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Results for “VASCULAR RESISTANCE”

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PubMed1994

Correlation between peripheral vascular resistance and time to peak flow during reactive hyperaemia.

Earlier studies have proposed that the time to reach peak hyperaemic flux recorded with laser Doppler (tp) is a simple and accurate method of evaluating ischaemic limbs and possibly a method of estimating the peripheral vascular resistance (PR). The aim of this study was to investigate the relationship between the tp and changes in limb vascular resistance caused by arterial stenosis. Forty postocclusive hyperaemia tests with arterial stenoses of different pressure gradients were performed in four pigs. A laser Doppler fluxmeter was used to record postocclusive hyperaemia in the skin of one hind limb. A specially designed tourniquet was used for the arterial occlusion. Proximal and distal to the occlusion level a snare was used to form different grades of stenosis. The PR (mmHg.ml-1.min-1) was either estimated by infusion of a known blood volume into the tested limb over a given time period with simultaneous measurement of pressure or calculated on the basis of measurements of limb blood flow and blood pressure gradients. The tp was closely related to total limb vascular resistance assessed by the blood infusion method (r = 0.83, p < 0.0003) and to the resistance calculated from volume blood flow and intraarterial pressures (r = 0.86, p < 0.0001). This study suggests that the tp accurately reflects limb vascular resistance in an experimental model. Thus tp may be used as a quantitative indicator of overall blood flow impairment, and should be evaluated in patients with lower-limb atherosclerosis.

Animals↗

PubMed1994

Leuprolide acetate depot for the treatment of uterine leiomyomas. Changes in bone density, uterine volume and uterine vascular resistive index.

This study measured the changes in uterine volume, uterine vascular resistive index and lumbar vertebral bone density before and after a six-month course of leuprolide acetate depot in women with uterine leiomyomas. All nine patients studied were black. The high baseline bone density of black women may provide a greater scope for the use of gonadotropin agonists as compared to women in the general population. A significant reduction in uterine volume was achieved in the patients with leuprolide therapy. Uterine vascular resistive indices were not altered consistently following leuprolide therapy in women with leiomyomas.

Adult↗

PubMed1995

Segmental pulmonary vascular resistance following wood smoke inhalation.

OBJECTIVES: To locate the specific site (i.e., pulmonary arteries, veins, or capillaries) of increased pulmonary vascular resistance after wood smoke inhalation and to demonstrate whether the prostanoids, thromboxane B2 or 6-keto-prostaglandin F1 alpha, play a role in these vascular resistance changes. DESIGN: Prospective, randomized, controlled trial. SETTING: Laboratory at a university medical center. SUBJECTS: Five mongrel dogs. INTERVENTIONS: The isolated canine left lower lobe preparation was used to measure changes in the pressure drop across the pulmonary arteries, veins, and capillaries. The left lower lobe was surgically isolated and perfused by a pump primed with autologous blood. The arterial and venous occlusion technique and the vascular pressure-flow relationship were used to assess changes in pulmonary vascular resistance. After baseline measurements, the left lower lobe was exposed to wood smoke for 2.5 mins and measurements were repeated. MEASUREMENTS AND MAIN RESULTS: Smoke exposure caused an immediate (5 mins post-inhalation) increase in the total pressure gradient across the lobe (baseline = 9.8 +/- 0.5 torr [1.3 +/- 0.06 kPa]); smoke inhalation = 24.3 +/- 3.9 torr [3.24 +/- 0.5 kPa]; p < .05). Total pressure drop was partitioned longitudinally into pressure drops across arteries, veins, and the middle vessels. The increase in total pressure drop was associated with a moderate increase in the pressure drop across the middle vessels (baseline = 1.1 +/- 0.2 torr [0.14 +/- 0.02 kPa]; smoke inhalation = 5.2 +/- 1.1 torr [0.69 +/- 0.14 kPa]; p < .05); a large increase in the pressure drop across the veins (baseline = 4.8 +/- 1.3 torr [0.64 +/- 0.17 kPa]; smoke inhalation = 20.7 +/- 3.4 torr [2.7 +/- 0.45 kPa]; p < .05), and no significant change in the pressure drop across the arteries (baseline = 3.7 +/- 0.4 torr [0.49 +/- 0.05 kPa]; smoke inhalation = 4.8 +/- 0.5 torr [0.64 +/- 0.06 kPa]; p = NS). Increases in the pressure drop across the middle and venous vessels were transient and no longer significantly different from baseline 15 mins after smoke inhalation. Similarly, analysis of the pulmonary artery/blood flow data demonstrated that the mean slope and pressure intercept were greater than baseline only at 5 mins postsmoke inhalation (p < .05). Thromboxane B2 did not significantly change from baseline values after smoke exposure and prostaglandin F1 alpha demonstrated a slight but significant decrease 30 mins postsmoke. Pulmonary edema was measured gravimetrically (wet/dry weight ratio) and smoke significantly increased lung water in the left lower lobe (wet/dry weight ratio = 6.55 +/- 0.4) as compared with the normal left upper lobe (wet/dry weight ratio = 4.97 +/- 0.2). CONCLUSIONS: We conclude that smoke causes an intense but transient increase in the pressure drop across the venous segment that may accelerate the formation of pulmonary edema, which is not mediated by changes in thromboxane B2 or prostaglandin F1 alpha.

Analysis of Variance↗

PubMed2005

[The effects of inhaled nitric oxide on pulmonary vascular resistance in patients after total cavopulmonary connection].

OBJECTIVE: To study the effects of inhaled nitric oxide (NO) on pulmonary vascular resistance in patients after total cavopulmonary connection (TCPC). METHODS: Fifty-two patients after TCPC were evaluated, of them 24 patients were administered with inhaled nitric oxide in the early postoperative period. The cardiac index (CI) and pulmonary vascular resistance (PVR) were compared before and after inhaled NO. RESULTS: In experimental group, after inhaled NO, partial pressure of oxygen in artery/fraction of inspired oxygen increased from 161 +/- 17 to 193 +/- 23 (t = 2.75, P < 0.01); CI from (2.86 +/- 0.24) L.min(-1).m(-2) to (3.13 +/- 0.22) L.min(-1).m(-2) (t = 2.25, P < 0.05); PVR decreased from (4.2 +/- 0.5) U/m(2) to (3.8 +/- 1.4) U/m(2) (t = 2.29, P < 0.05); central venous pressure (CVP) from (17.0 +/- 1.8) mm Hg to (15.0 +/- 1.1) mm Hg, decreased 11.7%. Compared with the control group, respirator time decreased from (86 +/- 27) h to (54 +/- 18) h (t = 2.29, P < 0.05); ICU time from (6 +/- 2) d to (4 +/- 2) d (t = 2.32, P < 0.05); But hydrothorax drainage and length of stay had no significant difference. CONCLUSIONS: Though inhaled NO, there is no significant long-term effects in patients after TCPC, but it may play an important role in the management of low cardiac output syndrome and high cava pressure caused by reactive elevated pulmonary vascular resistance in the early postoperative period of TCPC.

Administration, Inhalation↗

PubMed1984

Blockade of GABA receptors in periventricular forebrain of anesthetized cats: effects on heart rate, arterial pressure, and hindlimb vascular resistance.

Pharmacologic antagonism of GABAergic inhibition in the periventricular forebrain of anesthetized cats caused dose related sympathetically mediated increases in heart rate and arterial pressure in vagotomized cats, and suppression of reflex vagal activation in vagus-intact preparations where sympathetic effects are prevented by cervical spinal cord transection. In the present study performed in cats with intact autonomic pathways, similar administration of the GABA antagonist bicuculline methiodide (BMI) produced dose-related increases in arterial pressure, heart rate, and, when perfusion pressure in the autoperfused hindlimb was measured, vascular resistance. Furthermore, the relationship between heart rate and hindlimb vascular resistance changes suggested that the effects on heart rate reflected the combined sympathetic and vagal baroreflex effects of BMI. Intraventricular administration of muscimol, a potent GABA agonist, elicited abrupt and parallel reversal of BMI-induced effects on systemic arterial pressure and vascular resistance while attempts to acutely denervate the hindlimb at the height of the BMI response by cutting the femoral and sciatic nerves sharply reversed the increase in hindlimb vascular resistance in most experiments. The results suggest that the cardiovascular changes observed represent an integrated pattern consisting of excitation of sympathetic nerves innervating the heart and vasculature along with suppression of reflex evoked vagal excitability.

Adrenergic Fibers↗

PubMed2004

Testicular size and vascular resistance before and after hydrocelectomy.

OBJECTIVE: We sought to determine whether there is an association between hydroceles and testicular size and vascular resistance. SUBJECTS AND METHODS: Twenty-three patients with a mean age of 42.8 years who had a unilateral idiopathic hydrocele and who underwent unilateral hydrocelectomy were included in the study. Testicular size and resistive (RI) and pulsatility (PI) indexes of the intratesticular arteries on the involved and uninvolved sides were measured before and after the hydrocelectomy. RESULTS: We found statistically significant differences in the testicular volumes between the normal side (mean +/- SD, 15.40 +/-3.41 mL) and the side with the hydrocele (20.67 +/- 4.01 mL) before surgery (p < 0.001) and in the volumes in the side with the hydrocele before (20.67 +/- 4.01 mL) and after (16.20 +/- 2.99 mL) surgery (p < 0.001). No such a difference in volume was seen in the normal side before (15.40 +/- 3.41 mL) and after (15.28 +/- 3.24 mL) surgery (p = 0.200). The mean decrease in volume in the testis with the hydrocele after hydrocelectomy was 21%. There were statistically significant differences of RI and PI values between the normal testis (0.59 +/- 0.07 and 1.02 +/- 0.34, respectively) and the testis with hydrocele (0.79 +/- 0.11 and 1.70 +/- 0.56, respectively) before surgery (p < 0.001). In the testis with the hydrocele, we found a statistically significant decrease in RI and PI values (0.62 +/- 0.05 and 1.00 +/- 0.14, respectively) of intratesticular arteries after surgery (p < 0.001). The mean decreases in RI and PI values after hydrocelectomy were 21% and 36%, respectively. CONCLUSION: There is an association between the development of an idiopathic hydrocele and testicular size and vascular resistance. We believe that the increase in volume and vascular resistance is due to an increase in impedance to venous and lymphatic flow.

Adult↗

PubMed1989

Progressive improvement in pulmonary vascular resistance after percutaneous mitral valvuloplasty.

Percutaneous mitral valvuloplasty has been proposed as a nonsurgical technique for treating high-risk patients with mitral stenosis who are deferred from mitral valve replacement. The effect of this technique on patients with pulmonary hypertension, however, has not been fully evaluated. Accordingly, serial assessment of pulmonary vascular resistance was made in 14 patients with critical mitral stenosis and pulmonary hypertension (pulmonary vascular resistance greater than 250 dynes.sec/cm5 or mean pulmonary artery pressure greater than 40 mm Hg or both) who underwent percutaneous balloon dilatation of the mitral valve. Balloon valvuloplasty was performed with either one (n = 10) or two (n = 4) balloons through the transseptal approach, and it resulted in significant improvement in mean mitral gradient (from 18 +/- 4 to 9 +/- 4 mm Hg, p less than 0.001), systemic blood flow (from 3.7 +/- 1.2 to 5.0 +/- 2.2 l/min, p less than 0.001), and calculated mitral valve area (from 0.7 +/- 0.2 to 1.6 +/- 0.7 cm2, p less than 0.001). Immediately after balloon mitral valvuloplasty, pulmonary vascular resistance fell from 630 +/- 570 to 447 +/- 324 dynes.sec/cm5. Repeat catheterization 7 +/- 4 months after valvuloplasty showed further improvement of pulmonary hypertension in 12 of the 14 patients, with a mean pulmonary vascular resistance for the group as a whole of 280 +/- 183 dynes.sec/cm5, p less than 0.005. In two patients, mitral valve restenosis to a mitral valve area less than 1.0 cm2 was associated with a return of pulmonary hypertension to predilatation values.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed2004

Renal vascular resistance in glomerular diseases--correlation of resistance index with biopsy findings.

Duplex Doppler sonography has been recognized as a noninvasive method to evaluate hemodynamic features of renal blood 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 glomerular diseases has not yet been clearly determined. The aim of the present study was to evaluate renal vascular resistance in patients with glomerular diseases by measuring intrarenal arterial resistance (RI) and to correlate RI with renal functional tests and other clinical and laboratory data. The Doppler parameters were also correlated with histopathological findings in the kidney which underwent the percutaneous biopsy. Duplex Doppler sonography was used to measure RIs in intrarenal arteries in 50 patients with glomerular diseases and 60 age-matched control subjects. The renal vascular resistance index (RI) was determined by the use of Doppler sonography. The mean RI in 50 patients with glomerular diseases was 0.68 +/- 0.09, which was statistically significantly higher than in 60 control subjects (the mean RI was 0.596 +/- 0.035). In a group of patients with membranoproliferative glomerulonephritis the mean RI was 0.817 +/- 0.624 which was statistically significantly higher than in other groups of glomerulonephritis. The renal vascular (resistance) RI significantly correlated with serum creatinine, creatinine clearance and beta2 microglobulin. Qualitative duplex sonography measure of renal arterial resistance-resistive index does not appear to be reliable in distinguishing different types of glomerulonephritis.

Adult↗

PubMed1976

Reflex increase in coronary vascular resistance in patients with ischemic heart disease.

To assess possible coronary vasoconstriction in patients with ischemic heart disease, we measured coronary vascular resistance in 12 patients with normal hearts and 12 with coronary disease before and during the initial 50 seconds of cold pressor test, a stimulus known to produce systemic vasoconstriction. Control coronary vascular resistance was similar in the two groups, and although it did not change in patients with normal vessels, it rose by 27 per cent (P less than 0.005) in the group with coronary disease during the cold pressor test. In three of 12 patients with coronary disease coronary flow actually declined despite an increase in arterial pressure; in four, angina was precipitated. Phentolamine abolished increases in arterial pressure and coronary vascular resistance during the test in three patients with coronary disease. Adrenergically mediated coronary vascular tone may be an important determinant of coronary blood flow and may contribute to ischemia in patients with coronary disease.

Adrenergic alpha-Antagonists↗

PubMed1985

Thromboxane is not responsible for the high pulmonary vascular resistance in fetal lambs.

The factors responsible for the high pulmonary vascular resistance in the fetus are not well known. Thromboxane (TX) A2 is a potent pulmonary vasoconstrictor. To determine whether TXA2 may play a role in fetal pulmonary vasoconstriction, we infused the specific TX synthetase inhibitor U63,557A into eight chronically instrumented fetal lambs (134-137 days gestational age, full term 145 days) and measured pulmonary blood flow, pulmonary and systemic arterial pressure, and heart rate. U63,557A (3 mg/kg as a bolus then 3 micrograms/kg/min for 120 min infused in the main pulmonary artery) did not change pulmonary blood flow, pulmonary mean arterial pressure, and pulmonary vascular resistance during the infusion and during 2 h following the end of the infusion. During the infusion, TXB2 arterial plasma concentrations decreased from 106.1 +/- 17.5 to 8.7 +/- 2.9 pg/ml. In three of the fetal lambs, immediately after the 2-h infusion of U63,557A, we infused the leukotriene end-organ antagonist FPL 57231 into the main pulmonary artery (1 mg/kg/min for 60 min). TXA2 synthesis inhibition did not prevent the pulmonary vasodilation induced by FPL 57231. Pulmonary blood flow increased from 64.8 +/- 24.4 to 669.5 +/- 65.6 ml/min/100 g lung tissue during the FPL 57231 infusion. We conclude that TXA2 does not play a role in the maintenance of elevated fetal pulmonary vascular tone, either directly or as a mediator of leukotriene action.

Animals↗

PubMed1981

Correlation between plasma sodium acetate concentration and systemic vascular resistances.

Acetate in dialysis fluid induces during haemodialysis a fall in systemic vascular resistance. In patients with hepatic insufficiency, acetate concentrations are higher than in patients without hepatic insufficiency and in such patients vascular sensitivity to acetate is perhaps potentiated by modifications of acid base status. The close inverse correlations between acetate concentrations and systemic vascular resistance are strong indications that acetate is a major factor involved in the genesis of 'dialysis hypotension'.

Acetates↗

PubMed2002

Intravenous sildenafil lowers pulmonary vascular resistance in a model of neonatal pulmonary hypertension.

Persistent pulmonary hypertension secondary to meconium aspiration syndrome is an important cause of morbidity and mortality in the neonatal population. We investigated the use of the phosphodiesterase-5 inhibitor sildenafil, in its intravenous form, as a pulmonary vasodilator in a model of meconium aspiration syndrome. Pulmonary hypertension was induced in 18 piglets, by endotracheal instillation of human meconium, 6 piglets subsequently received an infusion of intravenous sildenafil for 2 hours, 6 received inhaled nitric oxide for 2 hours, and 6 control animals received no additional intervention. Meconium aspiration increased pulmonary vascular resistance by 70%, and increased oxygenation index by over 100%. Pulmonary vascular resistance remained elevated for the remainder of the study period in control animals. Inhaled nitric oxide reduced the pulmonary vascular resistance by 40% after 2 hours of treatment; intravenous sildenafil completely reversed the increase in pulmonary vascular resistance within 1 hour of commencing the infusion. Neither agent had an effect on systemic hemodynamics. Sildenafil also increased cardiac output by 30%, but while doing so did not adversely influence oxygenation. Intravenous sildenafil is a selective and highly effective pulmonary vasodilator, which is at least as effective as inhaled nitric oxide, in this model of neonatal persistent pulmonary hypertension.

Administration, Inhalation↗

PubMed2002

The endothelin antagonist BQ123 reduces pulmonary vascular resistance after surgical intervention for congenital heart disease.

OBJECTIVE: Postoperative pulmonary hypertension in children after surgical intervention for congenital heart disease has been attributed to failure of the pulmonary endothelium to provide adequate vasodilation. Although we have shown that the impaired vasodilatory component attributable to the l-arginine-nitric oxide pathway is almost completely reversible, a nonrestorable component persists, implying an additional vasoconstrictive mechanism in postoperative pulmonary endothelial dysfunction. In this study of children after surgical intervention for congenital heart disease, we measured endothelin-1 levels and used BQ123, a selective endothelin-A receptor antagonist, together with inhaled nitric oxide to discriminate dysfunctional pulmonary endothelial vasodilation from endothelin-mediated pulmonary vasoconstriction. METHODS: All children were examined early after surgical intervention in the intensive care unit. Pulmonary vascular resistance (with respiratory mass spectrometry), as well as arterial and venous endothelin-1 levels (measured by means of a quantitative enzyme-linked immunosorbent assay), were determined in 7 children (age range, 3.3-13.7 months; median age, 6.3 months) with intracardiac shunting defects at baseline and during ventilation with a fraction of inspired oxygen of 0.65, with additional BQ123 (0.1 mg/kg infused over 20 minutes), and with inhaled nitric oxide (20 ppm). RESULTS: Pulmonary vascular resistance decreased from 7.7 +/- 3.4 at baseline to 6.1 +/- 2.8 Woods units. m(-2) (P =.022) at a fraction of inspired oxygen of 0.65 and to 4.7 +/- 2.7 Woods units. m(-2) (P =.013) during BQ123 infusion. Inhaled nitric oxide had no further effect on pulmonary vascular resistance. Left atrial endothelin-1 levels (1.35-5.12 pg/mL; mean, 2.4 pg/mL) correlated significantly with the decrease in pulmonary vascular resistance in response to BQ123 infusion (r(2) = 0.89, P =.003). CONCLUSION: Postoperative elevation of pulmonary vascular resistance in children after surgical intervention for congenital heart disease is responsive to endothelin-A blockade with BQ123. Increased levels of endothelin-1 predict the response to this therapy, which might become an important addition to the clinical armamentarium in postoperative pulmonary hypertensive disease.

Adolescent↗

PubMed1994

Abnormal diurnal variation of blood pressure, cardiac output, and vascular resistance in cardiac transplant recipients.

BACKGROUND: An attenuated or absent nocturnal decline in blood pressure has repeatedly been documented in cardiac transplant recipients. The present study was aimed at investigating the hemodynamic mechanism underlying this abnormality. METHODS AND RESULTS: In 23 cardiac transplant recipients (11 to 36 months after transplantation) and in 23 control subjects matched for age and 24-hour mean arterial pressure, invasive 24-hour ambulatory blood pressure was measured by means of the Oxford technique. Beat-to-beat relative values of stroke volume were determined by means of a pulse-contour method, and relative changes of cardiac output (stroke volume x heart rate) and total peripheral vascular resistance (blood pressure/cardiac output) over the 24-hour period were calculated. The nocturnal decline in blood pressure was 20 +/- 8% (mean +/- SD) in control subjects but only 5 +/- 9% (P < .001) in cardiac transplant recipients. In control subjects, the nocturnal decline in blood pressure was associated with a nocturnal fall in cardiac output of 24 +/- 13%, whereas vascular resistance compared with daytime value did not change. The small nocturnal decline in blood pressure in cardiac transplant recipients was associated with an attenuated nocturnal fall in cardiac output of 14 +/- 12% (P < .05 versus control subjects). In addition, vascular resistance compared with daytime value was increased by 9 +/- 9% (P < .05) during the night. Both in cardiac transplant recipients and in control subjects, the nocturnal changes in blood pressure were correlated with the nocturnal changes in cardiac output but not with the nocturnal changes in total peripheral vascular resistance. CONCLUSIONS: This study confirms the attenuated nocturnal fall in blood pressure in cardiac transplant recipients. Hemodynamically, this attenuated blood pressure decline is characterized by a reduced nocturnal fall in cardiac output, and it is associated with a nocturnal increase in vascular resistance.

Adolescent↗

PubMed2006

Carotid baroreflex regulation of vascular resistance in high-altitude Andean natives with and without chronic mountain sickness.

We investigated carotid baroreflex control of vascular resistance in two groups of high-altitude natives: healthy subjects (HA) and a group with chronic mountain sickness (CMS), a maladaptation condition characterized by high haematocrit values and symptoms attributable to chronic hypoxia. Eleven HA controls and 11 CMS patients underwent baroreflex testing, using the neck collar method in which the pressure distending the carotid baroreceptors was changed by applying pressures of -40 to +60 mmHg to the chamber. Responses of forearm vascular resistance were assessed from changes in the quotient of blood pressure divided by brachial artery blood velocity. Stimulus-response curves were defined at high altitude (4338 m) and within 1 day of descent to sea level. We applied a sigmoid function or third-order polynomial to the curves and determined the maximal slope (equivalent to peak gain) and the corresponding carotid pressure (equivalent to 'set point'). The results showed that the peak gains of the reflex were similar in both groups and at both locations. The 'set point' of the reflex, however, was significantly higher in the CMS patients compared to HA controls, indicating that the reflex operates over higher pressures in the patients (94.4 +/- 3.0 versus 79.6 +/- 4.1 mmHg; P < 0.01). This, however, was seen only when subjects were studied at altitude; after descent to sea level the curve reset to a lower pressure with no significant difference between HA and CMS subjects. These results indicate that carotid baroreceptor control of vascular resistance may be abnormal in CMS patients but that descent to sea level rapidly normalizes it. We speculate that this may be explained by CMS patients having greater vasoconstrictor activity at altitude owing to greater hypoxic stimulation of chemoreceptors.

Adult↗

PubMed1993

The effects of acidosis and alkalosis on long bone vascular resistance.

This study used an ex vivo perfusion model to investigate the direct effects of acidosis and alkalosis on the vascular resistance of the canine tibia. Baseline vascular resistance (BVR) and the vascular smooth muscle response to bolus doses of norepinephrine (NE) (0.025-3.2 nmol) and periarterial sympathetic nerve stimulation (NS) (10-25 Hz: 9 V, 2 ms pulses, 10 s) were studied. In Group I, these parameters were measured at normal pH (duration 7.34-7.44) and then during acidosis (pH 7.2-7.33). In Group II, they were measured at normal pH and then during alkalosis (pH 7.47-7.58). In Group III (control), they were measured serially at a normal pH. Alkalosis increased BVR by 56% (p < 0.0001). Acidosis attenuated (18% reduction) and alkalosis enhanced (66% increase) the vasoconstrictor action of NE (p < 0.0001). Acidosis also attenuated (11% reduction) the effect of sympathetic NS (p = 0.012). It is concluded that perfusion pH influences the sensitivity of long bone resistance vessels to circulating NE and sympathetic NS. Thus, local concentration of hydrogen ions may provide bone with a mechanism to autoregulate blood flow.

Acidosis↗

PubMed1993

Much more potent baroreflex sympathetic control of vascular resistance in the resting human limb than previously believed.

The concept that, in man, the sympathetic control of the resting limb vascular resistance is truly limited and thus strikingly different from animal species, was challenged in the present study. Analyses were performed in healthy male volunteers of reflex forearm vascular resistance changes evoked by lower body negative pressure (LBNP) ranging from low (15 mmHg) to high and barely tolerated (85 mmHg) levels. Graded LBNP was associated with graded increases in resistance. At high 85 mmHg LBNP the responses were pronounced with a rise in forearm resistance to no less than 120 mmHg ml-1 min 100 + ml soft tissue, on average, corresponding to a 377% increase above control. This drastic response seemed entirely neurogenic in origin and calculations, based on the likely assumption that a similar response occurred in all skeletal muscle and skin/(subcutaneous fat), showed that it permitted a marked increment in total systemic vascular resistance because of the fact that these tissues constitute so large a proportion of the body mass. The conclusion was reached that the studied tissues may serve as main targets for powerful homeostatic reflexes. It is also suggested, in contrast to current views, that the high-pressure arterial rather than the low-pressure cardio-pulmonary baroreceptors may be the main mediators of haemodynamically important vasoconstrictor responses.

Adult↗

PubMed1995

Role of nitric oxide in regulation of vascular resistance in postnatal intestine.

Studies were conducted to determine whether endothelial production of nitric oxide (NO) participates in the regulation of vascular resistance in postnatal swine intestine. In vivo, intra-arterial infusion of the arginine analogue NG-monomethyl-L-arginine (L-NMMA, 10(-4) M) increased intestinal vascular resistance 34% in 3-day-old animals and 9% in 35-day-old animals (P < 0.01); similar findings were noted during infusion of 10(-3) M L-NMMA. Mechanical augmentation of gut flow rate induced intestinal vasodilation in both age groups; L-NMMA eliminated this flow-induced dilation in intestine of 3- but not 35-day-old animals. In vitro, precontracted mesenteric artery rings from both age groups relaxed to a similar extent in response to the endothelium-independent nitrovasodilator sodium nitroprusside (SNP) and the calcium ionophore A-23187; the effect of A-23187, but not SNP, was eliminated by mechanical disruption of the endothelium. Acetylcholine (ACh) and substance P (SP), agents with vascular effects that are secondary to receptor-mediated activation of NO, caused greater relaxation of rings from younger than from older animals, and this effect was attenuated by L-NMMA or methylene blue. Unstimulated accumulation of guanosine 3',5'-cyclic monophosphate (cGMP) occurred to a similar extent in vessel segments from both groups. ACh and SP increased cGMP accumulation in segments from 3- but not from 35-day-old animals. We conclude that the NO-cGMP axis participates to a greater extent in regulation of intestinal vascular resistance in 3- than in 35-day-old swine.

Aging↗