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PubMed1988

Effects of CGS-13080, a thromboxane inhibitor, on pulmonary vascular resistance in patients after mitral valve replacement surgery.

Pulmonary hypertension with an elevated pulmonary vascular resistance was observed during the immediate recovery period in patients who underwent mitral valve surgery. In eight such patients, intravenous infusion of CGS-13080, imidazo(1,5-a)pyridine-5-hexanoic acid (a thromboxane synthetase inhibitor), at a dose range of 0.08-0.1 mg/kg/hr, effectively reduced pulmonary hypertension (from a mean pulmonary arterial pressure of 36 +/- 2 to 31 +/- 2 torr) and pulmonary vascular resistance (from 339 +/- 38 to 238 +/- 37 dynes.sec.cm-5) within 30 minutes and remained reduced for the entire infusion period (48 hours in five patients and 18 hours in three patients). Mean arterial pressure or systemic vascular resistance were not significantly affected by the drug infusion. Serum thromboxane B2 levels (a stable metabolic product of thromboxane A2) were significantly reduced after administration of the compound, with the maximum effect of greater than 90% reduction. All patients tolerated the drug infusion without significant side effects.

6-Ketoprostaglandin F1 alpha↗

PubMed2000

Noninvasive measurement of pulmonary vascular resistances by assessment of cardiac output and pulmonary transit time.

RATIONALE AND OBJECTIVES: Pulmonary vascular resistance is of special interest in many diseases. Usually it is determined invasively by catheterization, but cardiac output and pulmonary transit time can be ascertained by several noninvasive methods. METHODS: Fourteen heart recipients (age 34-71 years) were examined by electron-beam CT of the heart. Cine and flow studies were performed using a total of 60 mL of contrast and a breath-hold of 20 seconds. RESULTS: A mathematical model for calculating pulmonary vascular resistances from noninvasively measured cardiac outputs and pulmonary transit times was developed. Right-sided heart catheterization served as the reference method. CONCLUSIONS: The formula created seems to allow a clinically valid estimate of pulmonary vascular resistance from noninvasively acquired data.

Algorithms↗

PubMed1982

Influence of tocopherol, its chromane compound, phytyl chains and superoxide dismutase on increased vascular resistance and permeability due to arachidonate metabolism in isolated rabbit lung.

In the model of isolated, ventilated rabbit lungs, perfused with isoionic and isooncotic fluid, the addition of arachidonic acid to the perfusion fluid or the liberation of arachidonic acid by the Ca-ionophore A 23187 result in an increase in pulmonary vascular resistance and permeability. The former can be ascribed to cyclooxygenase products, the latter to lipoxygenase products of arachidonic acid. The effect of alpha-tocopherol, its chromane compound, alpha-tocopherolquinone, phytol, 2-methyl-1,4-naphthoquinone, 2-methyl-3-phytyl-1,4-naphthoquinone and of superoxide dismutase (SOD) on the increase in pulmonary vascular resistance and permeability was investigated. A membrane effect of the phytyl side chain and an antioxidative effect of the chromane compound can be distinguished: phytol increase the arachidonate-induced rise of pulmonary vascular resistance and permeability, whereas the chromane compound decreases both to a large degree. Methyl-phytyl-naphthoquinone and methyl-naphthoquinone gave equivalent results. SOD decreases the enhanced vascular resistance and the vascular leakage. The possibility of antioxidative therapy in acute pulmonary lesions with vascular leakage and increased vascular resistance is discussed.

Animals↗

PubMed1981

[Increase of pulmonary vascular resistance and permeability due to the metabolism of free arachidonic acid (author's transl)].

Release and metabolism of arachidonic acid are supposed to form the common final pathway of different stimuli on the pulmonary vascular endothelium. In a model of isolated, ventilated and perfused rabbit lungs we investigated the influence of increased availability of free arachidonic acid on pulmonary vascular resistance and permeability. Addition of arachidonic acid to the perfusion fluid or release of arachidonic acid by Ca-ionophore A 23187 regularly produces a characteristic biphasic increase of the pulmonary vascular resistance as well as a continuous increase in permeability, followed by pulmonary edema. Inhibition of cyclooxygenase by indomethacin prevents the augmentation of vascular resistance, the increase of vascular permeability however is enhanced. thus the raise in pulmonary vascular resistance can be ascribed to cyclooxygenase products, the increased pulmonary vascular permeability to lipoxygenase products of arachidonic acid.

Animals↗

PubMed1979

Humoral regulation of vascular resistance after 30 days of pulmonary artery constriction.

In an earlier study of guinea pigs with constriction of the pulmonary artery (PA) for 30 days, hindquarters' vascular resistance was maintained primarily by humoral mechanisms. In the present study, we investigated the contribution of circulating catecholamines, angiotensin II, and other constrictor stimuli to hindquarters' vascular resistance by observing vasodilator responses to specific competitive antagonists. Pressure-flow curves indicated vascular resistances in isolated, perfused, sympathectomized hindquarters of anesthetized guinea pigs. Phentolamine produced significantly greater (P less than 0.05) vasodilatation in animals with constriction of pulmonary artery than in sham animals [Sar1-Ala8]angiotensin II produced no vasodilation in either group. After alpha-adrenergic blockade, papaverine produced similar vasodilatation and similar final perfusion pressures in both groups. It appears that circulating catecholamines and augmented vasoconstrictor responsiveness to norepinephrine are totally responsible for the increased humoral regulation of vascular resistance in this experimental model of right ventricular hypertrophy.

Angiotensin II↗

PubMed1991

Vascular resistance of uterine arteries: physiological effects of estradiol and progesterone.

To determine if reproductive hormones played a role at physiological levels on vascular resistance of uterine arteries, we studied young women having inactive ovaries who received exogenous estradiol (E2) and progesterone (P). Six women, ages 27 to 36 with absent or nonfunctioning ovaries, received transdermal E2 and vaginal P after a 28-day replacement regimen duplicating E2 and P levels seen in the menstrual cycle. Vascular resistance of uterine arteries was evaluated before treatment (baseline), on days 13 to 14 and on days 26 to 27, using transvaginal pulsed Doppler combined with real-time imaging. Doppler waveforms were analyzed by the pulsatility index (PI). Baseline evaluation showed narrow systolic Doppler flow waves with a PI of 5.2 +/- 0.4, mean +/- SEM. On cycle day 13, Doppler waveforms showed a marked broadening with uninterrupted diastolic flow indicative of a profound decrease in vascular resistance. This was reflected by a significant decrease in PI to 1.3 +/- 0.3, mean +/- SEM. Doppler measurements made on days 26 to 27 showed no significant change. Our results indicate that at physiological levels, E2 affects vascular resistance of uterine arteries. This represents a new parameter of estrogen action, readily measurable by a noninvasive technique that, in the future, may help for assessing the efficacy of various estrogenic treatments.

Adult↗

PubMed1989

Increases in coronary vascular resistance initiated by blockade of CNS GABAergic tone occurs in the hindbrain.

The purpose of this study was to determine the site of action in the CNS responsible for producing picrotoxin-induced sympathetic mediated increase in coronary vascular resistance. To do this, picrotoxin, was administered either into the lateral cerebral ventricle, with the perfusion restricted to the forebrain, or into the fourth ventricle, to perfuse only the hindbrain and spinal cord, in chloralose-anesthetized cats, while monitoring coronary blood flow from the anterior descending branch of the left coronary artery, arterial pressure, heart rate and electrocardiogram (ECG). There was no difference between administration into the forebrain and hind-brain in terms of changes in coronary vascular resistance, ECG, arterial pressure and sinus rate when 600 micrograms of picrotoxin was used. Administration into either area elicited significant increases in coronary vascular resistance, arterial pressure and sinus rate, as well as changes in the ST segment and occasional ventricular tachyarrhythmias. However, a separation of effects was noted between the forebrain and the hindbrain when 200 micrograms of picrotoxin was administered. Administration of this dose into the forebrain did not significantly alter coronary vascular resistance or the ST segment, although significant increases in arterial pressure and sinus rate occurred in these animals. In contrast, administration of this dose into the hindbrain elicited significant increases in coronary vascular resistance, ST segment, arterial pressure and sinus rate. These results indicate that the most sensitive site for eliciting picrotoxin-induced increase in coronary vascular lies in the hindbrain.

Animals↗

PubMed1975

Vascular resistance in peripheral blood vessels at normotension and at local orthostatic hypertension in healty humans.

The effect of changes in orthostatic pressure on vascular resistance in subcutaneous adipose tissue was examined in the forearm at normal tension and in the leg at local orthostatic hypertension in three normal subjects. Blood flow in subcutaneous tissue was measured by the local xenon-133 washout technique. Changes in orthostatic pressure were achieved by postural changes of the extremity. At levels above the heart where venous pressure is constant, there was autoregulation of blood flow over a wider arterial blood pressure range in leg than in forearm. When transmural pressure increased 25 mm Hg or more vascular resistance increased about 50 per cent in the dependent forearm and 300 per cent in the dependent leg. The effect of ischemia on vascular resistance was investigated in cutaneous tissue of hand and foot by means of the 131I-Antipyrine initial slope technique. Vascular resistance after maximum dilatation achieved after 20, 30, and 35 min of ischemia was less in vessels of the hand than in vessels of the foot. Thus, adaptive structural changes of vessels subjected to increased blood pressure are present in cutaneous and subcutaneous adipose tissues in normal subjects.

Adipose Tissue↗

PubMed1983

Effect of captopril on renal vascular resistance, renin, prostaglandins and kinin in the isolated perfused kidney.

Vasodilatory and natriuretic effects of captopril were studied in the isolated hog kidney perfused with modified Krebs-Ringer solution. Renal arterial infusion of captopril caused increases in releases of renin, prostaglandins (PGE2, 6-keto-PGF1 alpha and PGF2 alpha) and kinin, and was accompanied by a decrease in the renal vascular resistance and an increase in urinary sodium excretion. Indomethacin administered with captopril diminished the saluretic effect of captopril and evoked an increase in kinin, but was associated with a marked decrease in prostaglandin and renin releases, while renal vascular resistance remained decreased. Indomethacin alone did not alter vascular resistance and kinin; however, renin and prostaglandin releases were decreased. Aprotinin administered with captopril showed a decrease in releases of prostaglandins, renin and kinin without any change in vascular resistance. These results suggest that increased release of kinin induced by captopril contributes to a reduction in renal vascular resistance. Increased prostaglandin release after captopril administration may be caused by an increase in kinin without direct involvement of captopril in prostaglandin synthesis. Renal prostaglandins may enhance sodium excretion and mediate renin secretion in captopril perfusion.

Animals↗

PubMed2005

Effects of norepinephrine and histamine on vascular resistance in isolated perfused mouse liver.

Mice have frequently been used for a variety of physiological studies because of the development of genetic engineering. However, the characteristics of hepatic vessels such as the vascular resistance distribution and the reactivity to various vasoconstrictors are not known in mice. We therefore determined the basal levels of segmental vascular resistances and the effects of histamine and norepinephrine on the vascular resistance distribution of mice. The liver of male non-inbred ddY mice was excised and perfused via the portal vein with 5% bovine albumin-Krebs solution at a constant flow rate. The sinusoidal pressure was measured by the double occlusion pressure and used to determine the presinusoidal (R(pre)) and postsinusoidal (R(post)) resistances. The basal R(post) comprised 53 +/- 1% of the total hepatic vascular resistance. The norepinephrine and histamine increased R(pre) in a greater magnitude than R(post) with liver weight loss. However, the response to histamine was weaker than that to norepinephrine. Moreover, histamine-induced vasoconstriction showed tachyphylaxis. In conclusion, the presinusoidal and postsinusoidal resistances of mouse livers were similar in magnitude. The presinusoidal vessels predominantly contract in response to norepinephrine and histamine in mouse livers.

Animals↗

PubMed1991

Segmental vascular resistance during pulsatile and steady perfusion in 3- to 5-wk-old rabbit lungs.

To determine the mechanisms by which pulsatile perfusion reduces vascular resistance in isolated lungs, we compared the effects of pulsatile versus steady perfusion on total and segmental vascular resistance in isolated lungs of 3- to 5-wk-old rabbits. Lungs were perfused alternately with steady and pulsatile flow for 45-min periods at a constant total arteriovenous pressure drop. Blood flow was adjusted to keep mean pulmonary arterial pressure at 20 cmH2O, when left atrial and airway pressures were 8 and 6 cmH2O, respectively. We partitioned the pulmonary circulation into three longitudinal vascular segments, i.e., arteries, microvessels, and veins, by measuring pressures in 20- to 50-microns-diameter subpleural arterioles and venules by the micropipette servo-nulling method. We found that in the isolated, perfused 3- to 5-wk-old rabbit lung, in which arteries and veins are the main sites of resistance, pulsatile flow results in a 20-36% reduction in total vascular resistance, mainly due to a reduction in arterial and venous resistances. The decrease in total vascular resistance was similar in lungs that were untreated or treated with papaverine, indicating that the effect of pulsatile flow was not due to active vasomotion. The reduction in arterial resistance was greater than that in veins (31-55 vs. 19-22%), especially when pulse amplitude was high (5-10 vs. 20-30 cmH2O). Total vascular resistance was also lower after 45 min of pulsatile perfusion with a pulse rate of 200 pulses/min than 80 pulses/min (0.126 +/- 0.04 vs. 0.154 +/- 0.059 cmH2O.min.ml-1.kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2004

Effects of terbutaline on peripheral vascular resistance and arterial compliance.

In a double blind, randomized placebo-controlled crossover study we characterized how terbutaline affects the mean and short-term fluctuations of peripheral vascular resistance and arterial compliance. The study was carried out in six young and healthy male subjects in the supine and upright positions by recording continuously electrocardiography and finger arterial blood pressure. On average, large intravenous terbutaline doses reduce maximally by 50% the mean systolic-diastolic pressure decay time (windkessel time), by 30% the mean vascular resistance, and by 20% the mean arterial compliance. Terbutaline reduces differently the beat-to-beat variability of peripheral vascular resistance and arterial compliance. The effects can be explained by beta-adrenoceptor activation that mediates smooth muscle relaxation in small resistance arteries and large conduit arteries. Differences between vascular resistance and compliance lowering actions could be explained by differences in the beta-adrenoceptor-mediated vascular relaxation and sympathetically mediated vascular contraction between small and large arteries.

Adrenergic beta-Agonists↗

PubMed2004

Angiotensin II receptor modulation of renal vascular resistance and neurotransmission in young and adult spontaneously hypertensive rats.

BACKGROUND/AIMS: Angiotensin (Ang) II modulates vascular resistance and sympathetic neurotransmission through Ang II type 1 (AT1) receptors. Recent studies reported an involvement of AT2 receptors. We investigated whether AT2 receptors participate in modulation of vascular resistance and sympathetic neurotransmission in spontaneously hypertensive rats (SHR). METHODS: Kidneys of 6- and 16-week-old normotensive (WKY) and SHR were isolated and perfused. RESULTS: Noradrenaline release induced by renal nerve stimulation (RNS) was increased in SHR (WKY: 1,837 +/- 128, SHR: 2,310 +/- 192 pg/g). Ang I- and II-induced pressor responses and enhancement of noradrenaline release were greater in SHR than in WKY. Pressor responses to Ang I and II were greater in adult compared with young SHR. The AT1 receptor antagonist EXP3174 (0.1 microM) blocked Ang I- and II-induced renal vasoconstriction and noradrenaline release to RNS in both strains. In contrast, the selective AT2 receptor antagonist PD 123319 (1 microM) had no influence in young and adult WKY and SHR. CONCLUSION: Ang I and II had a greater impact on renal vascular resistance and neurotransmission in SHR, which was more pronounced in adult SHR. All effects are mediated by the AT1 receptor and no modulatory influence of the AT2 receptor could be found.

Aging↗

PubMed2000

Renal vascular resistance in essential hypertension: duplex-Doppler ultrasonographic evaluation.

Duplex Doppler ultrasonography has been validated as a noninvasive method to evaluate hemodynamic features of renal blood flow in renal and intrarenal arteries in patients with various renal diseases. The significance of duplex Doppler sonography in the evaluation of renal vascular resistance in essential hypertension has not yet been clearly determined. The aim of the present study was to evaluate the renal vascular resistance in patients with essential hypertension by measuring intrarenal arterial resistance (RI) and to correlate RI with renal functional tests and other clinical and laboratory data. Duplex Doppler ultrasonography was used to measure RIs in intrarenal arteries in 128 patients with essential hypertension and 61 age-matched normotensive control examinees. The renal vascular resistance index (RI) was determined by use of Doppler ultrasound. Hypertension was classified according to the 1997 Joint National Committee Guidelines (JNC-VI). Mean RI in hypertensive patients was 0.66 +/- 0.05 (+/- sd) and in healthy controls 0.60 +/- 0.03 (+/- sd) (p = 0.0001). RI correlated significantly with patient's age (r = 0.577, p = 0.001), duration of hypertension (r = 0.335, p= 0.001), stage of hypertension according to the JNC-VI classification (r = 0.315, p = 0.006), creatinine clearance (r = -0.383, p = 0.001), systolic blood pressure (SBP, r = 0.41, p = 0.001) and mean blood pressure (MBP, r = 0.30, p = 0.002). RI values did not correlate significantly with plasma renin concentration (r = -0.198 NS), diastolic blood pressure (DBP, r = 0.17, p = 0.06), and cardiac pulse (r = -0.10, p = 0.16). Multiple regression analysis showed that independent variables for RI were the patient's age (multiple R = 0.53, signif. F = 0.001) and systolic blood pressure (multiple R = 0.57, signif. F = 0.03). The renal Doppler resistance index (RI) is increased in essential hypertension and it correlates with renal functional tests as well as with patient's age, duration of hypertension, with a stage of hypertension according to the JNC-VI classification, and with systolic and mean blood pressure. The increased renal vascular resistance (RI) in hypertensive patients could be a sign of developing hypertensive nephrosclerosis and consequently renal failure. The utilization of the renal vascular resistance index (RI), provides a new noninvasive parameter in the followup of patients with essential hypertension.

Adult↗

PubMed1992

Longitudinal distribution of pulmonary vascular resistance after endotoxin administration in sheep.

BACKGROUND AND METHODS: Pulmonary hypertension may increase pulmonary capillary pressure and exacerbate pulmonary edema in acute respiratory failure. The effects of pulmonary hypertension on pulmonary capillary pressure depend on the longitudinal distribution of pulmonary vascular resistance. Since pulmonary hypertension occurs during acute respiratory failure, we hypothesized that acute respiratory failure may produce time-dependent changes in the longitudinal distribution of pulmonary vascular resistance. Therefore, we measured pulmonary capillary pressure and the longitudinal distribution of pulmonary vascular resistance in an animal model of acute respiratory failure. Escherichia coli endotoxin (2.5 to 5.0 micrograms/kg) was administered over a 1-hr period in eight anesthetized sheep. Pulmonary and systemic hemodynamics, including pulmonary artery occlusion pressure (PAOP), pulmonary capillary pressure, and the longitudinal distribution of pulmonary vascular resistance, were measured over the next 5 hrs. Pulmonary capillary pressure was estimated by analysis of the pressure decay following pulmonary artery balloon inflation. RESULTS: Endotoxin administration resulted in sustained pulmonary hypertension for the subsequent 5 hrs of the study. Pulmonary capillary pressure was increased 7 mm Hg above baseline at 0.5 and 0.75 hrs during the infusion of endotoxin but returned to baseline values at 1.5 hrs. Despite sustained pulmonary hypertension, pulmonary capillary pressure remained at baseline values for the duration of the study. Similar to pulmonary capillary pressure, pulmonary venous (or postcapillary) resistance was increased approximately four-fold over baseline at 0.5 and 0.75 hrs after initiating endotoxin administration, but returned to baseline values by the end of endotoxin administration and remained at baseline values throughout the remainder of the study. In contrast, pulmonary arterial (or precapillary) resistance remained at values approximately three times baseline during the infusion and throughout the duration of the study. CONCLUSIONS: In this experimental model of acute respiratory failure, the effects of endotoxin on the longitudinal distribution of pulmonary vascular resistance are time-dependent. If these data from animals can be extrapolated to humans, we speculate that the importance of pulmonary venoconstriction in exacerbating pulmonary edema may vary over time in patients with acute respiratory failure.

Animals↗

PubMed2005

Are there changes in leg vascular resistance during laparoscopic cholecystectomy with CO2 pneumoperitoneum?

BACKGROUND: The prompt haemodynamic response to carbon dioxide insufflation during laparoscopic cholecystectomy suggests involvement of the sympathetic system. The aim of the present study was to examine if a change in vascular resistance in leg skeletal muscle could be an important mechanism behind the increased afterload. Furthermore, the arterio-venous differences of the catecholamines were measured in the leg before and during insufflation of carbon dioxide into the peritoneal cavity. METHODS: Ten patients (ASA I) scheduled for laparoscopic cholecystectomy were included. After induction of anaesthesia, catheters were introduced percutaneously into the radial artery, the femoral vein and the cubital vein for pressure monitoring and blood sampling. The arterial blood flow in the legs was measured by mercury-in-Silastic strain gauge venous occlusion plethysmography. Vascular resistance in the right leg (LVR) was calculated from the formula: (MAP-FVP)/calf blood flow. Measurements were made before and 5 min after insufflation of pneumoperitoneum. RESULTS: Induction of pneumoperitoneum increased the heart rate (P < 0.05) and also increased mean arterial pressure and femoral vein pressure as well as the calculated leg vascular resistance (P < 0.01). Calf blood flow did not change significantly in either leg. Both arterial and venous noradrenaline concentrations were higher after insufflation (P < 0.01). CONCLUSION: In patients without heart or lung disease, pneumoperitoneum at an intra-abdominal pressure level of 11-13 mmHg increased the peripheral vascular resistance in the leg while the arterial blood flow in the leg was unaffected. Catecholamine levels increased, but were still low. Therefore, we suggest that the increase in peripheral vascular resistance is caused by increased myogenic activity in the resistance vessels secondary to increased arterial and transmural pressure rather than by increased neurogenic sympathetic activity.

Adolescent↗

PubMed1994

Role of EDRF in the regulation of regional blood flow and vascular resistance at rest and during exercise in conscious dogs.

The contribution of endothelium-derived relaxing factor (EDRF) to the regulation of regional vascular resistance and tissue blood flow at rest and during acute moderate exercise was studied in chronically instrumented conscious dogs. Radioactive microspheres were injected before and during exercise to measure regional blood flow. An infusion of nitro-L-arginine (L-NA), an analogue of L-arginine, was used to inhibit the synthesis of EDRF and resulted in a significant increase in mean arterial pressure, associated with significantly elevated vascular resistance in heart, skeletal muscle, renal and splanchnic circulations and with decreases in tissue blood flow in those regions at rest. Acute exercise caused a typical redistribution of blood flow, in which there was vasodilation in heart and working skeletal muscles, accompanied by vasoconstriction in kidney and splanchnic circulations. L-NA resulted in significantly elevated vascular resistance during vasodilation in heart and working skeletal muscles and also significantly increased vasoconstriction in renal cortex, stomach, pancreas, liver, and colon during exercise. Blood flows during exercise were largely unaffected by L-NA treatment. Our results suggest that whereas EDRF functions to regulate basal vascular tone and vascular resistance during exercise, EDRF has a minor role in determining the pattern of the redistribution of tissue blood flow during exercise.

Acetylcholine↗

PubMed1975

Effect of prostaglandin E2 on pulmonary vascular resistance in intact dog, swine and lamb.

The effects of prostaglandin E2 (PGE2) on pulmonary vascular resistance in the intact dog, swine and lamb were studied using a right heart catheterization technique to isolate and perfuse the left lower lung lobe at controlled blood flow. Infusion of PGE2 into the lobar artery increased lobar arterial perfusion pressure but did not alter pressure in the left atrium in all 3 species. The increase in lobar arterial pressure was associated with a rise in pressure in the small intrapulmonary lobar vein in the dog but no change in pressure in these veins in the swine and lamb. Infusion of PGE2 into the iliac artery produced a marked decrease in perfusion pressure in the hindlimb of the dog. The effects of PGE2 on the canine lung occurred in the absence of any significant change in arterial blood gases, pH, hematocrit or rate and volume of respiration, and this substance increased pulmonary vascular resistance when the lung was perfused with dextran instead of blood. These results show that in dog, swine and lamb, PGE2 increases pulmonary vascular resistance; however, the site of vasoconstriction is different in the dog and swine or lamb. In the swine and lamb vasoconstriction occurred primarily in vessels upstream to the small veins, presumably small arteries, whereas in the dog lung, the pre- and postcapillary vessels were actively constricted by this naturally occurring substance.

Animals↗