Changes In Central Venous Pressure Research Articles

Extravascular fluid uptake during cardiopulmonary bypass in hypertensive dogs

We investigated the effects of increases in central venous pressure (CVP) and carotid baroreceptor-induced vasodilation on the rate of extravascular fluid uptake during cardiopulmonary bypass in normotensive and Goldblatt hypertensive dogs. Carotid sinus baroreceptors were selectively perfused to control the level of vasodilation. Central venous pressure was controlled by changing the height of the venous outflow cannula. Extravascular fluid uptake was determined from the rate of change in reservoir volume. After 3 hours of bypass, total fluid accumulation was 56.11 ± 14.16 mL/kg in normotensive dogs, significantly less than in hypertensive dogs (110.90 ± 23.20 mL/kg) ( p < 0.05). Raising CVP from 1 to 5 mm Hg increased the rate of extravascular fluid uptake in both normotensive (from 0.05 ± 0.25 to 0.85 ± 0.22 mL · kg −1 · min −1; p < 0.05) and hypertensive dogs (from 0.68 ± 0.28 to 2.57 ± 0.46 mL · kg −1 · min −1; p < 0.01)). At a constant CVP, baroreceptor-induced vasodilation increased the rate of extravascular fluid uptake in normotensive (from 0.25 ± .15 to 0.81 ± .22 mL · kg −1 · min −1) and in hypertensive dogs (from 0.84 ± .12 to 1.72 ± .32 mL · kg −1 · min −1; p < 0.05). Hypertensive dogs were more sensitive to changes in CVP and to baroreceptorinduced vasodilation. The results of this study imply that elevations in CVP or the use of vasodilators may lead to increased extravascular fluid uptake during bypass; this effect may be exacerbated in the hypertensive state.

The cerebral and systemic effects of movement in response to a noxious stimulus in lightly anesthetized dogs. Possible modulation of cerebral function by muscle afferents.

Afferentation theory predicts that agents or maneuvers that stimulate muscle stretch receptors (i.e., muscle afferents) will produce cerebral stimulation. From this theory it follows that, regardless of the source (e.g., drug effect, active muscle movement), increases in stretch receptor activity should result in a similar effect on the brain. The present study tested the hypothesis that active muscle movement in lightly anesthetized subjects would result in cerebral stimulation. Studies were conducted in six dogs who were lightly anesthetized with halothane (0.70% end-expired). The following physiologic variables were quantified before and for 6 min after the initiation of a standardized (1-min duration) noxious stimulus to the trachea and the skin overlying the hind limb: cerebral blood flow, cerebral metabolic rate for oxygen (CMRO2), cerebral perfusion pressure, cerebral vascular resistance, electroencephalogram activity, electromyogram activity, arterial carbon dioxide partial pressure (PaCO2), central venous pressure, and serum epinephrine and norepinephrine concentrations. Response to stimulation was evaluated initially in unparalyzed dogs and later was evaluated in the same dogs after they were paralyzed with intravenous pancuronium (0.2 mg/kg). In unparalyzed dogs, stimulation produced episodes of coughing plus head and limb movement during the 6-min study period. Accompanying the movement was activation of the electromyogram, an increase in electroencephalogram frequency, and a reduction in electroencephalogram amplitude. There also was a 35% increase in cerebral blood flow, a 25% decrease in cerebral vascular resistance, and a 7% increase in CMRO2 versus the baseline values for each variable. There were no significant increases in either cerebral perfusion pressure, central venous pressure, PaCO2, or serum norepinephrine concentration to account for the cerebral effects; however, serum epinephrine concentrations increased by 61%. In pancuronium-paralyzed dogs, noxious stimulation resulted in a 5% increase in cerebral blood flow, a 7% decrease in cerebral vascular resistance, and an 5% increase in CMRO2 versus baseline levels. Electroencephalogram frequency was increased, but amplitude was unchanged. Central venous pressure, electromyogram activity, and serum norepinephrine concentration were unaffected. The serum epinephrine response was similar to that observed when the dogs were not paralyzed. These data support the hypothesis that active muscle movement in lightly anesthetized subjects has an effect on the brain that is mediated in part by muscle afferent receptors. This cerebral response was manifested as electroencephalogram activation, cerebral vasodilation unrelated to central venous pressure changes, and an increase in cerebral blood flow greater than that required to meet metabolic demands. Paralysis with pancuronium abolished movement induced by stimulation (and, thus, the muscle afferent response) and also attenuated the cerebral blood flow, cerebral vascular resistance, and electroencephalogram responses.

Hemodynamic Responses of the Venous System during Global Brain Ischemia Related to the Reflex Bradycardia in the Rabbit.

Global brain ischemia in anesthetized rabbits induces a pressor response, bradycardia, apnea, and a reduction in cardiac output. The bradycardia is virtually abolished by bilateral aortic denervation (ADN). To elucidate hemodynamic responses in the venous system and the role of bradycardia in these responses during brain ischemia, central venous pressure (CVP), femoral venous pressure (FVP), and circulation time (CT) of a dye in large veins were simultaneously measured before and after ADN. Cardiopulmonary blood volume (CPBV) and circulating blood volume (CBV) were also measured using a dye-dilution technique in separate experiments. Before brain ischemia, the value of CVP, FVP, mean arterial pressure (MAP), and heart rate (HR) were 0.2 +/- 1.2 cmH2O, 8.9 +/- 1.9 cmH2O, 76 +/- 16 mmHg, and 274 +/- 35 beats/min, respectively (n = 8, mean +/- SD). During brain ischemia, CVP, FVP, and MAP significantly increased to 5.8 +/- 2.6 cmH2O, 11.1 +/- 2.4 cmH2O, and 159 +/- 10 mmHg, respectively. HR decreased to 113 +/- 54 beats/min. After ADN, the changes of CVP, FVP, and HR evoked by brain ischemia were significantly suppressed to 2.4 +/- 1.6 cmH2O, 9.8 +/- 2.1 cmH2O, and 210 +/- 61 beats/min, respectively; however, the increase in MAP was not affected. During brain ischemia, CVP correlated negatively with HR, and positively with CT. CPBV tended to decrease and CBV significantly increased by 3.7 +/- 2.5 ml/kg from that before brain ischemia. It seems that the increased amount in CBV evoked by brain ischemia mainly exists in large veins. From these results we conclude that bradycardia is a major determinant of the blood volume in the cardiopulmonary system and prevents its overflow into pulmonary circulation during global brain ischemia in the rabbit when afterload to the left ventricle is extremely increased.

Cardiac output and regional hemodynamics during recurrent seizures in rats

Altered cardiovascular function in status epilepticus may contribute to mortality in patients. We investigated changes in cardiac output and regional hemodynamics during 2 h of recurrent PTZ-induced seizures in anesthetized, paralyzed rats using radioactive microspheres, thermodilution methods, and the pulsed Doppler technique. Cardiac output fell 30–60% during recurrent seizures in 17 of 27 animals. The fall in cardiac output was sudden in onset and occurred primarily in association with seizures accompanied by prolonged increases in MABP but no change in central venous pressure. Total peripheral resistance (TPR) rose during early seizures in association with vasoconstriction of renal and certain splanchnic vascular beds. Ictal increases in TPR became attenuated during late seizures, due to failure of renal and splanchnic beds to constrict. Therefore, derangements in both cardiac and vascular function occur during late seizures. These derangements may contribute to both cerebral hypoperfusion and sudden death in status epilepticus.

Core-peripheral temperature gradient in children: does it reflect clinically important changes in circulatory haemodynamics?

Following open heart surgery, changes in core and peripheral skin temperature and changes in the core-peripheral temperature gradient were measured in 10 children. These were correlated with changes in cardiac index, systemic vascular resistance index, mean arterial pressure and urinary output. During the study intervals, which lasted 1 h each, no changes in medical management were made. Using Spearman's rank correlation, only a change in central venous pressure was found to correlate with a change in the core-peripheral temperature gradient. We conclude that a change in the core-peripheral temperature will give valuable information about the patient's intravascular volume.

Studies of cardiopulmonary bypass in children: implications for the regulation of brain natriuretic peptide

The aim was to examine the influence of cardiopulmonary bypass on brain natriuretic peptide (BNP) and on hormones of importance in the control of sodium and water balance and blood volume. Nine patients (mean age 4 years, range 2-9) undergoing cardiac surgery were studied. Blood samples were taken before, during, and up to 24 h after bypass. Plasma levels of BNP, atrial natriuretic peptide (ANP), arginine vasopressin (AVP), plasma renin activity, aldosterone, and catecholamines were measured. Preoperative concentrations of plasma BNP [573(SEM 68) pg.ml-1] and ANP [332(74) pg.ml-1] were greatly increased (p < 0.05) before bypass in all patients when compared to normal levels in children [BNP = 31(4) pg.ml-1; ANP = 27(3) pg.ml-1, n = 28]. With general anaesthetic and sternotomy, there were large reductions (p < 0.05) in both plasma BNP [180(62) pg.ml-1] and plasma ANP [163(59) pg.ml-1]. During bypass, there were no further significant decreases in plasma ANP or BNP concentrations compared with preoperative levels. Postoperatively, plasma BNP gradually increased for 12 h, to 170(28) pg.ml-1, whereas plasma ANP showed a further small decrease, to 107(20) pg.ml-1. However, postoperative plasma levels of both ANP and BNP remained well below preoperative values (p < 0.01). Plasma AVP increased rapidly within 15 min of the onset of bypass, reaching a peak value of 153(5) pg.ml-1 after 45 min. Off bypass, plasma AVP decreased slowly and was still almost 10-fold above preoperative levels 12 h after end of bypass [137(11) pg.ml-1]. Mean central venous pressure decreased during the onset of bypass, from 4.3(1.9) to 0.4(1.1) mm Hg (p < 0.05), and increased again at the end of bypass, to 9.0(3.3) mm Hg (p < 0.05); there was little further change during the postoperative period. The major source of plasma BNP in patients with congenital heart disease is the cardiac ventricle. The lower plasma ANP and BNP levels and the narrow band of change in central venous pressure following surgical repair of cardiac abnormalities may be a response to improved cardiac function.

Central cardiovascular pressures during graded water immersion in humans

Thermoneutral (34.9 degrees C) water immersion (WI) was conducted with 12 upright seated normal males at four consecutive water levels (5-10 min each): knee (reference), xiphoid process, fourth intercostal space, and sternoclavicular notch. Thereafter, water was let out of the tank and the experiment was repeated from the neck to the knees at the same levels. Arterial pulse pressure (PP), central venous pressure (CVP), and transmural CVP (TCVP = CVP - esophageal pressure; n = 4) gradually increased with increasing water levels (P < 0.05). Heart rate (HR) decreased at WI to the xiphoid process (P < 0.05) and thereafter remained at this level, whereas mean arterial pressure remained unchanged. There was a closer linear correlation between HR and PP (r = -0.35, P < 0.01) than between HR and CVP (r = -0.13, P > 0.05). Furthermore, there was a significant positive linear correlation between CVP and TCVP (r = 0.83, P < 0.01). We conclude that WI in humans induces an increase in cardiac filling pressures with an increase in PP and a consequent decrease in HR. Furthermore, changes in CVP accurately reflect changes in cardiac distension (TCVP) during WI.

Effect of exercise training on cardiopulmonary baroreflex control of forearm vascular resistance in humans

We studied the stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR) in four groups of male volunteer subjects: i) unfit, ii) physically fit, iii) before and after 10 wk of endurance training (chronic blood volume expansion), and iv) before and after acute blood volume expansion. We assessed the relationship between reflex stimulus, i.e., changes in central venous pressure and response, i.e., FVR, during unloading of cardiopulmonary mechanoreceptors with lower body negative pressure (LBNP, 0 to -20 mm Hg). The slope of the linear relationship between FVR and CVP, the index of the responsiveness of this baroreflex, was significantly diminished (> 50%) in the fit subjects compared with the unfit. The slope of the FVR-CVP relationship was inversely correlated with the subject's total blood volume, suggesting that blood volume expansion was related to the attenuated CP baroreflex. In the exercise training study, maximal oxygen consumption and blood volume increased following 10 wk of endurance training (N = 14) but were unchanged in the time control group (N = 7). The slope of the FVR-CVP relationship was significantly reduced (32%) following 10 wk of training but was unchanged in the time control group. The reduction in slope of the FVR-CVP relationship was inversely related to the increase in blood volume associated with exercise training. Acute blood volume expansion 8 ml.kg-1 body weight with 5% human serum albumin solution) significantly reduced the slope of the FVR-CVP relationship. These data support the hypothesis that the attenuated forearm vascular reflex in physically fit individuals is related to a training-induced hypervolemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of NG-Nitro-L-Arginine on Effective Vascular Stiffness in Dogs

It has been reported that there is a continuous release of nitric oxide (NO) that contributes to the regulation of vascular tone in the arterial system. In contrast, the role of NO on vascular tone in the venous system is controversial. We examined the effect of NG-nitro-L-arginine (LNNA), an NO synthase inhibitor, on venous tone in dogs. Venous tone was evaluated by effective vascular stiffness (EVS), which was calculated from the changes in central venous pressure recorded simultaneously with changes in blood volume. LNNA (10 mg/kg, i.v.) increased EVS from 0.21 +/- 0.04 to 0.30 +/- 0.03 mmHg.kg/ml as well as increasing the systemic vascular resistance. NG-Nitro-D-arginine had no effect on EVS. The LNNA-induced increase in EVS was partly reversed by L-arginine, but not by D-arginine, indicating that the increase in EVS was attributable to a blockade of NO synthesis. Since the present study was conducted under ganglion blockade, nitroxidergic nerve terminals do not seem to be the source of NO in this case. These findings suggest that NO (endothelium-derived relaxing factor) is constantly released in the venous system and contributes to the regulation of total systemic venous tone.

Perfusion de dopamine par voie veineuse centrale. Variation de la dose lors de la mesure de la pression veineuse centrale

The changes in the doses of dopamine administered at a steady rate which occur during central venous pressure (CVP) measurement were studied. A workbench model with a single lumen central venous catheter was devised with which a mathematical model was constructed to calculate the alterations due to changes in different variables : central venous pressure, dopamine dose, collateral infusions. The average time for CVP measurement was 2 min. The volume of 5 % glucose solution filling the manometer was 2.3 ml. The dopamine bolus generated by CVP measurement was equivalent to a dose of 85 μg · kg −1 · min −1. The delay required for a return to the initial dose was 2 h 42 min. Changes in CVP led to inversely proportional changes in dopamine dose. These also depended on the level to which the measuring tube was filled before carrying out the measurement. High initial rates of dopamine infusion required shorter times for a return to initial dopamine doses. The bolus and time for recovery were also inversely proportional to the volume of infusion fluids given at a steady rate on the same venous line. This model was tested in a patient suffering from bacterial pneumonia and septic shock (60 years, 55 kg). CVP measurement resulted in a bolus dose of 17 μg · kg −1 · min −1, leading to a 43 % decrease in aortic flow rate and 60 % in the ejection volume. After about 25 min, heart rate and mean arterial blood pressure had returned to their initial values, although aortic flow rate remained 30 % below initial values. This problem is also met with other drugs, such as heparin. Several solutions are suggested to avoid these abrupt changes in drug doses. Venous access reserved for this is the best way out. As an alternative, a three-way tap may be placed on the CVP line as close as possible to the patient, so as to reduce the volume of fluid within the common tubing, and, therefore, the drug bolus.

Analysis of systemic and pulmonary vascular responses to PACAP and VIP: role of adrenal catecholamines.

Systemic and pulmonary vascular responses to pituitary adenylate cyclase-activating polypeptide (PACAP), a novel peptide with 68% sequence homology to vasoactive intestinal peptide (VIP), were investigated in the anesthetized cat. Intravenous injections of PACAP in doses of 0.1-3.0 nmol/kg produced decreases in arterial pressure (AP) at low doses and biphasic changes (decreases followed by increases) at higher doses, which were accompanied by increases in central venous pressure (CVP) and cardiac output (CO), and decreases and biphasic changes in systemic vascular resistance (SVR). In contrast, VIP in doses of 0.1-3.0 nmol/kg produced only dose-dependent decreases in AP and SVR and produced little change in CVP and CO. PACAP produced increased pulmonary arterial pressure (PAP), left atrial pressure (LAP), and increases in pulmonary vascular resistance (PVR). PACAP increased heart rate (HR) and right ventricular contractile force (RVCF), while VIP had no effect. Increases in AP and SVR in response to PACAP were changed to decreases following the administration of phentolamine or after adrenalectomy. Under constant flow conditions, PACAP and VIP produced dose-dependent decreases in lobar arterial pressure when tone was elevated, with PACAP being threefold more potent than VIP. Meclofenamate and nitro-L-arginine methyl ester (L-NAME) had no effect on pulmonary responses to the peptides. PACAP produced dose-dependent biphasic changes in hindquarters perfusion pressure, whereas VIP produced only decreases that were unchanged by indomethacin, L-NAME, and glibenclamide. Phentolamine and adrenalectomy eliminated the hindquarters pressor response to PACAP and D-Phe2-VIP, a VIP antagonist, reduced responses to VIP but not to PACAP. These data suggest that responses to PACAP and VIP are mediated by distinct receptors and that pressor responses to PACAP are due to the release of catecholamines from the adrenal gland.

Atrial natriuretic factor and right atrial pressure in patients undergoing chronic haemodialysis

To quantitate the mutual relationship between central venous pressure (CVP) and circulating atrial natriuretic factor (ANF) during haemodialysis, nine end-stage renal failure patients on chronic haemodialysis underwent ultrafiltration (UF) and biochemical correction (3 h) separated by 1 h (no dialysis, ND). During UF CVP and circulating ANF decreased significantly in all patients from basal levels (0.5±1.0 vs 5.4±2.0 mmHg and 58±16 vs 95±19 pmol/l respectively,P<0.01 for both), while microhaematocrit increased significantly (29.5±1 vs 26.0±1%,P<0.01). During ND, CVP and ANF rose significantly (P<0.05 for both) in seven of the nine patients, while microhaematocrit returned towards basal values. In two patients CVP did not change during ND and circulating ANF remained unchanged. A significant correlation between CVP and circulating ANF was found (end-basal to end-UF,r=0.72,P<0.05; end-UF to end-ND,r=0.77,P=0.025;n=7). As expected, during biochemical correction plasma creatinine and K+ decreased significantly and consistently in all the patients (from 875±74 to 400±56 μmol/l and from 4.7±0.07 to 4.0±0.04 mEq/l, respectively;n=9,P<0.01 for both) as did body weight during UF (65.6±7 vs 67±5 kg;n=9,P<0.05). No significant changes were seen for systolic and diastolic blood pressure, heart rate and plasma renin activity at any time. Our data provide further evidence that the regulation of circulating ANF is synchronized with changes in CVP. They also quantitate the mutual relationship between CVP and ANF in end-stage renal failure.

Effect of complete cardiac denervation on atrial natriuretic factor release in baboons.

We investigated the influence of cardiac innervation on atrial natriuretic factor (ANF) release in baboons. For this purpose, plasma ANF levels were measured in control conditions and in response to head-down (-45 degrees) and head-up tilt (+45 degrees) in six anesthetized baboons before and after complete cardiac denervation obtained by orthotopic autotransplantation of the heart. Cardiac denervation did not modify baseline plasma ANF levels (60.4 +/- 17 pg/ml before and 63.1 +/- 16 pg/ml after heart autotransplantation). In contrast the significant ANF responses to changes in central venous pressure (CVP) induced by postural maneuvers (-45 degrees, + 16.2 +/- 4 pg/ml; +45 degrees, -18.5 +/- 4 pg/ml) were markedly altered after cardiac denervation (-45 degrees, +5.8 +/- 2 pg/ml; +45 degrees, -7.6 +/- 1 pg/ml). The changes in CVP and systemic blood pressure evoked by the postural challenges were comparable before and after cardiac denervation. These results demonstrate that cardiac nerves play a role in the control of ANF release.

Naloxone potentiates cardiopulmonary baroreflex sympathetic control in normal humans.

Naloxone, an opioid antagonist, augments baroreflex mechanisms in animals; this occurrence suggests that endogenous opioids blunt baroreflex responses. Limited human studies suggest an inhibitory action of endogenous opioids on baroreflex-mediated vagal responses during arterial baroreceptor deactivation. To evaluate the potential effect of endogenous opioids on cardiopulmonary baroreflex mechanisms in humans, we measured arterial and central venous pressures, heart rate, and efferent muscle sympathetic nerve activity (MSNA, by peroneal microneurography) during unloading of cardiopulmonary baroreceptors with incremental lower body negative pressure (LBNP, from 0 to -15 mm Hg) and during the cold pressor test in 21 normal subjects (aged 24 +/- 1 [mean +/- SEM] years). In 14 subjects, we performed LBNP before and after naloxone (0.15 mg/kg i.v.) and placebo (n = 11) on separate days. In six of these 14 subjects and an additional seven subjects (n = 13), studies were also performed before and after administration of a lower dose of naloxone (0.075 mg/kg i.v.) on separate days. Neither dose of naloxone significantly altered control arterial or central venous pressures or heart rate. Control MSNA was reduced after the higher but not after the lower dose of naloxone. Comparable reductions in central venous pressure were produced by LBNP in all groups before and after naloxone or placebo, whereas LBNP did not alter arterial pressure. Cardiopulmonary baroreflex sympathetic sensitivity, which was derived as the slope of the linear regression relation between percent change in total MSNA (units) per absolute change in central venous pressure (mm Hg) during incremental LBNP, was significantly augmented after both the high dose (from 18.6 +/- 4.7%/mm Hg to 39.3 +/- 8.1%/mm Hg, p = 0.001) and low dose of naloxone, whereas placebo had no effect. MSNA responses to the cold pressor test were not altered by either dose of naloxone. Thus, naloxone selectively potentiates cardiopulmonary baroreflex regulation of sympathetic neural activity in normal humans. These findings suggest that endogenous opioids exert a tonic inhibitory effect on sympathetic responses to orthostatic stress in normal humans.

Effects of hypotensive anesthesia with sodium nitroprusside or isoflurane on hemodynamic and metabolic changes.

The hemodynamic and metabolic changes during induced hypotension with isoflurane (isoflurane group) or sodium nitroprusside (SNP group) were observed in twelve mongrel dogs. These hypotensive effects were evaluated at 30 and 60 minutes after the mean arterial blood pressure was lowered to 50% from the control. Hemodynamic changes were evaluated by measuring systemic arterial blood pressure, heart rate, central venous pressure, pulmonary capillary wedge pressure, cardiac output, systemic vascular resistance and pulmonary vascular resistance. Metabolic changes were evaluated by measuring serum lactate and pyruvate, arterio-venous oxygen content difference and oxygen extraction rate. We also compared the ventilatory effect of hypotensive anesthesia by blood gas analysis. The results were as follows: 1. Isoflurane inhalation 2-4% or SNP infusion 10-20 micrograms/kg/min was required to reduce the mean arterial pressure to 50% of the control. 2. Heart rate was decreased slightly in the isoflurane group but significantly decreased in the SNP group. 3. There were no significant changes in central venous pressure and pulmonary capillary wedge pressure in either group. 4. Cardiac output was reduced in both groups but was more severe in the isoflurane group. 5. Systemic vascular resistance was decreased by 36% in the isoflurane group and 47% in the SNP group. 6. Acidosis was apparent and did not recover to the control until 30 minutes after recovery in the SNP group. 7. Arterio-venous oxygen difference was increased during hypotension in the isoflurane group probably due to decreased cardiac output. 8. The lactate/pyruvate ratio increased slightly in the SNP group.(ABSTRACT TRUNCATED AT 250 WORDS)

Diminished baroreflex control of forearm vascular resistance following training

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR units in mm Hg.min.100 ml.ml-1) were studied in 14 volunteers before and after 10 wk of endurance training. We assessed the relationship between reflex stimulus (changes in central venous pressure, CVP) and response (FVR) during unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP, 0 to -20 mm Hg). Changes in CVP during LBNP were estimated from pressure changes in a large peripheral vein in the dependent arm of the subject in the right lateral decubitus position. Maximal oxygen uptake (VO2max) and total blood volume increased with endurance training from 37.8 +/- 1.4 ml.min-1.kg-1 and 63.6 +/- 2.1 ml.kg-1 to 45.3 +/- 1.4 ml.min-1.kg-1 and 69.3 +/- 2.8 ml.kg-1, respectively (P less than 0.05). Reflex forearm vasoconstriction occurred in response to a reduction in estimated CVP, and the absolute change in FVR per unit of CVP was reduced from -5.96 +/- 0.79 to -4.06 +/- 0.52 units.mm Hg-1 (P less than 0.05) following exercise training but was unchanged from -6.10 to 0.57 to -6.22 +/- 0.94 units.mm Hg-1 for the time control group (N = 7). Resting values for FVR were similar before and after exercise training; however, resting estimated CVP was elevated from 9.5 +/- 0.5 mm Hg before training to 11.3 +/- 0.6 mm Hg after training.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in cerebrospinal fluid pressure and spinal cord perfusion pressure prior to cross-clamping of the thoracic aorta in humans

Little is known about what influences cerebrospinal fluid pressure (CSFP) during anesthesia prior to aortic cross-clamping (AXC). Therefore, this study measured the effect of anesthetic induction, of various drugs administered during the course of surgery. prior to AXC, and of hemodynamic changes on CSFP, and calculated spinal cord perfusion pressure (SCPP = mean arterial pressure [MAP] - CSFP) in 11 patients undergoing surgery on the descending thoracic aorta. A lumbar drainage catheter was placed to facilitate drainage of CSF and to measure CSFP. Anesthesia was induced with fentanyl, 50 μg/kg, and midazolam, 1 mg, using a pancuronium-metocurine mixture for neuromuscular blockade. Data were collected prior to and after (1) anesthetic induction, (2) mannitol to augment diuresis, (3) sequential use of sodium nitroprusside (SNP) and isoflurane (ISO) to lower MAP by 20%, (4) drainage of spinal fluid, (5) intrathecal injection of papaverine (IP), and (6) AXC. Statistical comparisons of recorded data were made using the least squares mean method and Friedman test. Linear regression was used to test for correlation between CSFP and hemodynamics. Anesthetic induction affected neither hemodynamics nor CSFP. Mannitol significantly increased heart rate, central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), and CSFP ( P < 0.05). SNP or ISO altered neither CVP, PCWP, CO, nor CSFP, which remained elevated at the postmannitol infusion level. ISO, unlike SNP, caused a significant decrease in SUP ( P < 0.005). Subsequent drainage of 20 mL of CSF improved SCPP ( P < 0.05). IP did not have any effect on hemodynamics or CSFP. CSFP showed a strong correlation with CVP ( r = 0.86). It is concluded that drugs commonly administered prior to AXC significantly influence CSFP and SCPP, and cannot be discounted as a factor contributing to the acute increase in CSFP observed during AXC. CSFP correlates with changes in CVP, which reflects increased intracranial and intraspinal venous blood volume, probably caused by cumulative effects of events during anesthesia and surgery.

Phlebotomy Reverses the Hemodynamic Consequences of Thoracic Aortic Cross-clamping

In dogs (n = 11) anesthetized with sodium pentobarbital (to an isoelectric EEG), the authors investigated the influence of thoracic aortic cross-clamping (AXC) on systemic hemodynamics and cerebrospinal fluid pressure (CSFP) with concurrent measurement of total brain flow (tCBF) and regional (cervical, thoracic, and lumbar) spinal cord blood flow (SCBF). The effect of phlebotomy (to control the hemodynamic consequences of AXC) on tCBF and SCBF was assessed. Radioactive microspheres were injected at four time periods in each animal: 1) at baseline; 2) with application of the AXC; 3) after phlebotomy, to reduce the proximal mean arterial pressure (MAPp) to baseline values; and 4) 2 min after removal of the AXC (mean AXC time 68 +/- 6 min). With application of the AXC, the MAPp, central venous pressure (CVP), and CSFP significantly increased (104 +/- 6 to 156 +/- 6 mmHg, 3.4 +/- 0.4 to 5.2 +/- 0.7 mmHg, and 3.3 +/- 0.7 to 5.2 +/- 0.8 mmHg, respectively), while distal mean aortic pressure (MAPd) significantly decreased (98 +/- 6 to 14 +/- 1 1 mmHg). Phlebotomy (24 +/- 3 ml.kg-1) significantly decreased MAPp (to 106 +/- 6 mmHg), CVP (to 1.6 +/- 0.6 mmHg), and CSFP (to 1.2 +/- 1.1 mmHg). The CSFP changed in parallel with the changes in CVP, a result suggesting that the alterations in CSFP depended on cardiac preload. The spinal cord perfusion pressure (SCPP; SCPP = MAPd - CSFP) was unchanged after phlebotomy, since both MAPd and CSFP decreased. The tCBF and cervical SCBF were unchanged when MAPp increased by 50% with application of the AXC; this indicated that autoregulation was intact.(ABSTRACT TRUNCATED AT 250 WORDS)

Reflexogenic neuronal and humoral responses to selective stimulation of low-pressure cardiopulmonary receptors in man

This study was conducted to determine the relative importance of efferent muscle sympathetic nerve activity (MSA), vasopressin (ADH) and atrial natriuretic peptide (ANP) in the short-term neurohumoral response to moderate changes in low-pressure cardiopulmonary receptor activity. The low-pressure receptors were stimulated and unloaded, respectively, by autotransfusion of blood (450 ml) and the application of lower body negative pressure (LBNP, -20 mmHg), and in 11 healthy men we measured MSA in the left peroneal nerve, indirect blood pressure, ECG, central venous pressure (CVP) and venous plasma concentrations of ANP and ADH (radioimmunoassay). Total MSA rose by 30% during LBNP and decreased during a rapid autotransfusion of blood, and the changes in MSA were significantly related to changes in CVP. The plasma concentrations of ADH and ANP were not significantly affected by either procedure. It is suggested that during moderate short-term changes in venous return, MSA responded more rapidly and/or at a lower threshold than the ADH and ANP systems.

Regulation of Vascular Compliance and Stress Relaxation by the Sympathetic Nervous System.

We measured the changes in central venous pressure (CVP) and circulating blood volume (CBV) in dogs consequent to fluid infusion under halothane anesthesia, and compared the CVP and CBV responses to those obtained after blocking the autonomic nervous system by total spinal anesthesia (TSA) and stimulating the alpha receptor with methoxamine (MTX). Under TSA, the change in CVP consequent to fluid infusion was less than that under halothane anesthesia, while with MTX, the change in CVP was larger than that under halothane anesthesia. The recovery time of CVP response toward the baseline level after the end of fluid infusion was fastest under halothane anesthesia, while the recovery time of CVP was two times longer under TSA and MTX. Based on the relationship between changes in CVP and BV, we quantified effective vascular compliance and stress relaxation using mathematical analysis. The effective vascular compliance increased to 13.3 +/- 3.2 ml.mmHg-1.kg-1 under TSA as compared to 5.6 +/- 0.3 ml.mmHg-1.kg-1 under halothane anesthesia, and it decreased to 2.6 +/- 0.2 ml.mmHg-1.kg-1 with MTX. Stress relaxation was determined as the time constant in the unit response of CVP. The time constant for stress relaxation was 39 +/- 7 min under halothane, 74 +/- 12 min with TSA, and 92 +/- 25 min with MTX. These results suggest that the autonomic nervous system modifies cardiac preload by changing effective vascular compliance and stress relaxation.