinephrine and 5-hydroxytryptamine. The results indicate that the present perfusion method seems to be a good alternative for studying contractile activity and endothelium function of isolated vascular tissues.

Animals↗

PubMed1978

Influence of hypoxia on the longitudinal distribution of pulmonary vascular resistance.

We have examined the influence of hypoxia on the longitudinal distribution of vascular resistance and intravascular pressure in isolated cat lungs using the low-viscosity bolus technique. Hypoxia increased total vascular resistance, decreased total lung blood volume, and moved the maximum local resistance downstream away from the main pulmonary artery. The circumference of the main pulmonary artery was increased and the extravascular lung water (double indicator dilution technique) was decreased by hypoxia. Thus, it would appear that distension of the large pulmonary arteries and a decrease in the amount of lung tissue perfused contributed to the change in resistance distribution brought about by hypoxia.

Animals↗

PubMed1985

Pulmonary and systemic hemodynamic responses to ketamine in infants with normal and elevated pulmonary vascular resistance.

Avoidance of ketamine has been recommended in children with pulmonary hypertension or with limited right ventricular reserve, despite absence of data about the effects of ketamine on pulmonary vascular resistance (PVR) in children. Ketamine has been associated with increased PVR in studies of adults; in these studies adults were spontaneously breathing through unprotected airways, despite ketamine's known effects of ventilatory depression and partial loss of airway. The authors measured pulmonary and systemic hemodynamic responses to ketamine during spontaneous ventilation in 14 intubated infants who were receiving minimal ventilatory support with an intermittent mandatory ventilation (IMV) of 4 at an FIO2 of 0.3-0.4. No significant changes were found in cardiac index (CI), pulmonary vascular resistance index (PVRI), or systemic vascular resistance index (SVRI) in a group of seven infants with normal PVRI or in another group of seven infants with preexisting increased PVRI. Results did not differ in infants receiving diazepam sedation. The authors conclude that ketamine has little effect on baseline hemodynamics in mildly sedated infants whose airway and ventilation are maintained; in particular, PVRI is little changed by ketamine administration in ventilated infants with either normal or increased baseline PVRI.

Blood Gas Analysis↗

PubMed1983

Vascular resistance during cardiopulmonary bypass. Its effect on cardiac performance in the immediate post-bypass period.

A clinical study was undertaken to measure changes in systemic vascular resistance during cardiopulmonary bypass in 56 adults. Forty-five patients showed a rise in systemic vascular resistance and 77% required no inotropic support in the immediate post-bypass period. Eleven of the 33 patients undergoing valve replacement surgery showed only a small increase or an actual decrease in systemic vascular resistance and required inotropic support. These results were statistically significant. Factors affecting cardiac performance are discussed.

Cardiopulmonary Bypass↗

PubMed1993

Effect of nitric oxide and cyclooxygenase products on vascular resistance in dog and rat lungs.

Pulmonary vascular resistance decreases with increased cardiac output. Because nitric oxide (NO) and prostacyclin are potent vasodilators that are released with increased shear stress, their roles in the control of pulmonary vascular pressure were evaluated using isolated blood-perfused rat and dog lungs. Lungs were perfused with an initial arteriovenous pressure gradient (Ppa-Ppv) of 15 cmH2O; Ppa and Ppv were increased by the same amount, and the flow was measured. In rat lung (n = 6), the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) decreased pulmonary blood flow by approximately 50% at the same pressure (P < 0.05), whereas the cyclooxygenase inhibitor indomethacin (n = 6) had no effect. In dog lungs (n = 6), indomethacin decreased pulmonary blood flow by approximately 50% at the same pressure gradient (P < 0.05), whereas L-NAME (n = 6) had no effect. Furthermore, the flow increase that occurs as venous and arterial pressures are elevated together (so that Ppa-Ppv is constant) was inhibited by L-NAME in rat lungs and by indomethacin in dog lungs (P < 0.05 for each). Plasma guanosine 3',5'-cyclic monophosphate (cGMP) rose with increased absolute pressure in rat lung [from 71 +/- 17 to 274 +/- 104 pM (P < 0.05)], and this increase was blocked by L-NAME. Plasma cGMP was unchanged in dog lung, but the ratio of prostacyclin to thromboxane tended to be higher.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Effects of different training intensities on the cardiopulmonary baroreflex control of forearm vascular resistance in hypertensive subjects.

We recently reported that ambulatory blood pressure decreased during the awake period after training at low intensity but not after training at moderate intensity in subjects with mild to moderate hypertension. The reasons for the failure of moderate-intensity training to reduce blood pressure are not clear. In the present article, we report the effects of different training intensities on cardiopulmonary baroreflex control of forearm vascular resistance, left ventricular function, vascular reactivity, and resistive vessel structure. After moderate-intensity training, the cardiopulmonary baroreflex control of forearm vascular resistance was significantly attenuated, left ventricular performance was enhanced, and vascular reactivity and resistive vessel wall thickness in the calf were reduced compared with values after the control sedentary period. No significant changes in these indexes were found after low-intensity training compared with sedentary values. These results indicate that attenuation of the cardiopulmonary baroreflex control of skeletal muscle vascular resistance after training at moderate intensity may contribute to the lack of antihypertensive effects, as seen from unchanged ambulatory blood pressure levels during the awake period, after training at this intensity. A decreased vascular smooth muscle response to sympathetic nervous stimulation appears to be partly involved in the alteration in the baroreflex control of forearm vascular resistance after moderate-intensity training. Although these findings should be confirmed in a greater number of subjects, the present results point to a key mechanism that might explain why moderate endurance exercise training fails to lower arterial blood pressure in hypertensive subjects.

Adult↗

PubMed1989

Effects of distention and neostigmine on jejunal vascular resistance, oxygen uptake, and intraluminal pressure changes in ponies.

The influence of distention (high baseline intraluminal pressure) and neostigmine methylsulfate on intestinal vascular resistance, oxygen uptake, and intraluminal pressure changes (rhythmic contractions) was studied in terminal jejunal segments, which were perfused at a constant rate, in 16 anesthetized ponies. When baseline intraluminal pressure was increased to 10 mm of Hg, the intestinal vascular resistance and amplitude of rhythmic contractions were increased. Neostigmine induced cyclic increases in amplitude of rhythmic contractions whether intraluminal pressure was 0 or 10 mm of Hg. Neostigmine also increased intestinal oxygen uptake at intraluminal pressures of 0 mm of Hg, but not at 10 mm of Hg, and vascular resistance was not altered at either intraluminal pressure. The results indicate that intestinal hemodynamics are adversely affected by distention. Further, neostigmine did not adversely affect intestinal hemodynamics while increasing rhythmic contractions, suggesting that neostigmine may be useful in the treatment of ileus in equids.

Animals↗

PubMed1985

[The effect of oxedrine on the left ventricle and peripheral vascular resistance].

The sympathomimetic substance oxedrine (Sympatol) influences, by means of its affinity to alpha- and beta-receptors, cardiac performance and peripheral vascular tone. We studied in 12 healthy male volunteers the influence of intravenous oxedrine on left ventricular contractility parameters as estimated by TM-echocardiography, on cardiac index as well as on arterial blood pressure and peripheral vascular resistance. Under continuous intravenous infusion of 4 mg/min oxedrine the systolic and mean arterial blood pressure increased significantly (p less than 0.005) while the diastolic pressure and heart rate remained unchanged. The cardiac index increased (p less than 0.001) and the peripheral vascular resistance decreased significantly (p less than 0.01). The echocardiographically determined left ventricular contractility parameters, i.e. systolic shortening fraction (SF) as well as maximal velocity of shortening of the left ventricular diameter (VCFmin) also increased significantly (p less than 0.001 and 0.005, resp.). An increase in left ventricular contractility and cardiac index with concomitant decrease of peripheral vascular resistance and without increase in heart rate implies an economical increase in cardiac performance under intravenous infusion of oxedrine.

Adult↗