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PubMedDate not supplied

Low systemic vascular resistance after cardiopulmonary bypass: incidence, etiology, and clinical importance.

BACKGROUND: Low systemic vascular resistance during and immediately after cardiac surgery in which cardiopulmonary bypass is utilized is a well-known phenomenon, characterized as vasoplegia, which appears with an incidence ranging between 5% and 15%. The etiology is not completely elucidated and the clinical importance remains speculative. METHODS: In this prospective clinical trial, we assessed the incidence of postoperative low systemic vascular resistance in 800 consecutive patients undergoing elective coronary artery bypass grafting and/or valve replacement. We have attempted to identify the predictive factors responsible for the presence of low systemic vascular resistance and we have examined the subsequent postoperative outcome of those patients who developed early postoperative vasoplegia. The severity of vasoplegia was divided into three groups according either to the value of systemic resistance and/or the dose of vasoconstrictive agents necessary to correct the hemodynamic. RESULTS: Six hundred twenty-five patients (78.1%) did not develop vasoplegia, 115 patients (14.4%) developed a mild vasoplegia, and 60 patients (7.5%) suffered from severe vasoplegia. Low systemic vascular resistance did not affect hospital mortality but was the cause for delayed extubation and prolonged stay on the intensive care unit (ICU). Logistic regression analysis identified temperature and duration of cardiopulmonary bypass, total cardioplegic volume infused, reduced left ventricular function, and preoperative treatment with angiotensin-converting enzyme (ACE)-inhibitors, out of 25 parameters, as predictive factors for early postoperative vasoplegia. CONCLUSION: The occurrence of low systemic vascular resistance following cardiopulmonary bypass is as high as 21.8%. The etiology of this clinical condition is most probably multifactorial. Mortality is not affected by vasoplegia, but there is a trend to higher morbidity and prolonged stay in the ICU.

Aged↗

PubMed2002

Sympathetic nerve hyperactivity is associated with increased peripheral vascular resistance in hypopituitary patients with growth hormone deficiency.

OBJECTIVE: Hypopituitary patients with untreated GH deficiency have increased cardiovascular mortality. Sustained vasoconstriction is an important factor in the development of hypertension and insulin resistance. This study was designed to see whether peripheral vascular resistance was increased in subjects with GH deficiency and to examine the mechanisms involved. METHODS: Nine patients with GH deficiency and nine matched control subjects were studied. Calf vascular resistance was measured by venous occlusion plethysmography and sympathetic vasoconstrictor nerve activity by peroneal microneurography. RESULTS: Subjects with GH deficiency had a significantly lower blood flow (by 31%) and higher vascular resistance (by 48%) than the control group. In addition, they had a significantly higher sympathetic vasoconstrictor activity (by 67%) and this correlated with the vascular resistance (r = 0.45; P < 0.04). CONCLUSIONS: Patients with GH deficiency have an increased peripheral vascular resistance that is contributed to by an increase in central sympathetic vasoconstrictor discharge to the peripheral vasculature. This could be important in the development of cardiovascular disease in this condition.

Adult↗

PubMed1991

Prostaglandin inhibition prevents the fall in pulmonary vascular resistance as a result of rhythmic distension of the lungs in fetal lambs.

Prostaglandins (PG) are vasoactive factors involved in the regulation of pulmonary vascular resistance at birth. However, their physiologic importance is unclear. We hypothesized that PG are important regulators of pulmonary vascular resistance during static and rhythmic distension of the lungs. To test this hypothesis, we studied seven near-term fetal lambs treated with meclofenamate (a PG synthetase inhibitor) and six controls. The fetal lambs were instrumented on a long-term basis with vascular catheters to measure pulmonary arterial pressures, left atrial pressures, and pulmonary blood flow (radionuclide-labeled microsphere method). The fetal airway was intubated, and the ductus arteriosus wall was infiltrated with formalin to assure full patency during the study period. Pulmonary vascular resistance was calculated during baseline and during sequential in utero static distension of the fetal lungs, rhythmic distension, and ventilation with oxygenation. We found that during rhythmic distension, inhibition of PG synthesis abolished the 4-fold decrease in pulmonary vascular resistance seen in the control group. In contrast, during static distension, pulmonary vascular resistance did not change in either group, and during ventilation with oxygenation, pulmonary vascular resistance decreased 12-fold in both groups. We conclude that PG are important regulators of pulmonary vascular resistance during rhythmic distension but are not essential for the regulation of pulmonary vascular resistance during static distension or during ventilation with oxygenation.

Animals↗

PubMed1987

Differential regulation of regional vascular resistance by the rostral and caudal ventrolateral medulla in the rat.

Regional vascular resistance changes were determined following chemical excitation and inhibition of the rostral vasopressor (RVLM) and caudal vasodepressor (CVLM) areas in the ventrolateral medulla. Mesenteric, renal and hindquarter vascular resistances were assessed in paralyzed and artificially ventilated urethane-anesthetized rats instrumented with pulsed-Doppler flow probes. Microinjection of the excitatory amino acid L-glutamate in the RVLM elicited a significant dose-related transient increase in blood pressure, heart rate and resistance of mesenteric, renal and hindquarter vascular beds. A similar dose-related hemodynamic profile was obtained following microinjection of muscimol, a GABAmimetic, in the CVLM. In contrast, significant dose-related decrease in blood pressure, heart rate and resistance in mesenteric and hindquarter vascular beds was observed following glutamate-induced excitation of the CVLM and muscimol-induced inhibition of the RVLM. Changes in renal vascular resistance were inconsistent in this second hemodynamic profile. Intravenous administration of the alpha 1 adrenergic antagonist, prazosin, abolished all of the hemodynamic effects elicited by excitation of the RVLM except the tachycardia. Intravenous atropine methylnitrate blocked the bradycardia associated with excitation of the CVLM but did not alter the vascular resistance changes. These results indicate that the changes in heart rate did not contribute significantly to the resistance profiles described. The changes in vascular resistance elicited by excitation and inhibition of the RVLM were correlated with increase and decrease in the greater splanchnic nerve activity, respectively. In conclusion, neuron pools in the RVLM and CVLM exert differential effects upon resistance in different vascular beds via changes in sympathetic outflow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Incremental pulmonary vascular resistance increases with elevation of pulmonary venous pressure.

The aim of this study was to determine whether elevation of pulmonary venous pressure affects incremental pulmonary vascular resistance. We vascularly isolated the left lower lobe of the lung and perfused with blood using a pulsatile pump. Blood flow to the isolated lobe was decreased in 6 to 7 steps from about 8 to 1 ml/kg/min. Incremental pulmonary vascular resistance was estimated from the slope of the pressure-flow relationship between pulmonary arteriovenous pressure difference and pulmonary blood flow at different pulmonary venous pressures. Incremental pulmonary vascular resistance increased as pulmonary venous pressure was elevated. This result suggests that an increase in cardiac output, i.e., an increase in pulmonary blood flow, results in a larger increase of pulmonary arterial pressure in high pulmonary venous pressure than in low pulmonary venous pressure.

Animals↗

PubMed1995

Platelet-activating factor increases vascular resistance in rat hindquarters by thromboxane A2.

The effects of platelet-activating factor (PAF) on vascular resistance and capillary permeability were studied in the isolated rat hindquarter. Six groups were studied (n = 30): control; PAF alone (1.4 microM); and PAF (1.4 microM) pretreated with ibuprofen (30 mg/kg), thromboxane A2 (TxA2)-receptor antagonist (BM-13505, 2 mg/kg), PAF-receptor antagonist (WEB-2086, 5 mg/kg), or dexamethasone (5 mg/kg). The vascular resistance was calculated, and the reflection coefficient (sigma) was determined as an index of capillary permeability. Exogenous PAF caused a threefold increase in vascular resistance peaking at 5 min and a 2.5-fold increase in capillary permeability. The increased vascular resistance caused by PAF alone was significantly attenuated by ibuprofen, BM-13505, and dexamethasone. The PAF-induced permeability was neither attenuated by ibuprofen nor BM-13505. However, both the increased vascular resistance and permeability were blocked and attenuated by WEB-2086 and dexamethasone, respectively. We conclude that TxA2 mediates the PAF-induced increased vascular resistance; however, the increased vascular permeability is independent of the formation of TxA2 in the isolated hindquarter.

Animals↗

PubMed1977

Cardiovascular correlates of attention in normal and psychiatrically disturbed children. Blood pressure, peripheral blood flow, and peripheral vascular resistance.

Blood pressure, peripheral blood flow, and peripheral vascular resistance were measured in normal adults and children and in children with autism and severe disturbances in personality development while the individuals were engaged in a variety of attentional tasks. The tasks were designed to elicit outward direction of attention (and intake of sensory input) or inward direction of attention (and relative rejection of external sensory input). During tasks involving sensory rejection, normal adults and normal children showed increased blood flow and decreased peripheral vascular resistance; with sensory intake, blood flow was decreased and resistance was increased. The most severely impaired children showed little alteration in their physiological response to task requirements. Autistic children had higher mean blood flow and lower peripheral vascular resistance than normal children and adults. Some autistic children characteristically may be in a state of sensory rejection associated with generally higher levels of arousal or defense against environmental bombardment.

Adolescent↗

PubMed1996

The association among gastric mucosal pH, endotoxemia, and low systemic vascular resistance after cardiopulmonary bypass.

OBJECTIVE: Previously, it was found that a number of patients suffer a "low systemic vascular resistance syndrome" after cardiopulmonary bypass, and this was hypothesized to be secondary to endotoxemia, resulting from intestinal ischemia during bypass. DESIGN: Prospective cohort. SETTING: University teaching hospital. PARTICIPANTS: Thirty-two patients undergoing cardiac surgery. INTERVENTIONS: A number of variables relating to adequacy of tissue perfusion were measured at seven time periods perioperatively: cardiac output, systemic vascular resistance, oxygen delivery and consumption, oxygen extraction ratio, gastric mucosal pH, serum lactate, and endotoxin levels. MEASUREMENTS AND MAIN RESULTS: Investigators could not find any association between systemic vascular resistance and mucosal pH or endotoxin levels after bypass. There were significant changes in oxygen flux and extraction ratio (p < 0.001) as well as serum lactate (p < 0.001). There was no significant change in endotoxin levels or mucosal pH. The systemic vascular resistance at 6 hours postbypass could be predicted from the vascular resistance reading at 1 hour postbypass by a regression equation. A significant correlation between systemic vascular resistance and mixed venous oxygen was found at 4 and 6 hours postbypass (p < 0.01) as well as with oxygen extraction (p < 0.01). There was a negative correlation between mucosal pH and serum lactate, particularly at 6 hours postbypass (p < 0.01). There was no correlation between mucosal pH and endotoxin levels, oxygen flux, or cardiac output. CONCLUSIONS: The investigators therefore could not find any evidence that intestinal ischemia during bypass, as measured by gastric mucosal pH, predisposes to endotoxemia, or low systemic vascular resistance after cardiac surgery.

Adult↗

PubMed1986

Relationship between tracheal mucosal thickness and vascular resistance in dogs.

We have measured changes in tracheal mucosal thickness and tracheal vascular resistance in the dog. A probe was used to detect changes in height with time of the tracheal epithelium relative to an underlying cartilage. Tracheal vascular resistance was determined by perfusing a cranial tracheal artery at constant flow and measuring inflow pressure. Various drugs injected close-arterially were tested in 20 greyhounds anesthetized with pentobarbital sodium. Bradykinin, histamine, and methacholine significantly (P less than 0.01) decreased vascular resistance (-39.3 +/- 3.7, -47.3 +/- 4.2, and -22.5 +/- 5.2%, respectively) and increased the thickness of the mucosa (119.0 +/- 25.0, 61.9 +/- 25.0, and 46.3 +/- 6.4 micron). Substance P, vasoactive intestinal peptide, prostaglandin F2 alpha, and prostaglandin E, had large vasodilator actions (-31.4 +/- 5.0, -34.3 +/- 2.2, -21.9 +/- 2.8, and -31.5 +/- 2.4%) but only small effects on mucosal thickness (12.3 +/- 3.9, 13.0 +/- 3.4, 16.7 +/- 6.5, and 8.7 +/- 2.9 micron, respectively). Phenylephrine hydrochloride increased vascular resistance (19.8 +/- 1.7%) and decreased mucosal thickness (-23.9 +/- 3.1 micron). Thus airway vascular resistance and mucosal thickness always change in opposite directions, but drugs have different relative actions on the two variables. Even with large vasodilatations, the absolute changes in mucosal thickness were small and were unlikely to have an appreciable effect on tracheal airway resistance.

Animals↗

PubMed1977

Effects of increased intracranial pressure on pulmonary vascular resistance of fetal and neonatal goats.

The effects of increased intracranial pressure on the pulmonary circulation were investigated in fetal and neonatal goats. Pulmonary vascular resistance and systemic arterial pressure increased with elevation of intracranial pressure in neonatal animals. Alpha-adrenergic blockade completely eliminated both of these responses. The response of the fetal pulmonary circulation was unlike that seen in the postnatal animal. Although there was a slight elevation of pulmonary vascular resistance initially, the predominant response was a decrease in resistance. The decrease in fetal pulmonary vascular resistance was unaffected by phenoxybenzamine, but reversed by propranolol. After the beta-adrenergic blockade, increased intracranial pressure produced an increase in pulmonary vascular resistance. Similarly, ventilation of fetal lungs resulted in an increase in pulmonary vascular resistance after increased intracranial pressure. These results demonstrate for the first time that pulmonary vascular resistance may be altered in fetal and neonatal animals by increasing intracranial pressure. The elevation of pulmonary vascular resistance after elevated intracranial pressure must be due to an active pulmonary vascular constriction.

Age Factors↗

PubMed1992

[Impaired cardiopulmonary baroreflex control of forearm vascular resistance in hypertrophic cardiomyopathy].

We tested the hypothesis that the cardiopulmonary baroreflex control of forearm vascular resistance is impaired in patients with hypertrophic nonobstructive cardiomyopathy (HNCM). Forearm vascular responses to lower body negative pressures (LBNP) at -20 mmHg and -40 mmHg and to lower body positive pressure (LBPP) at +20 mmHg and +40 mmHg were compared between 11 patients with HNCM and 6 normal subjects. Forearm blood flow was measured with a strain gauge plethysmograph and forearm vascular resistance was calculated by dividing mean blood pressure by forearm blood flow. The left ventricular end-diastolic dimension and the left atrial dimension changed with the increases in LBNP and LBPP in patients with HNCM and in normal subjects. The ranges of these changes were similar in the 2 groups. Mean blood pressure and heart rate did not change during LBNP and LBPP. LBNP increased but LBPP decreased forearm vascular resistance in normal subjects, but neither LBNP nor LBPP changed the resistance in patients with HNCM. Increases in the resistance to cold pressor tests did not differ between the 2 groups. In patients with HNCM, there was a negative correlation between forearm vascular resistance at LBNP -20 mmHg and the left ventricular wall thickness (r = -0.81, p < 0.01). These results suggest that the cardiopulmonary baroreflex control of forearm vascular resistance is impaired in hypertrophic cardiomyopathy and that this impairment may be associated with left ventricular wall thickness.

Adult↗

PubMed1990

Combined effects of autoregulation and vasoconstrictors on hindquarters vascular resistance.

Relative contributions of local autoregulatory tone and vasoconstrictor tone to skeletal muscle vascular resistance were studied in anesthetized rats during hypertension produced by vasoconstrictor infusion. Rats were instrumented with a Doppler flow probe on the sacral aorta (SA) to measure blood flow and to allow calculation of vascular resistance. An occluder was placed on the SA and used to produce stepwise reductions in local perfusion pressure. Pressure-flow curves for the hindquarters were obtained in the absence and presence of elevated mean arterial pressure (MAP) produced by infusion of angiotensin II (ANG II; 50-1,247 ng.kg-1.min-1) or phenylephrine (PE; 2.5-12.4 micrograms.kg-1.min-1). Both ANG II and PE infusion increased MAP. For example, MAP was increased by ANG II from 91 to 134 mmHg and by PE from 89 to 156 mmHg. In addition, infusions of ANG II and PE produced dose-dependent rightward shifts in the hindquarters pressure-flow relationship. To examine the effect of pressure on the dose-response relationships of ANG II or PE, local perfusion pressure was adjusted to remain constant at various pressure levels that were independent of MAP during drug infusions. This produced a series of distinct dose-response curves with each curve defined by a different pressure level and with each characterized by a different maximum change in vascular resistance. If local perfusion pressure was not held constant but was permitted to increase with MAP, a compound dose-response curve was obtained in which the combined effects of the change in local pressure (i.e., autoregulation) and vasoconstrictor dose on vascular resistance could be discerned. These data demonstrate that hindquarters blood flow autoregulation continues to occur in the presence of vasoconstrictors. Consequently, autoregulatory mechanisms may be stimulated by any increase in MAP whether associated with systemic vasoconstrictor infusion or activation of neurohumoral pressor systems. The result is an amplified rise in local vascular resistance.

Angiotensin II↗

PubMed2001

Pulmonary vascular resistance after cardiopulmonary bypass in infants: effect on postoperative recovery.

OBJECTIVE: We sought to define the contemporary clinical effect of increased pulmonary vascular resistance in infants after congenital heart operations with cardiopulmonary bypass. METHODS: Fifteen infants (median age, 0.31 years; median weight, 5.1 kg) underwent cardiac operations involving cardiopulmonary bypass (range, 49-147 minutes). Pulmonary vascular resistance was measured in the immediate postoperative period in the intensive care unit by means of the direct Fick principle, with respiratory mass spectrometry to measure oxygen consumption. The effect of ventilation with an inspired oxygen fraction of 0.65, with additional infusion of L -arginine, substance P, and inhaled nitric oxide, was assessed and subsequently correlated with the length of mechanical ventilation from the end of cardiopulmonary bypass to successful extubation. RESULTS: Overall, pulmonary vascular resistance at baseline (11.7 +/- 5.6 WU. m(2)) could be reduced to a minimum of 6.1 +/- 3.5 WU. m(2). The ventilatory time was 0.86 to 14.9 days (median, 1.75 days) and correlated directly with the lowest pulmonary vascular resistance value achieved during the pulmonary vascular resistance study (r (2) = 0.64, P <.01). The patient subgroup with mechanical ventilation of greater than 2 days had significantly higher pulmonary vascular resistance at all stages of the study protocol, and in this group there was a correlation of cardiopulmonary bypass time and ventilatory support time (r (2) = 0.48, P <.05). CONCLUSION: Increased pulmonary vascular resistance, either directly or as a surrogate of the systemic inflammatory response after cardiopulmonary bypass, continues to have a significant effect on postoperative recovery of infants after cardiac operations.

Analysis of Variance↗

PubMed1996

Insulin increases forearm vascular resistance in obese, insulin-resistant hypertensives.

OBJECTIVE: To determine whether acutely lowering insulin levels with somatostatin in obese, insulin-resistant hypertensive individuals reduces arterial pressure and forearm vascular resistance; and whether these changes are reversed by restoring insulin levels during continuing somatostatin infusion. SUBJECTS: Subjects were 11 obese (body mass index 36 +/- 4 kg/m2) insulin-resistant, hypertensive men (systolic/diastolic blood pressures 153 +/- 6/94 +/- 2 mmHg, aged 51 +/- 7 years, fasting insulin level 17 +/- 8 mU/l). METHODS: Arterial pressure, forearm blood flow and vascular resistance were measured during 2 h of somatostatin infusion and during 2h of somatostatin plus insulin infusion (hyperinsulinemic or euglycemic clamp). RESULTS: Somatostatin infusion decreased plasma insulin levels from 17 +/- 2 to <3 mU/l. Insulin infusion raised plasma insulin levels to 86 +/- 7 mU/l. The forearm vascular resistance decreased significantly during somatostatin infusion and increased significantly during infusion of somatostatin plus insulin. Somatostatin also caused small but significant reductions in arterial pressure whereas insulin infusion during somatostatin infusion increased arterial pressure. Control experiments in six obese hypertensives indicated that the changes in forearm vascular resistance (but not in arterial pressure) were caused neither by time nor by vehicle. Control studies in six young normotensives indicated that somatostatin does not block the vasodilator response to insulin previously demonstrated in this group. CONCLUSIONS: The present results suggest that insulin causes forearm vasoconstriction in obese, insulin-resistant hypertensive humans.

Adult↗

PubMed2005

Novel Doppler technique to assess systemic vascular resistance: the snuffbox technique.

BACKGROUND: To explore an alternative to the systemic vascular resistance index (SVRI) for monitoring peripheral circulation in patients in the intensive care unit (ICU), the resistive index (RI) in the upper extremity arteries was measured by using surface Doppler ultrasound. METHODS AND RESULTS: The correlation between RI and vascular resistance was assessed in vitro using a vessel phantom in a Donovan-type mock circulation system. In addition, 15 ICU patients who had undergone open-heart surgery were studied. Mean arterial pressure, central venous pressure and cardiac output were measured 30 times at 10 min intervals after patients returned to the ICU following surgery, and the SVRI was calculated from these parameters. At the same time points, 3 parts of the upper extremity arteries (brachial artery in the cubital fossa (BA), radial artery at the wrist (RA), and radial artery at the anatomical snuffbox (SB)) were scanned by Doppler ultrasound, and the resistance index (RI) for each artery region was calculated. In vitro, RI increased with higher vascular resistance, exhibiting a significant correlation (r = 0.982, p < 0.0001). In vivo, the average incidence angles at the BA and RA were larger than 60 degrees , while that at the SB was only 11.5+/-10.8 degrees. The overall correlation between SVRI and RI for all patients was not significant for the BA or RA, but was significant for the SB (p < 0.0001). In individual patients, the correlation of SVRI with RI at the BA or RA was significant in 3 patients only, whereas significant correlation for the SB was observed in all patients. Doppler waveform analysis at the SB revealed diastolic flow reversal with increased SVRI. CONCLUSIONS: Measurement at the SB provides an ideal ultrasound incidence angle for the measurement of blood flow velocity. Hence, RI measured in this way may serve as an indicator of peripheral vascular resistance, and may be effective for the evaluation of peripheral circulatory disturbance.

Aged↗

PubMed1985

Rostral pontine and caudal mesencephalic control of arterial pressure and iliac, celiac and renal vascular resistance. II. Separate control and topographic organization.

A dense mapping of the rostral pons and caudal mesencephalon was performed in 26 cats using electrical stimulation while measuring arterial pressure and iliac, celiac and renal vascular resistance to determine if these vascular beds are controlled separately. It was found that the central tegmental fields (CTF) of the mesencephalon contained a large area active in control of iliac vascular resistance and a smaller area active in control of renal vascular resistance. It was found that the marginal nucleus of the brachium conjunctivum (BCM) contained areas active in control of all three vascular beds studied. To determine if the BCM controlled regional vascular beds differently, the relationship between changes in vascular resistance in each bed and changes in arterial pressure were examined quantitiatively using regression analysis and the slopes of the regression lines were shown to be different (P less than 0.001). Further analysis of the relationships of changes in vascular resistance of pairs of vascular beds indicated that vascular beds are controlled differently in response to electrical stimulation of the BCM.

Animals↗

PubMed1999

Changes in skeletal muscle vascular resistance with weight gain: associations with insulin and sympathetic activity.

OBJECTIVE: This study was designed to characterize changes in peripheral vascular resistance with weight gain, and whether these changes are correlated with insulin and/or sympathetic activity. RESEARCH METHODS AND PROCEDURES: Femoral vascular resistance (FVR), mean arterial pressure, heart rate, and plasma insulin were measured before and during overfeeding in seven dogs with unilateral lumbar ganglionectomy (L3 to L6). Measurements were taken standing and while walking on a treadmill. RESULTS: There was a significant main effect of weight gain to increase mean arterial pressure (16.5+/-8.4 mmHg and 12.5+/-6.8 mmHg increase for standing and walking baseline, respectively) and heart rate (increase from week 1 of 31.6+/-10.6 beats/minute standing and 38.3+/-9.1 walking beat/minute). FVR increased immediately with overfeeding/ weight gain [standing: denervated (DNX):1.32+/-0.3 to 2.34+/-0.5; intact: 0.88+/-0.17 to 1.9+/-0.33 mmHg/mL.min(-1)], but returned to baseline with continued weight gain. Return of FVR to baseline occurred between weeks 2 and 3 of overfeeding in the DNX limb, but did not return to baseline until week 6 in the innervated limb. These changes were not correlated with plasma insulin levels. DISCUSSION: These data suggest that vascular resistance may be normal in the obese, but increases in vascular resistance occur early with weight gain (before changes in arterial pressure). This initial increase in vascular resistance could initiate the series of events leading to obesity-associated hypertension. Additionally, changing vascular resistance during weight gain may be influenced by sympathetic activity, because DNX limb FVR returned to baseline approximately 3 weeks earlier than the innervated limb.

Animal Feed↗

PubMed2002

Frequency modulation of mesenteric and renal vascular resistance.

The hypothesis was tested that low-frequency vasomotions in individual vascular beds are integrated by the cardiovascular system, such that new fluctuations at additional frequencies occur in arterial blood pressure. In anesthetized rats (n = 8), the sympathetic splanchnic and renal nerves were simultaneously stimulated at combinations of frequencies ranging from 0.075 to 0.8 Hz. Blood pressure was recorded together with mesenteric and renal blood flow velocities. Dual nerve stimulation at low frequencies (<0.6 Hz) caused corresponding oscillations in vascular resistance and blood pressure, whereas higher stimulation frequencies increased the mean levels. Blood pressure oscillations were only detected at the individual stimulation frequencies and their harmonics. The strongest periodic responses in vascular resistance were found at 0.40 +/- 0.02 Hz in the mesenteric and at 0.32 +/- 0.03 Hz (P < 0.05) in the renal vascular bed. Thus frequency modulation of low-frequency vasomotions in individual vascular beds does not cause significant blood pressure oscillations at additional frequencies. Furthermore, our data suggest that sympathetic modulation of mesenteric vascular resistance can initiate blood pressure oscillations at slightly higher frequencies than sympathetic modulation of renal vascular resistance.

Animals↗