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Results for “VASCULAR RESISTANCE”

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PubMed1993

Changes in blood flow and vascular resistance in the arm and leg during spinal anaesthesia and vasopressor therapy with methoxamine.

The effects of subarachnoid block with hyperbaric bupivacaine 0.5% on forearm and calf blood flow and vascular resistance were examined using venous occlusion plethysmography in 10 fit patients. Following blockade there was an increase in mean (SD) calf blood flow from 2.0 (0.4) to 2.6 (1.2) ml.100 ml-1.min-1 (p = 0.057), a decrease in mean (SD) calf vascular resistance from 55 (15) to 38 (14) R units (p < 0.01), a decrease in mean (SD) forearm blood flow from 3.1 (1.2) to 1.8 (0.9) ml.100 ml-1.min-1 (p < 0.01) and an increase in mean forearm vascular resistance from 38 (16) to 62 (24) R units (p < 0.01). Methoxamine 2 mg was administered intravenously when the mean arterial blood pressure decreased by 15%. There was a resultant marked increase in mean (SD) forearm blood flow from 1.8 (0.9) to 3.0 (0.8) ml.100 ml-1.min-1 (p < 0.001) but a decrease in mean (SD) calf blood flow from 2.6 (1.2) to 2.1 (1.4) ml.100 ml-1.min-1 (p = 0.11). Correspondingly, the mean (SD) forearm vascular resistance decreased from 62 (24) to 46 (17) R units (p < 0.01) with an increase in mean (SD) calf vascular resistance from 38 (14) to 56 (22) R units (p < 0.01). These findings indicate that whereas methoxamine produces the anticipated constrictor response in the calf vessels it causes a simultaneous reduction in vascular resistance in the forearm.

Adult↗

PubMed1992

Characterization of thromboxane and prostacyclin effects on pulmonary vascular resistance.

Although thromboxane and prostacyclin (PGI2) have long been described as major controllers of pulmonary vascular resistance, little has been reported on the characteristics of the interactions between the two arachidonic acid products. The current study uses segmental vascular resistance and compliance measurements to evaluate the actions of thromboxane and PGI2 in isolated blood-perfused rat lung. The thromboxane analogue U-46619 increases pulmonary vascular resistance by increasing only small artery resistance and decreases pulmonary vascular compliance in the middle compartment. Among the vascular effects of U-46619 are a maximum increase in resistance (RmaxU-46619) of 60.3 +/- 15.6 cmH2O.l-1.min.100 g-1 and a concentration required for 50% of maximum increase (K0.5,U-46619) of 1.60 +/- 0.85 nM for small artery resistance, a minimum vascular compliance (CminU-46619) of -0.93 +/- 0.58 cmH2O, and a K0.5,U-46619 of 1.10 +/- 1.60 nM for middle compartment compliance. Similar results were obtained for total resistance and total compliance. The effects of PGI2 on thromboxane-induced resistance and compliance changes were evaluated using K0.5,PGI2, RmaxPGI2, and CmaxPGI2 at each dose of thromboxane. PGI2 was more effective in reversing the thromboxane constriction at higher concentrations of thromboxane. These data show that the absolute concentration of PGI2 and thromboxane and not a simple ratio of thromboxane to PGI2 determines vascular tone.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1997

Bolus administration of eltanolone, thiopental, or etomidate does not affect systemic vascular resistance during cardiopulmonary bypass.

OBJECTIVE: To discover possible effects on systemic vascular resistance of the anesthetic induction agent eltanolone in comparison with thiopental and etomidate. The measurements were performed during cardiopulmonary bypass to maintain a constant cardiac output (approximately pump flow). DESIGN: The patients were prospectively randomized in three groups to receive either eltanolone, thiopental, or etomidate. SETTING: University hospital as a single center. PARTICIPANTS: Seventy-five patients scheduled for elective coronary artery bypass grafting. INTERVENTIONS: The anesthetic induction agents were repeated at the same dosage when cardiopulmonary bypass was instituted. The respective mean dosages were eltanolone, 0.41 +/- 0.1 mg/kg; thiopental, 2.88 +/- 0.62 mg/kg; etomidate, 0.26 +/- 0.06 mg/kg. MEASUREMENTS AND MAIN RESULTS: Systemic vascular resistance was calculated from the mean of a triple measurement (normal pump flow and +/- 20%). Points of measurement were before, and 2 and 5 minutes after injection of the hypnotic agent. None of the injected drugs made a significant change in the systemic vascular resistance. A small (not significant) decrease from 1,295 +/- 296 dyne/s/cm-5 to 1,196 +/- 323 dyne/s/cm-5 (mean +/- SD) was seen in the eltanolone group, whereas the other patients did not show any change during the study period. CONCLUSIONS: The reason for the significant reduction of the arterial pressure attributed to anesthetic induction by eltanolone may be more a cardiodepressive effect than a direct vasodilation.

Anesthetics, Intravenous↗

PubMed1975

Effects of alveolar and perfusion hypoxia and hypercapnia on pulmonary vascular resistance in the lamb.

The effects of ventilatory hypoxia and hypercapnia and perfusion hypoxia and hypercapnia on pulmonary vascular resistance were studied in the intact lamb using right heart techniques to isolate and perfuse the left lower lobe. Ventilatory hypoxia increased vascular resistance in the left lower lobe by constricting predominantly vessels upstream from small lobar veins, presumably small arteries. The response to hypoxia was not blocked by phentolamine and diphenhydramine in doses that markedly decreased pressor responses to norepinephrine and histamine in the lung. Perfusion hypoxia did not alter vascular resistance in the perfused lobe. Ventilatory hypercapnia increased vascular resistance in the lung by constricting mainly upstream vessels, whereas perfusion hypercapnia decreased resistance by dilating upstream vessels. These data indicate that histamine and catecholamines are not involved in the response to alveolar hypoxia. These results suggest that the sensor site for ventilatory hypoxia is close to the alveolus since the response is unrelated to lobar arterial Po2. It is concluded that systemic reflexes are not necessarily involved in the response of the pulmonary vascular bed to ventilatory hypoxia or hypercapnia and that the magnitude and rapidity of this response suggest that it may represent an important local mechanism for the control of ventilation-perfusion relationships in this species.

Animals↗

PubMed1994

Effect of erythrocyte heat treatment on pulmonary vascular resistance.

The effect of red blood cell deformability on the pulmonary vascular resistance was studied in isolated dog and rat lungs. Blood cells were incubated at 49 degrees C for 1 hr, to render them rigid. The resistance to blood flow in the lung was assessed either by calculating the pulmonary vascular resistance (PVR = arterial - venous pressure difference divided by flow rate) or by examining the vascular pressure-flow relationship for changes in slope and intercept. The resistance in the lung was first assessed during perfusion with normal blood and again during perfusion with rigid cells. The results showed that PVR in dog lungs increased by 15% during perfusion with heat-treated blood and that this increase in PVR was associated with a significant increase in the middle segment resistance (arterial-venous occlusion technique) and with an increase in critical closing pressure (pressure intercept of the pressure-flow curve). In contrast to the small effect in dog lungs, the PVR in rat lungs rose more than 400% during perfusion with heat-treated blood. The marked increase of PVR in rat lungs was prevented with papaverine (PVR increased only 58%), suggesting that vasoconstriction was a primary event in rat lungs. The rise in vascular resistance in rat lungs was further shown to be primarily due to the presence of rigid erythrocytes (RBC). The increase in PVR in the rat lungs was not due to mechanical obstruction of the vasculature but rather to constriction of arteries and veins (double occlusion technique). The conclusion from this study is that RBC deformability plays an important role in the pulmonary vasculature, primarily because of release of vasoactive substances and partially because of the potential mechanical obstruction of capillaries. These events are apparently species dependent and are attributed mostly to red blood cell deformability which decreases during heat treatment.

Animals↗

PubMed1992

Changes in vascular resistance during carotid occlusion in normal and baroreceptor-denervated rats.

In the present study, we investigated changes in mesenteric, renal, and hindquarter vascular resistance during the pressor response produced by bilateral carotid occlusion (BCO) in conscious, freely moving normal and denervated (aortic, carotid, or both) rats. BCO was performed using special previously implanted cuffs. In control normal rats, the increase in mean arterial pressure (MAP) during early and late responses (37 +/- 4 and 21 +/- 2 mm Hg, respectively) was related to increased renal (125 +/- 12% and 45 +/- 10%) and mesenteric (38 +/- 13% and 41 +/- 5%) but not hindquarter (14 +/- 4% and 8 +/- 7%) vascular resistance. In aortic-denervated rats, the greater MAP increase in early and late responses (57 +/- 4 and 44 +/- 4 mm Hg, respectively) compared with normal rats was related to a marked increase in hindquarter (137 +/- 26% and 106 +/- 26%) and mesenteric (104 +/- 14% and 66 +/- 9%) vascular resistance. In carotid-denervated rats, MAP increase and change in vascular resistance were similar to those values observed in control rats. Sinoaortic-denervated rats showed a greater MAP increase (34 +/- 4 mm Hg) during late response and a reduced increase in renal vascular resistance (46 +/- 6%) during early response.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1997

Renal vascular resistance in normal children--a color Doppler study.

To investigate the relationship between age and renal vascular resistance and to establish normative data of the systolic/diastolic ratio (S/D ratio), pulsatility index (PI), and resistant index (RI) of the renal artery in the normal pediatric population, we studied 252 normal children aged newborn to 13 years (a total of 449 kidneys) with a color Doppler unit. After the normality of the kidney was established, color flow mapping was performed to localize the segmental portion of the renal artery. Flow velocity waveforms were then obtained by pulsed Doppler, and S/D ratio, PI, and RI were calculated. Multiple regression analysis confirmed the age dependence of the S/D ratio, PI, and RI of the renal artery in normal children. Renal vascular resistance continuously declines after birth and stabilizes at the age of 102-130 months. Normative data for S/D ratio, PI, and RI of the renal artery in normal children were established for each age group. Since renal vascular resistance decreases with age and stabilizes at 8-10 years, we suggest using different normal ranges for each age group when studying renal vascular resistance in pediatric patients.

Adolescent↗

PubMed1994

Regulation of baseline vascular resistance in the canine diaphragm by nitric oxide.

1. The role played by nitric oxide (NO) in the regulation of blood flow to the canine isolated hemidiaphragm was evaluated by determining (a) the effects of the L-arginine analogues NG-nitro-L-arginine methyl ester (L-NAME), NG-nitro-L-arginine (L-NOARG), and argininosuccinic acid (ArgSA) on baseline vascular resistance and of the latter two agents on endothelium-dependent (acetylcholine, ACh) and endothelium independent (sodium nitroprusside, SNP) vasodilatation; (b) the effects of L- and D-arginine on baseline vascular resistance; and (c) the effects of L-glutamine, an inhibitor of intracellular recycling of L-citrulline to L-arginine, on baseline resistance and on the response to ACh and SNP. 2. L-NAME, L-NOARG and ArgSA (6 x 10(-4) M final concentration) increased baseline diaphragmatic vascular resistance to a similar extent (28.6 +/- 4.2%, 26.7 +/- 4.3% and 32.8 +/- 4.6% respectively). L-NOARG and ArgSA reversed the vasodilator effect of ACh but not of SNP. 3. L- and D-arginine had no effect on vascular resistance. 4. L-Glutamine (10(-3) M) increased baseline vascular resistance by 10 +/- 1.9% (P < 0.05) but did not alter responses to either ACh or SNP. 5. Basal NO release plays a role in the regulation of baseline diaphragmatic vascular resistance. L-Arginine analogues tested potently and specifically inhibited this process. Moreover, extracellular L-arginine appears to have no effect on baseline diaphragmatic vascular resistance.

Acetylcholine↗

PubMed1998

Adenosine receptor antagonism affects regional resting vascular resistance during rat peritoneal sepsis.

BACKGROUND: To identify vascular beds where endogenous adenosine plays a significant role as a mediator of resting perfusion alterations associated with sepsis, we tested the hypothesis that adenosine receptor blockade would cause differential regional increases in vascular resistance during intraperitoneal (ip) sepsis in the rat. MATERIALS AND METHODS: Rats (250-350 g) were catheterized and randomized to septic or nonseptic groups. Sepsis was induced with an ip injection of cecal slurry (150 mg/kg in D5W; 5 ml/kg), and baseline hemodynamics, cardiac output (CO), and blood flows (microspheres) were measured 24 h later. Animals then received the adenosine receptor antagonist 8-phenyltheophylline (8-PTH; 10 mM, 1.5 ml/kg), its vehicle (1.5 ml/kg), or normal saline (1.5 ml/kg), iv, and measurements were repeated. RESULTS: Septic animals treated with 8-PTH had a significant increase in skeletal muscle, hepatic portal, and cerebral vascular resistance with concomitant decreases in CO when compared with vehicle at 1 min. No significant resistance changes were observed in the renal, adipose, or coronary vasculatures. Adenosine receptor blockade caused a significant increase in +dP/dt and -dP/dt during sepsis, indicating that the reduced CO was not secondary to myocardial depression. CONCLUSIONS: These data suggest that adenosine receptor-mediated actions during sepsis affect vascular beds selectively and indicate a significant role for adenosine in resting perfusion redistribution in sepsis.

Adenosine↗

PubMed1989

Effect of endothelin-1 on regional vascular resistances in the pig.

The actions of endothelin-1 (ET-1) on vascular resistances were investigated and characterized in anesthetized pigs in vivo. Intravenously administered ET-1 (2-400 pmol/kg) caused dose-dependent increases in mean arterial blood pressure accompanied by a reduction in heart rate. ET-1 also increased renal, coronary, femoral, and bronchial vascular resistances. The kidney was about 10 times more sensitive to ET-1 than the other regions. The ET-1-induced vasoconstriction in the kidney was attenuated by nifedipine (100 micrograms/kg). The responses to ET-1 in the femoral and bronchial vascular beds were biphasic with an initial decrease followed by an increase in vascular resistance at high doses. It is concluded that ET-1 causes dose-dependent vasoconstriction in several vascular beds in vivo with the most pronounced effects in the renal circulation.

Animals↗

PubMedDate not supplied

Pharmacologic reduction of pretransplantation pulmonary vascular resistance predicts outcome after pediatric heart transplantation.

Pulmonary hypertension leading to donor right ventricular dysfunction remains a major risk factor associated with poor outcome after heart transplantation. This study evaluated a pretransplantation protocol to assess pulmonary vascular resistance index and its response to pharmacologic modulation. Cardiac catheterization was performed in 25 patients (mean age, 8.6 years [range, 1 to 17 years]; mean weight, 27.3 kg [range, 8.1 to 54 kg]) with end-stage heart failure. Mean pulmonary artery and capillary wedge pressures and cardiac index were measured in the baseline state and during administration of 100% oxygen, dobutamine at 10 micrograms/kg/min, and nitroprusside at 1 to 4 micrograms/kg/min. Transpulmonary pressure gradient and pulmonary vascular resistance index were calculated. In 22 survivors, hemodynamics were reassessed 1 and 4 weeks after transplantation. The mean cardiac index significantly increased (2.2 to 3.2 L/min/m2); transpulmonary pressure gradient (12.7 to 9.6 mm Hg) and pulmonary vascular resistance index (6.2 to 3.0 units/m2) decreased during the drug study. In 12 patients with a baseline pulmonary vascular resistance index of more than 6 units/m2, 10 survived heart transplantation. This study shows that pharmacologic reduction of the pulmonary vascular resistance index in the pretransplantation protocol predicts reduced pulmonary vascular resistance index and a favorable outcome after heart transplantation.

Adolescent↗

PubMed1991

Comparison between muscle sympathetic nerve activity and calf vascular resistance with head-up tilting in humans.

The purpose of this study was to determine the relationship between muscle sympathetic nerve activity (MSA) to calf muscle and calf vascular resistance with head-up tilting in humans. In nine healthy volunteers, we performed simultaneous measurements of MSA using microneurography and calf vascular resistance using electrical impedance plethysmography in the same leg. The volunteers were laid on a tilt table and the examinations with head-up tilting (0 degrees, 30 degrees, 60 degrees) were performed. Corresponding to the increase in angles of head-up tilting, MSA and calf vascular resistance significantly increased. A statistically significant positive linear correlation was demonstrated between MSA and calf vascular resistance. These data suggest that impedance plethysmographic measurement of calf vascular resistance can be reliably used to assess the status of MSA with head-up tilting.

Adult↗

PubMed1990

Regional vascular resistance during exercise: role of cardiac afferents and exercise training.

This study was designed to determine whether cardiac vagal afferents exert an inhibitory influence on increases in regional vascular resistance during exercise and to determine whether endurance exercise training enhances the inhibitory influence of cardiac vagal afferents. We measured changes in regional vascular resistance in 12 rabbits at rest and during running at 12.6 m/min, 20% grade, before and after reversible denervation of cardiac afferents (intrapericardial procainamide HCl, 2%). In addition, these procedures were repeated in five of these rabbits following an 8-wk endurance exercise training program. Because intrapericardial injections of procainamide anesthetize both the efferent as well as the afferent innervation to the heart, it was necessary to determine the effects of blocking the efferent innervation on the regulation of regional vascular resistance during exercise. Rabbits were instrumented with Doppler ultrasonic flow probes around the renal (R), mesenteric (M), ascending, and terminal aortic (TA) arteries. Catheters were positioned in the central ear artery and vein and pericardial sac. Mean arterial pressure, heart rate, cardiac output, R, M, TA, and systemic (S) resistances were determined. Exercise changed R (+37 +/- 4%), M (+88 +/- 9%), TA (-62 +/- 6%), and S (-34 +/- 3) resistances. Subsequent cardiac efferent blockade alone had no significant effect on regional vascular resistance during exercise. Combined efferent and afferent blockade resulted in significant increases in R (+62 +/- 6%) and M resistance (+134 +/- 13%) but did not alter TA (-51 +/- 4%) or S (-27 +/- 2%) resistance during exercise. Exercise training significantly enhanced the inhibitory influence of cardiac afferents on R and M regional vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

PubMed1996

Systemic vascular resistance index determined by thoracic electrical bioimpedance predicts the risk for maternal hypotension during regional anesthesia for cesarean delivery.

OBJECTIVE: Our purpose was to evaluate the predictive value of the baseline systemic vascular resistance index for the development of maternal hypotension during regional anesthesia for cesarean delivery. STUDY DESIGN: Patients receiving a standardized spinal or epidural anesthetic for nonemergency cesarean delivery were studied prospectively. Hemodynamic data were obtained noninvasively with an NCCOM-3 cardiac output monitor (Bomed Medical Manufacturing, Irvine, Calif.), which uses thoracic electrical bioimpedance to estimate stroke volume and cardiac output. Measurements obtained were indexed to body surface area. The systemic vascular resistance index was calculated from mean arterial pressure and thoracic electrical bioimpedance-derived cardiac index. Hemodynamic data obtained were analyzed to identify statistically significant predictors of maternal hypotension. RESULTS: Maternal hypotension occurred in 24 of 42 (57%) patients studied. The incidence of hypotension did not differ between the types of anesthesia: spinal 17 of 274 (62%) versus epidural 7 of 15 (47%, p=0.48). The mean interval to the onset of hypotension was 12.2 minutes (SD 2.2 minutes, range 2 to 24 minutes). Mean (SD) baseline maternal systolic blood pressure was higher in patients who had hypotension (145 torr [4]) than those who did not (129 torr [4], p=0.01). The mean (SD) baseline systemic vascular resistance index was higher in patients who had hypotension (633 [SD 36] dyne . cm . sec-5/m2) than those who did not (454 [SD 29] dyne . cm . sec-5/m2; p =0.001). With receiver-operator characteristic curves, a baseline systemic vascular resistance index of 500 had a sensitivity of 83%, a specificity of 78%, a positive predictive value of 83%, and a negative predictive value of 78% for maternal hypotension (odds ratio 17.5, 95% confidence interval 3.1 to 109.4). A baseline systolic blood pressure of 140 torr had a sensitivity and specificity of 42% and 72%, respectively (odds ratio 1.9, 95% confidence interval 0.4 to 8.8). CONCLUSIONS: Baseline systemic vascular resistance index obtained by noninvasive cardiac output monitoring with thoracic electrical bioimpedance and systolic blood pressure are useful to predict the risk for maternal hypotension with regional anesthesia. Patients with increased baseline systemic vascular resistance index or systolic blood pressure are at increased risk for hypotension.

Adult↗

PubMed1993

Relationships between ambulatory blood pressure, forearm vascular resistance, and left ventricular mass in hypertensive and normotensive subjects.

Ambulant 24 h blood pressure was recorded in 97 untreated hypertensive subjects (50 with, 47 without echocardiographic signs of left ventricular hypertrophy) and 45 matched normotensive subjects. Forearm vascular resistance was calculated from mean blood pressure and blood flow, which was measured by venous plethysmography during reactive hyperemia. Blood pressure variability was calculated by standard deviations of pressure values. Systolic 24 h blood pressure exhibited the closest correlation with left ventricular mass index in hypertensives (4 = 0.48; P < .001). No relation could be found between blood pressure fall during the night and left ventricular mass index. Furthermore, body weight was a significant correlate of left ventricular mass (r = 0.53; P < .001). Regression analysis indicated that body weight and 24 h blood pressure were the principal determinants of left ventricular mass. Blood pressure variability was significantly higher in hypertensive than in normotensive subjects (P < .05). The highest vascular resistance was found in hypertensive patients with left ventricular hypertrophy compared with the other groups (P < .05). A significant close correlation between systolic resting as well as 24 h blood pressure and vascular resistance was identified for the group of hypertensives and all subjects investigated. Furthermore, left ventricular mass index and vascular resistance were correlated (in hypertensives: r = 0.32; P < .01). The extent of left ventricular mass index and forearm vascular resistance are proportional to the severity of hypertension. As vascular resistance and left ventricular mass are also related, these findings could speak for a parallel development of total peripheral resistance and left ventricular hypertrophy in essential hypertension.

Adult↗

PubMed1995

Pulmonary vascular resistance in infants after cardiac surgery: role of carbon dioxide and hydrogen ion.

OBJECTIVE: The objective of this study was to describe the effects of altering arterial PCO2 and pH on pulmonary vascular resistance in infants after cardiopulmonary bypass for cardiac surgery. DESIGN: Prospective study (with each patient as his or her own control). SETTING: Cardiac intensive care unit in a children's hospital. PATIENTS: We studied 15 infants (ages ranging from 0.4 to 15.6 months; median 5.7) who were mechanically ventilated during the immediate postoperative period after corrective cardiac surgery. INTERVENTIONS: The study was designed to have the following three stages: In the baseline stage, the initial postoperative hemodynamic parameters were stabilized and body temperature was normalized. In the hypercarbia stage, with FIO2 at 0.40, the rate of ventilation was decreased to produce an end-tidal CO2 level of > 55 torr (> 7.3 kPa). This stage established a clinical model of increased pulmonary vascular resistance. With the minute ventilation held constant in order to maintain a constant PaCO2, the arterial pH was increased by administration of a 4-mEq/kg iv dose of sodium bicarbonate (sodium bicarbonate stage). Arterial blood gas and hemodynamic determinations were obtained after a 10-min stabilization period at each stage. Drug infusions were not altered during the study period. MEASUREMENTS AND MAIN RESULTS: In the hypercarbia stage (stage 2), the mean PaCO2 increased from 36 +/- 5 torr (4.8 +/- 0.7 kPa) (at baseline) to 55 +/- 16 torr (7.3 +/- 2.1 kPa) (p < .01). As a result, the mean arterial pH decreased from 7.48 +/- 0.05 to 7.31 +/- 0.03 (p < .01). During this stage, the mean pulmonary arterial pressure increased from 21 +/- 6 to 30 +/- 8 mm Hg (p < .01) but the cardiac index remained unchanged (3.7 +/- 1.2 to 3.8 +/- 1.2 L/min/m2). Pulmonary vascular resistance index increased from 4.1 +/- 2.0 to 6.0 +/- 3.1 U.m2 (p < .01). After the administration of sodium bicarbonate (stage 3), the arterial pH increased to 7.44 +/- 0.06 (p < .05), while the PaCO2 was unchanged. The pulmonary vascular resistance index decreased to 3.1 +/- 1.5 U.m2 (from 6.0 +/- 3.1 U.m2; p < .01) as a result of both a decrease in mean pulmonary arterial pressure (to 26 +/- 6 mm Hg; p < .01) and a concomitant increase in cardiac index to 5.1 +/- 1.6 L/min/m2 (p < .01). CONCLUSIONS: Increasing the arterial pH by the administration of sodium bicarbonate both lowers the pulmonary arterial pressure and increases the cardiac index, resulting in a decrease in pulmonary vascular resistance. These changes were observed without alteration in PaCO2. Metabolic alkalosis may have a role in the treatment of increased pulmonary vascular resistance in infants after cardiopulmonary bypass for cardiac surgery.

Carbon Dioxide↗

PubMed1999

Nitric oxide/cAMP interactions in the control of rat renal vascular resistance.

This study aimed to characterize the interaction between nitric oxide (NO)- and cAMP-related pathways in the control of renal blood flow. Using the isolated perfused rat kidney model, we determined the effects of inhibition of NO formation by Nomega-nitro-L-arginine methyl ester (L-NAME; 1 mmol/L) and of NO administration by sodium nitroprusside (SNP, 10 micromol/L) on renal vascular resistance under conditions of elevated vascular cAMP levels. cAMP levels were increased either by adenylate cyclase activation via isoproterenol or by inhibition of cAMP phosphodiesterases (PDEs) 1, 3, and 4. We found that L-NAME markedly increased vascular resistance and that this effect was completely reversed by SNP. Both isoproterenol and inhibitors of the cAMP PDEs lowered basal vascular resistance. In the presence of isoproterenol (3 nmol/L) and inhibitors of PDE-1 [8-methoxymethyl-l-methyl-3-(2-methylpropyl)-xanthine; 8-MM-IBMX, 20 micromol/L] and PDE-4 (rolipram, 20 micromol/L), L-NAME again substantially increased vascular resistance, and this effect of L-NAME was completely reversed by SNP. In the presence of the PDE-3 inhibitors milrinone (20 micromol/L) and trequinsin (200 nmol/L), however, both L-NAME and SNP failed to exert any additional effects. Because PDE-3 is a cGMP-inhibited cAMP PDE and because the vasodilatory effect of SNP was abrogated by the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ) (20 micromol/L), our findings are compatible with the idea that an action of NO on PDE-3 could account for the vasodilatory properties of NO on the renal vasculature. Moreover, our findings suggest that PDE-3 activity is an important determinant of renal vascular resistance.

Adenylyl Cyclases↗

PubMed1975

Relation of renin status to neurogenic vascular resistance in borderline hypertension.

The relation of renin-angiotensin status to general hemodynamics and to neurogenic vascular resistance was studied in patients with border-line hypertension. Plasma renin activity during standing was referred to a standard renin-urinary sodium nomogram derived from 18 normal subjects. Among 22 patients with borderline hypertension the renin level was high in 8, low in 4 and within normal limits in the remaining 10. In patients with borderline hypertension and high or normal levels of plasma renin activity, the blood pressure elevation was due to increased total peripheral vascular resistance. In contrast, in patients with low renin borderline hypertension, total peripheral resistance was not significantly elevated; the blood pressure elevation reflected a cardiac index 12 percent higher than that in normal subjects. The neurogenic contribution to total peripheral vascular resistance was assessed by studying the effects of alpha adrenergic blockade with phentolamine, after prior autonomic blockade of the heart with atropine (0.04 mg/kg body weight) and propranolol (0.2 mg/kg). Phentolamine (15 mg) produced an immediate reduction in total peripheral resistance of 12.0 +/- 6.7 percent in patients with high renin borderline hypertension (P less than 0.01) but no change in normal subjects or those with borderline hypertension and normal or low renin levels. Normalization of the blood pressure followed "total" autonomic blockade with atropine, propranolol or phentolamine only in patients with high renin borderline hypertension. It is concluded from these preliminary data that in high renin borderline hypertension the blood pressure elevation is sustained by neurogenic mechanisms. The elevated renin level in these patients is probably an expression of increased sympathetic nervous activity. Although the elevated plasma renin level may possibly be contributing to the generation of higher sympathetic tone, or data do not support a direct role of circulating angiotensin in the maintenance of the elevated vascular resistance.

Adolescent↗