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Results for “VASCULAR RESISTANCE”

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PubMed1980

Renin secretion and renal vascular resistance following prolonged administration of desoxycorticosterone (DOC) in rats drinking normal saline.

1. The effect of long-term administration of desoxycorticosterone (DOC)-saline on arterial blood pressure, renal vascular resistance and renin secretion rate was studied in the rat. 2. Renin secretion rate and peripheral plasma renin activity was markedly reduced in the DOC-saline treated rats. Renal vascular resistance was comparable to that found in a corresponding control group. Responsiveness to isoprenaline suggested that the beta-adrenoceptor mediating renin release was grossly intact. 3. A significant rise in blood pressure occurred in only 50% of the treated animals: However, no differences in weight gain, renal vascular resistance or renin levels were apparent when compared with animals which remained normotensive. 4. These findings indicate that suppression of renin secretion during prolonged DOC-saline administration cannot be directly attributed to changes in arterial pressure, renal vascular resistance or beta-adrenoceptor sensitivity.

Animals↗

PubMed1980

Regional differences in pulmonary vascular resistance in the same patient. A study of partial anomalous pulmonary venous return, intact atrial septum, and mitral stenosis before and after surgical correction.

Using hemodynamic and radionuclide perfusion data, we measured regional pulmonary vascular resistances in a patient with mitral stenosis and anomalous pulmonary venous drainage with intact atrial septum before and after surgical correction. Pulmonary vascular resistance in the right upper lung region that had anomalous drainage to a normal-pressure right atrium was compared to resistance of a region in the left upper lung similar in size that had normal drainage to a high-pressure left atrium. Preoperatively, pulmonary vascular resistance in both regions was elevated but was considerably higher in the left upper lung region. Postoperatively, pulmonary vascular resistance fell substantially in the left upper lung with the fall in left atrial pressure, whereas it changed minimally in the right upper lung after elimination of the left-to right shunt. These findings are related to vascular abnormalities on biopsies obtained from both regions.

Female↗

PubMed1995

Assessment of stenoses in the aortoiliac tract by calculation of a vascular resistance change ratio before and after exercise.

OBJECTIVES: Intraarterial pressure measurement is the most reliable method to assess haemodynamically significant stenoses in the aortoiliac tract. We have tried to develop a simple and quick, non-invasive method to assess stenoses of this type. DESIGN: Prospective semi-blinded clinical study. METHODS: It was postulated that a haemodynamically significant aortoiliac tract stenosis would result in a lesser degree of vascular resistance decrease after vasodilatation, compared to patients only suffering from femorodistal stenoses. We approximated vascular resistance by: (brachial pressure-ankle pressure)/femoral artery mean Doppler velocity. By dividing vascular resistance at rest by vascular resistance after exercise, we calculated the Resistance Change Ratio (RCR). PATIENTS AND RESULTS: In 34 patients (50 legs) with arterial stenoses, the pressure gradient over the aortoiliac segment was compared to the RCR. Legs were divided in three groups: group 1 consisted of 22 legs that showed a pressure gradient > 10 mmHg at rest; group 2 showed a pressure gradient > 10 mmHg after papaverine; group 3 showed a pressure gradient of 10 mmHg or less. The median RCR was: 0.74 (range: 0.23-4.04) for group 1, 0.71 (range: 0.36-1.80) for group 2 and 0.93 (range 0.36-2.06) for group 3. There was no significant difference between the groups (p = 0.19). CONCLUSION: The RCR could not be used to accurately detect stenoses in the aortoiliac.

Aorta, Abdominal↗

PubMed1997

The adrenal-renal vascular connection contributes to increase in renal vascular resistance during an experimental hypotension in the rat.

The adrenal vascular connection (ARVC) was described for the first time in the cat by Cow (1914) and by other authors in the dog, rat, rabbit and humans. The aim of the present study is to investigate the role of above connection in regulation of renal vascular resistance (RVR), and renal blood flow (RBF) during decrease in blood pressure in the rat. Animals were divided into three groups. In the first group, mean arterial pressure (MAP) was unchanged. In the second and the third group MAP was maintained at 50 mmHg. In addition in the third group, an alpha adrenergic receptor blockade was produced with intravenous infusion of phentolamine. After stabilisation of RBF, in all groups, the tissue between the adrenal gland and the kidney was cut. RBF and MAP were measured and recorded. In the first and the third group, the elimination of ARVC neither influenced RBF nor RVR. In the second group the elimination of ARVC caused increase in RBF and decrease in RVR (p < 0.01). Results of the present study provide the evidence that catecholamines reaching the kidney, directly from the adrenal gland through ARVC, during the severe hypotension are responsible for reducing of renal blood flow and increase in renal vascular resistance in the rat.

Adrenal Glands↗

PubMed1983

Hyaluronidase reversal of increased coronary vascular resistance in ischemic rat hearts.

Testicular hyaluronidase prevents increased coronary vascular resistance (CVR) during prolonged myocardial ischemia. The mechanism is unknown, but edema and contracture both have been suggested to increase CVR. Additionally, the extent of contracture has been inversely related to ATP levels. Therefore, isolated perfused ischemic rat hearts were treated with hyaluronidase, following a 25% increase in CVR, to determine whether 1) increased CVR was reversed, 2) edema or contracture was reduced, and 3) tissue ATP levels were increased. Three hours of low-flow ischemia decreased coronary flow (CF) from 17.4 +/- 0.13 to 12.6 +/- 0.2 ml X min-1 X g dry tissue-1. During the subsequent 2 h of ischemia, CF of vehicle-treated hearts continued to decline to 8.0 +/- 0.76 ml X min-1 X g dry tissue-1, whereas CF of hyaluronidase-treated hearts increased to 15.6 +/- 1.17 ml X min-1 X g dry tissue-1. These changes in CF persisted during postischemic perfusion. Furthermore, restoration of coronary vascular resistance by hyaluronidase was associated with a 19% reduction in tissue water compared with control ischemic hearts but not with a reduction in cardiac contracture or an increase in tissue ATP. These results suggest that treatment of ischemic hearts with hyaluronidase reverses increased CVR through a reduction in tissue edema.

Adenosine Triphosphate↗

PubMed1988

Vascular resistance is decreased in the luteal rat ovary by a 20 minute continuous infusion of noradrenaline.

The effect of a 20 min continuous infusion of noradrenaline (2 nanomoles/min) on the blood flow and vascular resistance of 2-, 6- and 11-day-old corpora lutea from adult pseudopregnant rats was studied. Pseudopregnancy was induced by mating with vasectomized male rats. The blood flow of the corpus luteum and the remaining ovary was measured with the microsphere technique. The basal blood flow varied between the luteal ages studied and was highest at day 6 of pseudopregnancy. Noradrenaline induced a two-fold increase in the blood flow of the corpus luteum at the luteal ages studied. The vascular resistance (blood pressure/blood flow) decreased for all luteal ages, while the vascular resistance for kidney, spleen and diaphragm was unchanged. Antidiuretic hormone was found to markedly decrease the luteal blood flow and the vascular resistance remained increased. The effect of noradrenaline infusion on the luteal blood flow thus in contrast to other vasoactive substances is biphasic, with an initial vasoconstriction followed by vasodilatation.

Animals↗

PubMed1994

Effect of inhaled nitric oxide on raised pulmonary vascular resistance in children with congenital heart disease.

OBJECTIVE: To study the short-term effects of inhaled nitric oxide in infants and young children with congenital heart disease. SETTING: A supraregional referral centre for children with congenital heart disease. PATIENTS AND METHODS: 22 infants and children aged 3-32 months (median age 5 months) with congenital heart disease undergoing preoperative cardiac catheterisation. All but one infant had intracardiac shunt lesions and 13 had increased pulmonary vascular resistance. During catheterisation the patients inhaled nitric oxide in a concentration of 40 parts per million in room air. Pulmonary and systemic haemodynamic variables were evaluated by means of measured oxygen consumption and the Fick principle before and after 10 minutes' exposure to nitric oxide. RESULTS: Inhaled nitric oxide did not affect the systemic circulation. There was a significant reduction in the pulmonary vascular resistance, but only in the 13 infants with pulmonary hypertension, in whom pulmonary vascular resistance was reduced by 34% from 8.6 (4.6) mm Hg.min.m2.l-1 (mean (SD)) to 5.7 (3.5) mm Hg.min.m2.l-1. The pulmonary circulation in infants with normal pulmonary vascular resistance was not affected. No statistically significant increase in methaemoglobin was seen, though there were large individual differences. No other side effects were seen. CONCLUSION: The present study shows that in infants with congenital heart disease inhaled nitric oxide reduced pathologically increased pulmonary vascular resistance without affecting systemic circulation and without important side effects with brief exposure.

Administration, Inhalation↗

PubMed2000

Adenosine and nitric oxide regulate regional vascular resistance via interdependent and independent mechanisms during sepsis.

OBJECTIVE: Adenosine receptor blockade increases regional resting vascular resistance during sepsis. In healthy subjects, part of adenosine's actions are mediated via stimulation of nitric oxide synthase. Because nitric oxide synthase activity is thought to be a major contributor to altered vascular tone in sepsis, we tested the hypothesis that some of the nitric oxide-mediated resting regional resistance during sepsis is secondary to endogenous adenosine stimulation of nitric oxide synthase. DESIGN: Prospective, randomized, controlled experiment. SETTING: Shock-trauma and basic science laboratory. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: Twenty-four hours after sepsis or sham induction, rats were separated into two groups (n = 6 to 10 in each group). Group 1 received a 10-min infusion of the adenosine antagonist 8-sulfophenyltheophylline (0.9 mg/kg x min) followed by a 10-min infusion of L-nitro-arginine-methyl ester (0.5 mg/kg x min). Group 2 similarly received L-nitro-arginine-methyl ester followed by 8-sulfophenyltheophylline in the presence of L-nitro-arginine-methyl ester. MEASUREMENTS AND MAIN RESULTS: Hemodynamic and blood flow measurements (microspheres) were made before infusions, 10 mins after the administration of each single-agent infusion, and 10 mins after combined-agent infusions were administered. No significant resistance alterations were observed in nonseptic rats. In septic rats, adenosine receptor blockade alone increased hepatosplanchnic and skeletal muscle vascular resistance, but no further increases were seen when L-nitro-arginine-methyl ester was added. Nitric oxide synthase inhibition alone increased hepatosplanchnic and skeletal muscle vascular resistances. When 8-sulfophenyltheophylline was added to the infusion, skeletal muscle vascular resistance increased significantly more than with L-nitro-arginine-methyl ester alone, but there were no further increases in hepatosplanchnic resistance. Renal and adipose vascular resistances increased with L-nitro-arginine-methyl ester infusions, and 8-sulfophenyltheophylline produced no effect. CONCLUSIONS: During sepsis, nitric oxide caused resting vasodilation independent of adenosine in the renal and adipose vasculature. In the hepatosplanchnic circulation, there is reciprocal adenosine-nitric oxide interaction in maintaining resting regional resistance. Skeletal muscle displayed a dual adenosine-mediated (nitric oxide-independent) and nitric oxide-mediated (adenosine receptors required) interaction to regulate resting resistance during sepsis. These data indicate that in the hepatosplanchnic and skeletal muscle vasculature, all of the resting nitric oxide-mediated vasodilation is secondary to endogenous adenosine action, but in adipose and renal vasculature, resting nitric oxide mediated vasodilation is independent of adenosine. Endogenous adenosine also appears to play a significant role in determining resting skeletal muscle resistance that is independent of nitric oxide synthase during sepsis.

Adenosine↗

PubMed1991

Effect of edema on segmental vascular resistance in isolated perfused rat lungs.

We have determined the effect of hydrostatic edema on total and segmental vascular resistances in the rat lung. Lungs of 12 adult rats, body weight 515 +/- 42 g, were isolated and perfused with blood. To investigate the role of vasoactivity on edema effects, we studied two groups of lungs; group I (n = 6) were untreated and group II (n = 6) were treated with papaverine hydrochloride to paralyze the vasculature. Initially blood flow was adjusted to keep pulmonary artery pressure approximately 15 cmH2O, left atrial and airway pressures being 8 and 7 cmH2O, respectively, and then kept unchanged thereafter (18 +/- 3 ml/kg/min). Hydrostatic edema was induced by raising venous pressure and pulmonary artery pressure measured continuously. In 4 lungs from each group, during baseline and after the development of severe edema, we partitioned the pulmonary circulation into arteries, microvessels, and veins by measuring pressures in 20-50 microns diameter subpleural arterioles and venules with the micropipette-Servonull method. Baseline total vascular resistance was similar in the two groups. Interstitial and early alveolar edema did not affect pulmonary vascular pressures. With severe edema (W/D ratio: 17 +/- 2), pressures in pulmonary artery and arterioles increased significantly in both groups; venular pressures did not change. Total resistance increased by 250% in group I and by 224% in group II lungs. Arterial resistance increased 3-5-fold in both groups, as did microvascular resistance. Venous resistances also increased in both groups, although to a lesser extent. The increase in total and segmental vascular resistances was not significantly different in the two groups of lungs. We conclude that in isolated rat lungs only severe edema results in an increase in total vascular resistance, mainly due to an increase in arterial and microvascular resistances, with a smaller increase in venous resistance. This appears to be a mechanical effect of edema on the vasculature and not a result of active vasomotion.

Animals↗

PubMedDate not supplied

Increased uterine and ovarian vascular resistance following Filshie clip sterilization: preliminary findings obtained with color Doppler ultrasonography.

The effect of Filshie clip sterilization on uterine and ovarian circulation was studied with color Doppler ultrasonography in 16 women before and twice after the operation. As a whole, the vascular resistance was slightly raised in the largest uterine artery and in the fundal parts of the uterine arteries; likewise in the ovarian arteries 2 days after sterilization. The resistance in the uterine arteries approached the presterilization level at 3 months after the operation, although these changes were not statistically significant. Two women had pelvic pain in the first days after the procedure, and they were compared with the symptom-free patients. Two days after sterilization, the patients with pain had significantly higher vascular resistance in all parts of the uterine arteries as compared to the symptom-free patients. After 3 months the difference had decreased in the largest uterine arteries and in the middle parts of the uterine arteries, but in the fundal parts the resistance was still higher than before sterilization. Vascular resistance in the ovarian arteries was increased in both groups, although the elevation was more pronounced in patients with pain. These preliminary findings imply that sterilization may cause an increase in the local vascular resistance, which is measurable by color Doppler sonography.

Adult↗

PubMed2001

Renal vascular resistance in progressive systemic sclerosis: evaluation with duplex Doppler ultrasound.

The study was planned to evaluate renal vascular resistance by means of duplex Doppler ultrasonography in patients with progressive systemic sclerosis (PSS) with or without signs of renal involvement. Twenty-two female patients with PSS (mean age 38.5 +/- 17.3 years) and 20 age-matched (mean age 36.7 +/- 7.2 years) female healthy controls participated to the study. Doppler indices of renal vascular resistance--resistive index (RI), pulsative index (PI), and systolic-to-diastolic flow velocities ratio (S/D ratio)--were determined on main renal artery and interlobar artery. RI, PI and S/D ratio were found to be increased in PSS patients with signs of renal involvement as compared to those without renal manifestations and healthy controls (p<0.0001 for all groups). Doppler indices of renal vascular resistance were closely related to the duration of the disease, age, and plasma renin activity. Doppler ultrasound is a useful and informative technique in the monitoring of PSS patients with renal involvement.

Adult↗

PubMed1995

Vascular resistance quantification in high flow resistance areas using the Doppler method.

The objective of the present study is to define and validate on an animal model (ewe) a new Doppler parameter for the assessment and monitoring of the vascular resistances in high resistance to flow areas (lower limbs, placenta with vascular disease). The high resistance index (HRI) was derived from the transmission line theory and defined as: HRI = D/S with S the amplitude of the systolic peak and D that of the diastolic reverse flow. Validation of the HRI was performed on adult ewes. Distal lower limb vascular resistances were evaluated from the Doppler femoral waveform (HRI) and compared with the classic vascular resistances (Rv), calculated from pressure and flow (mmHg/mL/min). The femoral flow variations were measured by duplex (echo-Doppler) method and the mean pressure through an arterial catheter inserted into the abdominal aorta. Two tests were used in this study: (1) A calibrated venous compression of the lower limbs extremity: The femoral flow dropped by 29%, the pressure and heart rate did not change, the HRI increased by 37% (p < 0.01), and the vascular resistance (Rv) by 46% (p < 0.01). (2) The intravenous injection of 1 mg adrenaline: The arterial pressure increased by 70% (p < 0.001), the heart rate and femoral flow dropped by 50% (p < 0.001), and 35% (p < 0.001), the HRI increased by 70% (p < 0.01) and the vascular resistances (Rv) by 140% (p < 0.01). During the two tests, the HRI changed in proportion with the "classic" vascular resistances.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1981

Determinants of systemic vascular resistance in children with congenital heart disease.

It is well known on the basis of acute experiments that changes in systemic arterial oxygen saturation, haemoglobin concentration and acid-base state produce changes in systemic vascular resistance. However, it is not known whether the same changes occur in the chronic state. In order to investigate this problem, we measured systemic vascular resistance in a population in whom chronic changes in these variables are common, namely 195 subjects with congenital heart disease. The significance of these factors was assessed by their ability to predict systemic vascular resistance in a multiple regression equation which also took account of the size of the patient. No matter how the size of the patient was allowed for, haemoglobin concentration, systemic arterial pH (or non-respiratory pH) and systemic arterial oxygen saturation were significantly (P less than 0.025) and positively correlated with systemic vascular resistance. We conclude that, as far as these factors are concerned, the mechanisms operating in the acute state continue to function in the chronic state.

Age Factors↗

PubMed1997

Pharmacological modulation of the human collateral vascular resistance in acute and chronic coronary occlusion assessed by intracoronary blood flow velocity analysis in an angioplasty model.

BACKGROUND: The pharmacological responsiveness of the coronary collateral circulation in humans has been studied only by indirect means. METHODS AND RESULTS: Patients with one-vessel disease and recruitable (n = 14) or spontaneously visible (n = 24) collateral vessels were studied during coronary angioplasty. Collateral flow in the recipient coronary artery was determined with a 0.014-in Doppler guide wire during balloon coronary occlusion and expressed as the diastolic blood flow velocity integral (dVi). Collateral blood flow velocity, mean aortic pressure (Pao), and coronary wedge pressure (Pw) were used to calculate the collateral vascular resistance index: Rcoll = (Pao-Pw)/ dVi (mm Hg/cm) and the peripheral vascular resistance index of the recipient coronary artery: R4 = Pw/dVi (mm Hg/cm). Adenosine (12 to 18 micrograms) and nitroglycerin (0.2 mg) were injected as a bolus in the donor coronary artery during subsequent balloon inflations to assess their effect on these hemodynamic variables. The administration of adenosine or nitroglycerin in patients with recruitable collateral vessels did not induce a change in dVi and Pw/Pao ratio. In patients with spontaneously visible collateral vessels, dVi increased from 8.0 +/- 4.5 to 10.8 +/- 8.0 cm (P = .01) after adenosine and from 7.4 +/- 4.5 to 10.3 +/- 6.9 cm (P = .003) after nitroglycerin. The Pw/Pao ratio remained unchanged after adenosine and nitroglycerin. Rcoll decreased from 10.3 +/- 9.5 to 8.6 +/- 8.5 mm Hg/cm (P = .01) after adenosine and from 11.6 +/- 10.4 to 8.3 +/- 8.9 mm Hg/cm (P < .001) after nitroglycerin. R4 decreased from 7.7 +/- 5.5 to 5.9 +/- 5.1 mm Hg/cm (P < .001) after adenosine and from 8.4 +/- 6.6 to 7.1 +/- 7.2 mm Hg/cm (P = .01) after nitroglycerin. CONCLUSIONS: Coronary collateral blood flow can be increased with adenosine and nitroglycerin in patients with one-vessel disease and spontaneously visible collateral vessels, which is in contrast to patients with recruitable collateral vessels. This effect is the result of a reduction in the collateral vascular resistance and peripheral vascular resistance of the recipient coronary artery.

Adenosine↗

PubMed1999

Carbon monoxide overproduced by heme oxygenase-1 causes a reduction of vascular resistance in perfused rat liver.

This study aimed to examine whether livers overexpressing heme oxygenase (HO)-1 could alter the vascular resistance through the vasorelaxing action of carbon monoxide (CO). The relationship among HO-1 expression, CO generation, and the vascular resistance was assessed in perfused rat livers pretreated with hemin, an inducer of HO-1. At 18 h after the hemin treatment, livers displayed marked increases in HO-1 expression in hepatocytes and venous CO flux and a reduction of the basal resistance. The reduction of the resistance in hemin-treated livers was canceled by administration of oxyhemoglobin, a reagent trapping both CO and nitric oxide (NO), but not by methemoglobin, which captures NO but not CO. Liposome-encapsulated oxyhemoglobin, which cannot access the space of Disse, did not cause vasoconstriction. Furthermore, these livers became less sensitive to endothelin-1, a vasoconstrictive peptide, than the untreated controls through mechanisms involving CO. On the other hand, at 12 or 24 h after the treatment when the HO-1 induction was not accompanied by CO overproduction, neither a decrease in the basal resistance nor vascular hyporeactivity to endothelin-1 was observed. These results suggest that CO overproduced in the extrasinusoidal compartment is a determinant of the HO-1-mediated vasorelaxation in the liver.

Animals↗

PubMed1989

Vascular resistance vs. perfusate osmolarity: the short term microvascular effect of hypotonic and hypertonic perfusion in the isolated kidney.

Vascular resistance changes were measured in response to alteration in perfusate osmolarity in isolated rabbit kidneys perfused at 10 degrees C. The data obtained were found to fit a simple mathematical model of the vascular resistance of the microcirculation in which it was assumed that variation in this parameter depended solely upon osmotic alterations in the size of the cells within and around the blood vessel walls. The model predicts that the volumetric changes due to the different osmolarities are produced in a tissue layer whose thickness is 30% relative to a fixed outer radius. This result is compatible with the hypothesis that the effects are predominantly due to changes of endothelial cell volume and other perivascular capillary cells. The analysis illustrates the significance of perfusate osmolarity as a determinant of vascular resistance, can be used to investigate the hemodynamic effects that occur during the introduction and removal of cryoprotective agents, and is relevant to the interpretation of results obtained with hypertonic solutions in blood volume restoration after hypovolemic shock.

Animals↗

PubMed1982

Vascular resistance and transit time of sickle red blood cells.

Changes in vascular resistance and mean transit time caused by the introduction either normal or sickled red blood cells (SSRBC) into the circulation were measured in the coronary and mesenteric vascular beds. The cat mesentery was perfused at constant flow through the superior mesenteric artery with a Ringer solution containing albumin. A rise in input pressure was observed after introducing RBC's. (10% hematocrit) at a constant rate, into the perfusate. The pressure rise caused by SSRBC's relative to that caused by normal RBC's represents the relative change in vascular resistance caused by the former cells as the perfusion flow was the same for both infusions. Similar measurements were performed in Ringer's perfused rabbit hearts in vitro. SSRBC's produced a 2 +/- 0.12 (M +/- SE) times relative increase in resistance in the mesentery and a 4 +/- 0.5 times increase in the coronary vasculature. Mean transit time, t was measured by monitoring the light transmission change caused by the injection of a small amount of RBC's into the arterial side of a Ringer's perfused rabbit heart. For normal RBC's t was 3.67 +/- 0.08 s and it rose to 6.1 +/- 0.6 s when SSRBC's were used. The simultaneous measurement of both mean transit time and pressure rise may help to identify the cell changes that cause circulatory impairment is SS cell anemia patients and it may also provide a convenient index to relate with the severity of the crisis.

Anemia, Sickle Cell↗

PubMed1987

Tilt test in essential hypertension. Differential responses in heart rate and vascular resistance.

Changes in hemodynamic parameters following 50-degree head-up tilt were studied in a population of 56 men, including 35 subjects with sustained essential hypertension and 21 age-matched normotensive controls. The increase in heart rate following tilt was similar in groups and exhibited the same reduction in response with age. The increase in vascular resistance following tilt was strongly and positively correlated with both age and baseline vascular resistance. The latter finding was observed mainly in hypertensive subjects. The study provided evidence that differentiated responses of heart rate and vascular resistance may be observed following orthostasis. In both normal and hypertensive subjects, the age dependence of heart rate response possibly reflected differences in baroreceptor reflex control of parasympathetic and sympathetic activity. In hypertensive subjects, the vascular response was amplified with age and baseline vascular resistance, suggesting a role for structural changes of the vessels in the increased vascular response.

Adult↗