Mean Arterial Blood Pressure Measurements Research Articles

Increased blood pressure in transgenic mice expressing both human renin and angiotensinogen in the renal proximal tubule.

The purpose of this study was to evaluate the physiological significance of a tissue renin-angiotensin system in the proximal tubule of the kidney. To accomplish this, we produced mice that express human renin (hREN) under the control of the kidney androgen-regulated promoter (KAP), which is androgen responsive. One of the lines expressed the hREN transgene primarily in the kidney. Renal expression of the transgene was undetectable in females but could be induced by testosterone treatment. Because the renin-angiotensin system is species specific, we bred KAP2-hREN mice with the mice expressing human angiotensinogen under the same promoter (KAP-hAGT) to produce offspring that expressed both transgenes. We measured mean arterial blood pressure (MAP) in the carotid artery of double-transgenic and control mice using radiotelemetry. Double-transgenic female mice had a normal baseline MAP (116 +/- 4 mmHg, n = 8), which increased by 15 mmHg after 2 wk of testosterone treatment, and returned to baseline after elimination of the testosterone pellet. The change in arterial pressure paralleled the change in plasma testosterone. There was no MAP change in testosterone-treated control littermates. We conclude that dual production of renin and angiotensinogen in the renal proximal tubule can result in a systemic increase in arterial pressure. These data support a role for a tissue-specific renin-angiotensin system in the renal proximal tubule that contributes to the regulation of systemic blood pressure.

Cocaine use as a predictor of outcome in aneurysmal subarachnoid hemorrhage.

The goal of this study was to analyze the relationship between cocaine use and outcomes of aneurysmal subarachnoid hemorrhage (SAH). A retrospective review was performed of the medical records of patients with intracranial aneurysms treated at a single institution between January 1996 and December 2001. Only patients who presented with SAH were included in the study. The covariates chosen for the statistical analysis included the following: patient age, sex, and race; systolic and mean arterial blood pressure measurements on hospital admission; Hunt and Hess and Fisher grades; pre-existent major systemic disease; and history of alcohol, tobacco, or cocaine use. The Glasgow Outcome Scale (GOS) was used to standardize outcome and was dichotomized such that a score between 1 and 3 was considered a poor outcome and a score of 4 or 5 was considered a favorable outcome. The records of 151 patients were reviewed and 108 of these presented with aneurysmal SAH. Of these 108 patients, 36 (33.3%) had used cocaine within 24 hours before presentation. A Hunt and Hess grade of IV or V was assigned to 20 (55.6%) of 36 patients who used cocaine, compared with eight (11.1%) of 72 patients who did not; this difference was found to be statistically significant (p < 0.0001). Twenty-eight patients (77.8%) in the cocaine user group and 20 patients (27.8%) in the non-cocaine user group experienced clinically significant, angiographically confirmed vasospasm during their hospital course (p < 0.0001). Cocaine use was associated with a 2.8-fold greater risk of developing vasospasm (95% confidence interval [CI] 1.86-4.22). A GOS score of 1, 2, or 3 was assigned to 33 patients (91.7%) in the cocaine user group and to 20 patients (27.8%) in the non-cocaine user group (p < 0.0001). Cocaine use was associated with a 3.3-fold greater risk of poor outcome (95% CI 2.24-4.85). This association was found to be independent of Hunt and Hess grade as well as of vasospasm. Cocaine adversely affects both the presentation of and outcome in patients with aneurysmal SAH who are undergoing treatment for this disease. The vasoactive properties of the drug appear to aggravate the already tenuous situation of SAH and increase both the occurrence and influence of cerebral vasospasm. Statistical analysis demonstrates that cocaine directly affects both presentation and outcome in a significant manner. It is the authors' interpretation of the results of this retrospective review that cocaine use negatively affects outcome to such an extent that it should be considered equal to the presence of a major systemic illness when determining Hunt and Hess grade.

Factors influencing the accuracy of oscillometric blood pressure measurement in critically ill patients

Comparison of oscillometric blood pressure measurement with two different devices (M3000A using a new algorithm and M1008A using an established algorithm, both Hewlett Packard) and evaluation of current recommendations concerning the relation between cuff size and upper arm circumference in critically ill patients. Prospective data collection. Emergency department in a 2000-bed inner-city hospital. A total of 30 patients categorized into three groups according to their upper arm circumference (I, 18-25 cm; II, 25.1-33 cm; III, 33.1-47.5 cm) were enrolled in the study protocol. INTERVENTIONS In each patient, two noninvasive blood pressure devices with three different cuff sizes were used to perform oscillometric blood pressure measurement. Invasive mean arterial blood pressure measurement was done by cannulation of the radial artery. Overall, 1,011 pairs of simultaneous oscillometric and invasive blood pressure measurements were collected in 30 patients (group I, n = 10; group II, n = 10; group III, n = 10). The overall discrepancy between both methods with the M3000A was -2.4 +/- 11.8 mm Hg (p <.0001) and, with the M1008A, -5.3 +/- 11.6 mm Hg (p <.0001) if the recommended cuff size according to the upper arm circumference was used (352 measurements). If smaller cuff sizes than recommended were used (308 measurements performed in group II and III), the overall discrepancy between both methods with the M3000A was 1.3 +/- 13.4 mm Hg (p <.024) and, with the M1008A, -2.3 +/- 11.5 mm Hg (p <.0001). The new algorithm reduced the overall bias of the oscillometric method but still showed a significant discrepancy between both methods of blood pressure measurement, primarily due to the mismatch between upper arm circumference and cuff size. The improvement of the algorithm alone could not result in a sufficient improvement of oscillometric blood pressure measurement. A reevaluation of the recommendations concerning the relation between upper arm circumference and cuff size are urgently required if oscillometric blood pressure measurement should become a reasonable alternative to intra-arterial blood pressure measurement in critically ill patients.

Indirect oscillometric and direct blood pressure measurements in anesthetized and conscious neonatal foals

AbstractObjective:To investigate the agreement between indirect oscillometric and direct blood pressure measurement in the equine neonate.Design:Prospective observational study.Setting:University Veterinary Teaching Hospital.Animals:Ten crossbred foals of 30–46 hours of age.Interventions:Six animals (Group 1) were anesthetized. Four animals (Group 2) were restrained on a mat. All animals were instrumented with a catheter in the greater metatarsal artery and an oscillometric blood pressure cuff over the coccygeal artery. Blood pressure was varied with dobutamine, phenylephrine, nitroprusside, and increased depth of anesthesia (Group 1) or dopamine (Group 2).Measurements and main results:Simultaneous direct and indirect blood pressure measurements were obtained from the greater metatarsal artery and the coccygeal artery, respectively. There was good agreement between the 2 methods for mean and diastolic blood pressures in both groups, but not for systolic pressure. The agreement was best in mean blood pressure of anesthetized foals (mean bias –1.07; limits of agreement – 9.39, 7.25 mmHg).Conclusions:Indirect oscillometry appears to be an acceptable method for measuring mean arterial blood pressure in both anesthetized and conscious neonatal foals, and may be a valid method of monitoring critically ill foals.

Different effects of eNOS and nNOS inhibition on transient forebrain ischemia

To clarify the functions of nitric oxide (NO) induced by either neuronal NO synthase (nNOS) or endothelial NO synthase (eNOS) after transient cerebral ischemia, we investigated the effects of l- N 5-(1-iminoethyl)ornithine ( l-NIO), a relatively selective eNOS inhibitor, and 7-nitroindazole (7-NI), a relatively selective nNOS inhibitor, on hippocampal dysfunction caused by cerebral ischemia. We measured mean arterial blood pressure (MABP), hippocampal blood flow, direct current (DC) potential, CA1 population spike (PS) and extracellular concentrations of glutamate from rat hippocampus after transient forebrain ischemia, which was induced by four-vessel occlusion for 10 min. l-NIO (20 mg/kg) and 7-NI (25 mg/kg) were administered intraperitoneally 20 min before ischemia. l-NIO, but not 7-NI, increased MABP before, during and after ischemia, compared with the vehicle group. 7-NI, but not l-NIO, reduced the amplitude of anoxic depolarization induced by ischemia. 7-NI recovered the PS amplitude in part 60 min after ischemia. 7-NI, but not l-NIO, reduced the ischemia-induced levels of glutamate. These results indicate that nNOS inhibition with 7-NI improves, at least in part, hippocampal dysfunction after ischemia, while eNOS inhibition with l-NIO worsens it.

Effects of Propofol Used with an Inhalation Anesthetic in the Neuroanesthetic Management on the Jugular Bulb Oxygen Saturation

Background: When we use a volatile anesthetic that increases cerebral blood flow (CBF) and propofol which decreases CBF in appropriate doses, respectively, an increase in ICP and cerebral ischemia can be prevented. The purpose of this study was to look for the proper method for balanced anesthesia using a jugular bulb oxygen saturation () that depends on the concentration of propofol used in combination with isoflurane- anesthesia. Methods: Randomly we divided these patients into group 1 (12 patients), group 2 (12 patients), and group 3 (15 patients). Using a Master TCI and injecting a volatile anesthetic continuously, we injected 2/ml of blood concentration to group 1, 3/ml to group 2 and 4/ml to group 3 and maintained a partial pressure of in the vein around 30 mmHg during the operation. After induction of anesthesia, injection of propofol, and the dura mater was opened, we measured mean arterial blood pressure, heart rate, respectively, measured partial pressure of , hematocrit, oxygen saturation sampling the arterial blood, measured oxygen saturation sampling jugular bulb. Results: There were no differences of mean arterial blood pressure, heart rate, hematocrit, arterial blood partial pressure of , oxygen saturation, or jugular bulb oxygen saturation among the groups. In addition, there were no statistical differences of variables measured before and after injecting propofol and the dura was opened. For 1 in group 1, 2 in group 2, and 3 in group 3, jugular oxygen saturation dropped below 50% after injecting propofol, but was not verified statistically. Conclusions: There were no significant hemodynamic effects when we used propofol with the volatile anesthetic in neuroanesthetic management.

Physiological elevation in plasma angiotensinogen increases blood pressure.

Hepatic angiotensinogen secretion is controlled by a complex pattern of physiological or pathophysiological mediators. Because plasma concentrations of angiotensinogen are close to the Michaelis-Menten constant, it was hypothesized that changes in circulating angiotensinogen affect the formation rate of ANG I and ANG II and, therefore, blood pressure. To further test this hypothesis, we injected purified rat angiotensinogen intravenously in Sprague-Dawley rats via the femoral vein and measured mean arterial blood pressure after arterial catheterization. In controls, mean arterial pressure was 131 +/- 2 mmHg before and after the injection of vehicle (sterile saline). The injection of 0.8, 1.2, and 2.9 mg/kg angiotensinogen caused a dose-dependent increase in mean arterial blood pressure of 8 +/- 0.4, 19.3 +/- 2.1, and 32 +/- 2.4 mmHg, respectively. In contrast, the injection of a purified rabbit anti-rat angiotensinogen antibody (1.4 mg/kg) resulted in a significant decrease in mean arterial pressure (-33 +/- 3.2 mmHg). Plasma angiotensinogen increased to 769 +/- 32, 953 +/- 42, and 1,289 +/- 79 pmol/ml, respectively, after substrate and decreased by 361 +/- 28 pmol/ml after antibody administration. Alterations in plasma angiotensinogen correlated well with changes in plasma renin activity. In summary, variations in circulating angiotensinogen can result in changes in blood pressure. In contrast to renin, which is known as a tonic regulator for the generation of ANG I, angiotensinogen may be a factor rather important for long-term control of the basal activity of the renin-angiotensin system.

Regional Brazilian Diet-Induced Low Birth Weight Is Correlated with Changes in Renal Hemodynamics and Glomerular Morphometry in Adult Age

Number of nephrons, renal hemodynamics, and glomerular morphometry were assessed in rats submitted to a multideficient diet which was developed from a basic regional diet consumed in a Brazilian region of sugarcane cultivation. We evaluated three groups of male Wistar rat offspring: (1) from dams fed a standard diet throughout mating, pregnancy and lactation (control group) and (2) from dams fed the multideficient diet during mating and pregnancy (MalN1 group) or (3) throughout mating, pregnancy, and lactation (MalN2 group). At adult age, the animals were anesthetized to measure mean arterial blood pressure and renal hemodynamics. The MalN1 group, as compared with the control group, showed unaltered body and kidney weights, nephron deficiency, a high mean arterial blood pressure, glomerular hypertrophy, and renal vasoconstriction. The MalN2 group showed the same nephron deficiency and mean arterial blood pressure levels as the MalN1 group. These animals exhibited lower body and kidney weights and no glomerular hypertrophy. In conclusion, the alterations induced by intrauterine malnutrition are compatible with the development of chronic renal failure.

Dementia and its associations in type 2 diabetes mellitus: The Fremantle Diabetes Study

Background: recent studies indicate that diabetes is an important risk factor for dementia in older patients, but the cause remains unknown. Objectives: to determine whether vascular or diabetes-related risk factors predict the development of dementia in older subjects with diabetes. Patients: 63 patients with type 2 diabetes of mean age 75.3 years. Methods: Subjects were screened for cognitive impairment using the Mini-Mental State Examination (MMSE) and informants who knew the subjects answered the Informant Questionnaire for Cognitive Decline in the Elderly (IQCODE). Probable dementia was diagnosed using highly specific criteria based on the combination of both tests. Potential risk factors for dementia obtained at the time of the cognitive test and annually from a median of 3.2 years previously were examined using univariate methods and simple general linear modelling. Results: since there was a significant association between MMSE and English speaking ability, ten non-Anglo–Celt patients were excluded from the analysis. Probable dementia was diagnosed in six of the remaining 53 subjects (11%). Dementia was significantly and independently associated with higher diastolic and mean arterial blood pressure measurements over the 3 years before assessment. Blood pressure declined over this time in the patients with probable dementia and was similar to that in non-demented subjects at the time of cognitive assessment. Conclusions: these preliminary data suggest that the high rate of dementia found in older people with diabetes may be explained by the high rate of hypertension in this population.

The roles of platelet-activating factor and endothelin-1 in renal damage after total hepatic ischemia and reperfusion.

This study was designed to verify the involvement of platelet-activating factor (PAF) in renal damage associated with hepatic ischemia and reperfusion (HIR) injury through the release of endothelin (ET)-1 and to determine the modulating effect of a specific PAF receptor antagonist on these insults in rats. Male rats pretreated with either normal saline as a vehicle (NS group) or intravenous TCV-309, a PAF receptor antagonist (TCV group), were subjected to 120 min of total hepatic ischemia under an extracorporeal portosystemic shunt. Plasma aspartate transaminase, creatinine, blood urea nitrogen, and ET-1 levels and the relative renal wet weight were determined under nonischemic conditions and at 1, 3, and 6 hr of reperfusion after hepatic ischemia. Changes in mean arterial blood pressure and renal tissue blood flow measurements in the kidney were determined throughout the experiment. Increased plasma aspartate transaminase, creatinine, blood urea nitrogen, and ET-1 levels and the relative renal wet weight after HIR in the NS group were significantly suppressed by TCV-309 pretreatment. Mean arterial blood pressure and renal tissue blood flow after HIR in the TCV group were significantly improved when compared with those in the NS group. These effects resulted in attenuation of structural hepatic and renal damage with the improvement of 7-day survival (62%). The present study demonstrates that renal damage as well as critical liver injury is produced after reperfusion following 120 min of total hepatic ischemia. A PAF receptor antagonist may be therapeutically useful to protect against these types of damage via indirect modulation of plasma ET-1 levels.

Arterial hypertension and renal allograft survival.

Several observational studies have investigated the significance of hypertension in renal allograft failure; however, these studies have been complicated by the lack of adjustment for baseline renal function, leaving the role of elevated blood pressure in allograft failure unclear. To examine the relationship between blood pressure adjusted for renal function and survival after cadaveric allograft transplantation. Nonconcurrent historical cohort study conducted from 1985 through 1997. University teaching hospital. A total of 277 patients aged 18 years or older who underwent cadaveric renal transplantation without another simultaneous organ transplantation and whose allograft was functioning for a minimum of 1 year. Follow-up continued through 1997 (mean follow-up, 5.7 years). Time to allograft failure (defined as death, return to dialysis, or retransplantation) by systolic, diastolic, and mean arterial blood pressure measurements at 1 year after transplantation. Multivariate Cox proportional hazards modeling demonstrated that nonwhite ethnicity, history of acute rejection, and nondiabetic kidney disease were significant predictors of failure (P = .01 for all). In addition, the calculated creatinine clearance at 1 year had an adjusted rate ratio (RR) for allograft failure per 10 mL/min (0.17 mL/s) of 0.74 (95% confidence interval [CI], 0.62-0.88). The RR per 10-mm Hg increase in blood pressure measured at 1 year after transplantation, after adjustment for creatinine clearance, was 1.15 (95% CI, 1.02-1.30) for systolic pressure, 1.27 (95% CI, 1.01-1.60) for diastolic pressure, and 1.30 (95% CI, 1.05-1.61) for mean arterial pressure. Supplemental analyses that did not include death as a failure event or reduce the minimum allograft survival time for study subjects to 6 months yielded results consistent with the primary analysis. There was no evidence of modification of the blood pressure-allograft failure relationship by ethnicity or diabetes mellitus. Systolic, diastolic, and mean arterial blood pressures at 1 year posttransplantation strongly predict allograft survival adjusted for baseline renal function. More aggressive control of blood pressure may prolong cadaveric allograft survival.

Accuracy of oscillometric blood pressure measurement according to the relation between cuff size and upper-arm circumference in critically ill patients

To evaluate the accuracy of oscillometric blood pressure measurement according to the relation between cuff size and upper-arm circumference in critically ill patients. Prospective data collection. Emergency department in a 2,000-bed inner city hospital. Thirty-eight patients categorized into three groups according to their upper-arm circumference (group I: 18-25 cm; group II: 25.1-33 cm; and group III: 33.1-47.5 cm) were enrolled in the study protocol. In each patient, all three cuff sizes (Hewlett-Packard Cuff 40401 B, C, and D) were used to perform an oscillometric blood pressure measurement at least within 3 mins until ten to 20 measurements for each cuff size were achieved. Invasive mean arterial blood pressure measurement was done by cannulation of the contralateral radial artery with direct transduction of the systemic arterial pressure waveform. The corresponding invasive blood pressure value was obtained at the end of each oscillometric measurement. Overall, 1,494 pairs of simultaneous oscillometric and invasive blood pressure measurements were collected in 38 patients (group I, n = 5; group II, n = 23; and group III, n = 10) over a total time of 72.3 hrs. Mean arterial blood pressure ranged from 35 to 165 mm Hg. The overall discrepancy between oscillometric and invasive blood pressure measurement was -6.7+/-9.7 mm Hg (p<.0001), if the recommended cuff size according to the upper-arm circumference was used (539 measurements). Of all the blood pressure measurements, 26.4% (n = 395) had a discrepancy of > or =10 mm Hg and 34.2% (n = 512) exhibited a discrepancy of > or =20 mm Hg. No differences between invasive and noninvasive blood pressure measurements were noted in patients either with or without inotropic support (-6.6 + 7.2 vs. -8.6 + 6.8 mm Hg; not significant). The oscillometric blood pressure measurement significantly underestimates arterial blood pressure and exhibits a high number of measurements out of the clinically acceptable range. The relation between cuff size and upper-arm circumference contributes substantially to the inaccuracy of the oscillometric blood pressure measurement. Therefore, oscillometric blood pressure measurement does not achieve adequate accuracy in critically ill patients.

Use of backrest elevation in critical care: a pilot study

Use of lower backrest positions occurs frequently and is a factor in the development of ventilator-associated pneumonia. To determine the usual bed elevation and backrest position in a medical intensive care unit and their relationship to hemodynamic status and enteral feeding. Data were collected in a 12-bed medical respiratory intensive care unit for 2 months. A protractor was used to measure the elevation of the head of the bed. Hemodynamic status was defined by systolic, diastolic, and mean arterial blood pressure measurements retrieved from each patient's flow sheet. The sample included 347 measurements of 52 patients. Mean backrest elevation was 22.9 degrees, and 86% of patients were supine. Backrest position differed significantly (P = .005) among nursing shifts (days, evenings, nights) but not for systolic (r = -0.04, P = .49), diastolic (r = 0.01, P = .83), or mean arterial blood pressure (r = -0.01, P = .84). Backrest elevation did not differ significantly between patients who were receiving enteral feedings and patients who were not (P = .23) or between patients receiving intermittent versus continuous nutrition (P = .22). Use of higher levels of backrest elevation (> or = 30 degrees) is minimal and is not related to use of enteral feeding or to hemodynamic status. The rationale for using lower backrest positions for critically ill patients may be based on convenience, the patient's comfort, or usual patterns in the unit. However, the dangers of supine positioning and its relationship to aspiration and ventilator-associated pneumonia should not be minimized.

Effect of Magnesium Sulfate on Kidney Function in the Newborn Rabbit

The aim of this study was to investigate the acute, short-term effects of the intravenous (i.v.) administration of magnesium (Mg) sulfate on renal function in the newborn rabbit. Eight anesthetized and mechanically ventilated, normoxemic, newborn New Zealand white rabbits were studied. We measured mean arterial blood pressure (MAP), urine volume (V), glomerular filtration rate (GFR), renal plasma flow (RPF) and calculated renal blood flow, filtration fraction (FF) and renal vascular resistance (RVR) under control conditions and in two experimental periods after the i.v. Mg sulfate load. Mg sulfate administration in a dose 100 mg/kg followed by 50 mg/kg/h caused a significant fall (p < 0.001) in MAP, GFR and RPF, whereas the RVR increased (p < 0.01). FF did not change significantly (p: NS/0.05) and V remained constant. These results show that the acute i.v. administration of Mg sulfate to newborn rabbits causes systemic vasodilatation with a fall in MAP. The increase in RVR, without consistent change in FF, suggests that the renal vasculature of the ‘immature’ neonatal rabbit reacts to these changes by preferential afferent arteriolar vasoconstriction.

Transplacental cocaine exposure. 3: Mechanisms underlying altered brain development.

In a mouse model of transplacental cocaine exposure we have demonstrated alterations in brain structure and function of offspring including disturbances of brain growth, disruption of neocortical cytoarchitecture, and transient as well as persistent behavioral deficits. One mechanism by which cocaine may alter fetal brain development is through cocaine-induced alpha-adrenergic-mediated (uterine) arterial vasoconstriction. In this study pregnant Swiss Webster (SW) mice were injected with cocaine HCl (20 or 40 mg/kg, SC) without any changes evident in mean arterial blood pressure (MAP) measurements. These physiology results suggest that in our mouse model, cocaine's transplacental effects on the fetus are not due to cocaine-induced maternal vasoconstriction, nor concomitant hypoperfusion of the fetus. In a separate series of experiments, pregnant SW dams were administered cocaine HCl at 40 mg/kg/day (COC 40), 20 mg/kg/day (COC 20), or 10 mg/kg/day (COC 10) [SC, divided in two daily doses, from embryonic day (E) 8 to E17 inclusive]. Additional groups of cocaine-treated dams were administered phentolamine (5 mg/kg, SC), a short-acting alpha-adrenergic antagonist, 15 min prior to each cocaine dose (Phent COC 40, Phent COC 20, Phent COC 10). Animals born to Phent COC 40 dams demonstrated transient postnatal brain growth retardation and behavioral deficits in first-order conditioning of P9 mice comparable to mice born to COC 40 dams, which received the same regimen of cocaine injections without phentolamine pretreatment. Like COC 40 offspring, Phent COC 40 offspring also demonstrated a persistent deficit in the blocking paradigm. The behavioral and growth findings confirm and extend the physiology data, and imply that in our rodent model, alpha-adrenergic mechanisms (including maternal vasoconstriction) are unlikely to mediate these toxic effects of transplacental cocaine exposure on developing brain.

Effects of naloxone on hemodynamic and sympathetic nerve responses to pain in normotensive vs. borderline hypertensive men

Pain sensitivity decreases with increasing resting blood pressure. This blood pressure–pain interaction may be mediated by endogenous opioids which have been shown to affect both blood pressure and nociception. To test this hypothesis, we measured mean arterial blood pressure (MAP), central venous pressure (CVP), heart rate (HR), muscle sympathetic nerve activity (MSNA), serum catecholamines, and individual pain rating scales during 2 min periods of noxious mechanostimulation (skin fold pinching) in nine young (26±2 year), male normotensive (NT) subjects and in 12 age and weight matched males with borderline hypertension (BHT). Measurements were performed before and after the i.v. administration of naloxone (0.15 mg/kg) and placebo in a randomized double-blind cross-over trial. In the pre-naloxone trials, pain led to similar changes in MAP, CVP, MSNA and plasma catecholamines in the two groups except for a higher increase in HR in the BHT group as compared to the NT group (3±1 vs. 1±1 bpm; P<0.005). Opioid blockade with naloxone increased MSNA responses to pain in the NT group (from 5±1 to 9±1 bursts/min, and, from 100±23 to 204±36 units/min, respectively; P<0.05) but did not significantly affect the MSNA response to pain in the BHT group. Pain induced responses of MAP, CVP, and catecholamines were not altered by naloxone in either group. Overall, there was a highly significant inverse correlation between pain perception and resting blood pressure which was not significantly affected by naloxone. The BHT subjects exhibited a lower pain perception compared to the NT subjects ( P<0.005). Naloxone increased pain rating in the NT group (from 194±9 to 218±13; P<0.005) but not in the borderline hypertensive group (160±8 vs. 168±10; P=0.36). Except for a decreased HR response in the BHT group, placebo had no effect on the responses to pain. Our data do not indicate a major role of the endogenous opioid system for the blood pressure–pain interaction in man. Endogenous opioids affect pain perception and sympathetic nerve activity responses to pain in normotensive men but their activity seems to be attenuated in borderline hypertensive subjects. Therefore, the lower pain sensitivity in human essential hypertension is probably mediated by non-opioid mechanisms.

Nitric oxide and vascular reactivity in pregnant rats with adriamycin nephropathy.

1. In previous studies we have shown that, after the administration of adriamycin, hypertension developed in rats who became pregnant (adriamycin-pregnant rats), whereas virgin animals remained normotensive. Subsequently, we showed that this hypertension was prevented by administration of L-arginine, suggesting that deficient synthesis of nitric oxide may be pathogenetic in this model. 2. To further assess the role of nitric oxide in this model, we measured mean arterial blood pressure after administration of L-arginine to adriamycin-pregnant rats or of NG-nitro-L-arginine-methyl ester (L-NAME) to normal pregnant rats. In other experiments, we assessed the response of isolated perfused arterial mesenteric vessels, precontracted with noradrenaline, to acetylcholine, L-arginine or L-NAME. 3. Blood pressure was decreased in normal pregnant rats, whereas it was elevated in adriamycin-pregnant rats. L-NAME treatment increased blood pressure in normal pregnant rats and L-arginine decreased it in adriamycin-pregnant rats. 4. Mesenteric vessels of adriamycin-pregnant rats exhibited an exaggerated vasoconstrictory response to noradrenaline, when compared with the blunted response observed in normal pregnancy. The addition of L-NAME in vitro induced a further contraction, significantly greater in normal pregnant rats. The vasodilatory response to acetylcholine and L-arginine was greater in vessels from adriamycin-pregnant rats. In contrast, responses to either nitroprusside or diazoxide were similar in all groups. 5. The results suggest a state of reduced nitric oxide synthesis in rats with adriamycin nephropathy, leading to vascular maladaption and hypertension in pregnancy.

Cardiorespiratory stability during transport of the critically ill

Inadequate secondary transport of the critically ill can result in systemic insults, most commonly hypotension and hypoxia [1-3]. We prospectively measured mean arterial blood pressure and oxygenation prior to and immediately post-transfer on 50 critically ill patients. We aimed to show that specialist transport using invasive monitoring, dedicated equipment and personnel results in cardiorespiratory stability during transport of the critically ill. Fifty consecutive patients were transferred according to our normal clinical practice. They were monitored with the portable Propak monitor and ventilated with an Oxylog 2000 ventilator. After appropriate resuscitation and stabilization they were established onto our ventilator and a mean arterial pressure was recorded from the Propak and a set of blood gases analysed using the Hewlett-Packard 'I-Stat' portable blood gas analyser. A second set of readings were taken on arrival at the destination unit but before transferring onto their monitors and ventilator. The MAP values were compared using a paired Student's t-test and (FiO2-PaO2) values using Mann-Whitney analysis. Transportation of the critically ill is increasing. All patients should be delivered to their destination in at least as good a condition as they left. This requires careful preparation, monitoring and continued support. Specialist regional teams dedicated to and trained for transport of the critically ill will best achieve these goals. Table 3Table 3: (abstract 22) Mean arterial pressure (M) and FiO2-PaO2 measured after resuscitation and after arrival at destination

Dissociation between the increase in systemic vascular resistance induced by acute nitric oxide synthesis inhibition and the decrease in cardiac output in anesthetized dogs.

The decrease in cardiac output (CO) that follows nitric oxide (NO) synthesis inhibition is thought to be the result of an increase in systemic vascular resistance (SVR). We investigated whether sodium nitroprusside (SNP) and iloprost prevent the decrease in CO induced by short-term administration of N omega-nitro-L-arginine methyl ester (L-NAME) in anesthetized dogs. The left femoral artery and vein were cannulated for mean arterial blood pressure (MABP) measurement and drug administration, respectively. A Swan-Ganz thermodilution catheter was inserted into the right femoral vein and allowed the determination of CO and the calculation of SVR, expressed as the cardiac index (CI) and the index of systemic vascular resistance (ISVR), respectively. L-NAME (0.01-10.0 mg/kg; n = 13) induced dose-dependent increases in MABP and in the ISVR. These changes were accompanied by significant decreases in both the CI and the heart rate. SNP (1 microgram/kg/min; n = 6) virtually abolished L-NAME-induced hypertension and significantly attenuated both the increase in the ISVR (< 3.0 mg/kg) and the decrease in CO. Iloprost (50 ng/kg/min; n = 6) also abolished L-NAME-induced hypertension and markedly attenuated the increase in SVR. However, the decrease in CO was not prevented by this vasodilator. These results clearly demonstrate that the increase in SVR is not the major factor accounting for the decrease in CO after short-term NO synthesis inhibition in anesthetized dogs.

Accuracy and reliability of noninvasive continuous finger blood pressure measurement in critically ill patients.

To evaluate the accuracy and reliability of noninvasive continuous finger blood pressure measurement in critically ill patients. Prospective data collection. Emergency department in a 2,000-bed hospital. Thirty-nine patients admitted to the emergency department requiring invasive arterial blood pressure monitoring were enrolled to the study protocol. Continuous noninvasive blood pressure measurement was performed on the middle phalanx of the second and third finger, using a test instrument which provides continuous arterial waveform display with the use of a finger cuff. Invasive mean arterial blood pressure measurement was done by cannulation of the radial artery and direct transduction of the systemic arterial pressure waveform. Three thousand one hundred eighteen pairs of simultaneous finger cuff and intra-arterial blood pressure measurements were collected in 1-min intervals from 39 patients over a total of 51.8 hrs. The overall discrepancy between both measurements was 0.10 mm Hg. The standard deviation of the differences was +/- 5.02 mm Hg. The mean bias in patients treated with catecholamines was 0.01 mm Hg and was not different from the bias observed in patients without catecholamines (mean bias: 0.23 mm Hg; p > .22). Whereas 95% of all comparisons between finger cuff and intra-arterial measurement had a discrepancy < or = +/- 10 mm Hg, 4.7% had a discrepancy between +/- 10.1 to 15 mm Hg and 0.3% exhibited a discrepancy > +/- 15 mm Hg. In 29 (74%) patients, the duration of errors > 10 mm Hg was < or = 1 min. In seven (18%) patients, the duration of errors > 10 mm Hg was between 2 to 3 mins and in three (8%) patients, the errors lasted for > 3 mins. Our data provide a guide to the accuracy and reliability of noninvasive finger blood pressure measurements in critically ill patients. Although most test instrument measurements were reliable, in 8% of all patients large discrepancies (> 10 mm Hg) between both measurements with a duration of > 3 mins were noted. Concerning the considerable risk for arterial cannulation, our preliminary data demonstrate that the test instrument (PORTAPRES, TNO Biomedical Instrumentation Research Unit; The Netherlands) is an advance in noninvasive monitoring of critically ill patients and may be useful in most emergency clinical settings.