Including Mean Arterial Blood Pressure Research Articles

HSD IS A BETTER RESUSCITATION FLUID FOR HEMORRHAGIC SHOCK WITH PULMONARY EDEMA AT HIGH ALTITUDE

To investigate the fluid tolerance of hemorrhagic shock with pulmonary edema (HSPE) at high altitude in unacclimated rats and the beneficial effect of 7.5% hypertonic saline/6% dextran (HSD). One hundred seventy-six Sprague-Dawley rats, transported to LaSa, Tibet, 3,760 m above the sea level, were anesthetized with sodium pentobarbital (30 mg/kg, i.p.) within 1 week. Hemorrhagic shock with pulmonary edema was induced by bloodletting (50 mmHg for 1 h) plus intravenous injection of oleic acid (50 microL/kg). Seventy-seven rats were equally divided into 11 groups (n = 7/group) including sham-operated control group; hemorrhagic shock control group; HSPE control group; HSPE plus 0.5-, 1.0-, 1.5-, 2.0-, or 3.0-fold volumes of lactated Ringer's solution (LR) groups; and HSPE plus 4, 6, and 8 mL/kg of HSD groups. Hemodynamic parameters including mean arterial blood pressure, left intraventricular systolic pressure, and the maximal change rate of intraventricular pressure rise or decline (+/-dp/dtmax) were observed at baseline and at 15, 30, 60, and 120 min after infusion; blood gases were measured at 30 and 120 min after infusion, and the water content of lung and brain was determined at 120 min after infusion. Additional 99 rats were used to observe the effect of these treatments on the survival time of HSPE rats; 0.5 volume of LR infusion slightly increased the mean arterial blood pressure, left intraventricular systolic pressure, and +/-dp/dtmax and prolonged the survival time of HSPE animals as compared with the HSPE group (P < 0.05 - 0.01); it did not increase the water content of lung and brain and had no marked influences on blood gases. One volume of LR infusion had somewhat improved the hemodynamic parameters for HSPE animals, but had no apparent effect on the survival time and the water content of lung and brain. Lactate Ringer's solution infusion, 1.5, 2, and 3 volumes, significantly deteriorated the hemodynamic parameters, increased the water content of lung, and decreased the survival time of HSPE animals. Hypertonic saline/6% dextran (4 - 8 mL/kg) significantly increased the hemodynamic parameters, improved the blood gases, decreased the water content of lung and brain, and prolonged the survival time of HSPE rats. Among the three dosages of HSD, 6 mL/kg of HSD had the best effect. The tolerance of fluid infusion for hemorrhagic shock with pulmonary edema at high altitude is significantly decreased. More than one volume of LR infusion would aggravate the pulmonary edema and exacerbate the resuscitation effect, but only one volume of LR cannot reach the effective volume resuscitation. Small volume of HSD could better resuscitate hemorrhagic shock with pulmonary edema at high altitude.

The Effect of the Nitric Oxide Synthesis Inhibitorl-NAME on Amitriptyline-Induced Hypotension in Rats

Hypotension induced by tricyclic antidepressants is multifactorial. Previous animal experiments suggest a contribution from nitric oxide production. Our study aimed to evaluate the role of nitric oxide in amitriptyline-induced hypotension using N-nitro-L-arginine methyl ester, a nitric oxide synthesis inhibitor, and 3-morpholino sydnonimine, a nitric oxide donor, in anesthetized rats. Amitriptyline intoxication was induced by the continuous infusion of amitriptyline 0.625 mg/kg/min throughout the experiment in anesthetized rats. Fifteen and 25 minutes after amitriptyline infusion began, two bolus doses of 10 mg/kg of N-nitro-L-arginine methyl ester (n = 8) or an equivalent volume of 5% dextrose solution (n = 8) was administered to each rat (Protocol 1). To investigate whether the effect of N-nitro-L-arginine methyl ester on blood pressure is counteracted by 3-morpholino sydnonimine, after the same protocol of amitriptyline infusion and 5 minutes after an N-nitro-L-arginine methyl ester bolus, a bolus of 3000 nmol/kg of 3-morpholino sydnonimine was administered (n = 8) to each rat (Protocol 2). To investigate the effect of N-nitro-L-arginine methyl ester on 3-morpholino sydnonimine induced hypotension, a group of rats received a continuous infusion of 0.54 mg/kg/h of 3-morpholino sydnonimine until 50% reduction was observed in mean arterial blood pressure followed by a bolus dose of 10 mg/kg of N-nitro-L-arginine methyl ester (n = 6) or 5% dextrose solution (n = 6) (Protocol 3). Outcome measures included mean arterial blood pressure, heart rate, and QRS duration in electrocardiogram. Student's t test and survival analysis were used for selected comparisons. For all parameters, the treatment groups were similar at baseline and at postamitriptyline periods before therapy was rendered. Amitriptyline infusion significantly reduced mean arterial blood pressure by 50.8 +/- 2.2% and prolonged QRS by 23.9 +/- 7.2% after 15 minutes. In Protocol 1, N-nitro-L-arginine methyl ester significantly increased mean arterial blood pressure compared to dextrose-treated control animals within 30 minutes (77.9 +/- 8.5% vs. 49.7 +/- 5.0% mmHg, p < 0.01, 95% CI 57.1-98.7%). QRS duration progressively increased during the amitriptyline infusion; however, there was no significant difference in QRS width between N-nitro-L-arginine methyl ester and control groups at any time point. N-nitro-L-arginine methyl ester increased survival time compared to controls (33.4 +/- 4.1 vs. 19.9 +/- 2.7 minutes, p < 0.01, 95% CI 25.4-41.3) but did not affect mortality. In Protocol 2 of continuous infusion of amitriptyline, 3-morpholino sydnonimine counteracted the N-nitro-L-arginine methyl ester-induced increase in mean arterial blood pressure. In both protocols, heart rate decreased significantly during amitriptyline infusion but there was no difference between treatment and control groups. In Protocol 3, N-nitro-L-arginine methyl ester bolus reversed 3-morpholino sydnonimine-induced hypotension compared to dextrose bolus. (83.8 +/- 5.7% vs. 54.6 +/- 4.8%, p < 0.01, 95% CI 69.2-98.4). N-nitro-L-arginine methyl ester is found to be effective in temporarily improving hypotension and prolonging survival time but does not affect overall mortality. Because this effect was antagonized by 3-morpholino sydnonimine, nitric oxide production appears to contribute to the pathophysiology of amitriptyline-induced hypotension.

The Effect of Calcium Channel Blockers on Cerebral Oxygenation During Tracheal Extubation

Calcium channel blockers are effective in stabilizing systemic hemodynamics during tracheal extubation. However, they may increase cerebral blood flow (CBF) during tracheal extubation because of cerebral vasodilation, even if systemic arterial blood pressure decreases. In this study, we observed changes in cerebral oxygenation during tracheal extubation by using near-infrared spectroscopy and evaluated the effect of nicardipine and diltiazem on the resultant changes. We studied 45 women undergoing elective gynecologic surgery. After surgery, the patients were randomly allocated to three groups (n = 15 each): saline (control), 0.02 mg/kg nicardipine, and 0.2 mg/kg diltiazem. After 2 min, we started to aspirate secretions for 2 min and then, extubated the trachea. Changes in cerebral oxygenated hemoglobin (Hbo2) and deoxygenated hemoglobin were measured during the extubation procedure for 9 min after drug treatment. Systemic hemodynamics, including mean arterial blood pressure, heart rate, end-tidal Co2, end-tidal sevoflurane concentration, and peripheral arterial oxygen saturation were also monitored. During extubation, Hbo2 increased significantly, presumably caused by the increase in CBF. Changes in deoxygenated hemoglobin were minimal. Compared with the control, nicardipine and diltiazem significantly inhibited the increase in mean arterial blood pressure. On the contrary, they significantly enhanced the increase in Hbo2. In conclusion, calcium channel blockers may increase CBF during extubation, even if these drugs stabilize systemic hemodynamics. Implications This study is a preliminary report evaluating the changes in cerebral oxygenation during the tracheal extubation. Cerebral oxygenated hemoglobin increased significantly, presumably caused by the increase in cerebral blood flow during extubation. In addition, these changes were enhanced by calcium channel blockers.

The Effect of Calcium Channel Blockers on Cerebral Oxygenation During Tracheal Extubation

Calcium channel blockers are effective in stabilizing systemic hemodynamics during tracheal extubation. However, they may increase cerebral blood flow (CBF) during tracheal extubation because of cerebral vasodilation, even if systemic arterial blood pressure decreases. In this study, we observed changes in cerebral oxygenation during tracheal extubation by using near-infrared spectroscopy and evaluated the effect of nicardipine and diltiazem on the resultant changes. We studied 45 women undergoing elective gynecologic surgery. After surgery, the patients were randomly allocated to three groups (n = 15 each): saline (control), 0.02 mg/kg nicardipine, and 0.2 mg/kg diltiazem. After 2 min, we started to aspirate secretions for 2 min and then, extubated the trachea. Changes in cerebral oxygenated hemoglobin (HbO(2)) and deoxygenated hemoglobin were measured during the extubation procedure for 9 min after drug treatment. Systemic hemodynamics, including mean arterial blood pressure, heart rate, end-tidal CO(2), end-tidal sevoflurane concentration, and peripheral arterial oxygen saturation were also monitored. During extubation, HbO(2) increased significantly, presumably caused by the increase in CBF. Changes in deoxygenated hemoglobin were minimal. Compared with the control, nicardipine and diltiazem significantly inhibited the increase in mean arterial blood pressure. On the contrary, they significantly enhanced the increase in HbO(2). In conclusion, calcium channel blockers may increase CBF during extubation, even if these drugs stabilize systemic hemodynamics. This study is a preliminary report evaluating the changes in cerebral oxygenation during the tracheal extubation. Cerebral oxygenated hemoglobin increased significantly, presumably caused by the increase in cerebral blood flow during extubation. In addition, these changes were enhanced by calcium channel blockers.

Physical Activity, Physical Fitness, and Coronary Heart Disease Risk Factors in Youth: The Québec Family Study

Objective. The relationships between physical activity, fitness, and CHD risk factors were investigated in 342 males and 268 females 9–18 years of age.Methods. Daily energy expenditure, moderate to vigorous physical activity, inactivity, and television viewing time were estimated. Indicators of physical fitness included submaximal work capacity, quadriceps muscle strength, sit-ups, and the sum of six skinfolds. Risk factors included mean arterial blood pressure and fasting blood levels of triglycerides, LDL-cholesterol, HDL-cholesterol, and glucose.Results. Canonical correlations between activity and risk factor profiles range from 0.22 to 0.45, while those between fitness and risk factor profiles range from 0.34 to 0.55, indicating that 5 to 20% and 11 to 30% of the variance in the risk profile is explained by activity and fitness, respectively.Conclusion. The results suggest that both physical fitness and level of habitual physical activity are strongly associated with CHD risk factors in this sample of youth.

Effects On Cerebral Perfusion Of Blood Withdrawal And Infusion Through The Umbelical Arterial (UAC) And Venous Catheters (UVC) In Preterm Infants† 1079

Objectives. To compare, using cerebral near-infrared spectroscopy (NIRS), the effects of blood withdrawal (W) and infusion (I) via, respectively, UAC with tip in the thoracic aorta and UVC. Method Twelve infants of 30 weeks (25-33) gestational age, 1175 g (760-1690) birth weight, mechanically ventilated for RDS were studied at 19 hours (2-25) postnatal age. The protocol involved W, through UAC of 3 ml/kg blood in 30 seconds, followed by I at the same rate, after recovery of the NIRS trace. The procedure was repeated 3 times for UAC and 3 times for UVC. NIRS (NIRO 500, Hamamatsu Photonics), a technique based on the differential absorption of NIR light by hemoglobin and cytochrome aa3 (CytO2), depending on their oxidation state, was used to assess changes in cerebral blood volume (DCBV), calculated from total hemoglobin, oxy- (DHbO2), deoxy-(DHb) hemoglobin and CytO2, time of max variation and recovery (from start of W and I). Vital parameters, including mean arterial blood pressure (MABP) were continuously measured. Results No significant change in Hb or CytO2, heart rate, pCO2 or pO2 was seen. Concordant changes in HbO2 and CBV indicate modifications of cerebral blood flow. MABP increased significantly during I-UVC and decreased during W-UVC. A positive correlation between MABP and CBV changes during W-UVC(r2 =0.41, p = 0.036) was observed. Conclusion Blood withdrawal and infusion via UVC cause significant MABP changes and related CBV oscillation which could potentially precipitate germinal matrix hemorrhage in preterm infants; utilizing the UAC this effect may be reduced or altogether avoided. Table

Direct effects of ropivacaine and bupivacaine on spinal pial vessels in canine. Assessment with closed spinal window technique.

Ropivacaine produces a vasoconstriction of cutaneous vessels in contrast to vasodilation produced by bupivacaine. To evaluate direct spinal microvascular actions of these local anesthetics, the authors investigated the concentration-related effects of ropivacaine and bupivacaine on spinal pial vascular diameters using the spinal window technique. Anesthetized dogs (n = 14) divided into two groups (ropivacaine, n = 7; bupivacaine, n = 7) were prepared for measurement of spinal pial vessel diameters by intravital microscopy in a spinal window preparation. The authors administered six concentrations of each drug (10(-8)-10(-3) M) under the window and directly measured the spinal pial arteriolar and venular diameters at sequential times. Physiologic data including mean arterial blood pressure (MAP) and heart rate (HR) were determined before and after topical application of each concentration of the drugs. In additional experiments (n = 18), the action of topical ropivacaine and bupivacaine solution on spinal vessels was evaluated in the presence of yohimbine, prazosin, and propranolol. Ropivacaine significantly constricted whereas bupivacaine dilated pial arterioles and venules, both in a concentration-dependent manner. Microvascular alteration was not blocked with any of the adrenoceptor antagonists tested (yohimbine, prazosin, propranolol), each of which per se did not affect pial vessel diameters. Topical application of ropivacaine or bupivacaine did not induce any change in MAP or HR. The present results indicate that ropivacaine constricts and bupivacaine dilates the pial vessels of the spinal cord in a concentration-dependent fashion, and the mechanisms involved in such actions do not seem to be mediated via alpha- or beta-adrenoceptor of spinal vasculature.

Transmyocardial laser revascularization induces cerebral microembolization.

Transmyocardial laser revascularization may vaporize fluid in the left heart, allowing bubbles to form. This study aimed to determine whether the laser pulse resulted in cerebral emboli and to examine changes in middle cerebral artery flow velocity and jugular bulb oxygen saturation (SjO2) during transmyocardial laser revascularization. Twelve patients (American Society of Anesthesiologists physical status III) were studied after the authors received institutional review board approval and the patients' informed consent. Monitored variables included mean arterial blood pressure (measured in millimeters of mercury), heart rate (measured as beats/min), and partial pressure of carbon dioxide (measured in millimeters of mercury). A 5-MHz transesophageal-sonography system was used to record intraventricular events after laser injection. Mean blood flow velocity (Vmean; measured in centimeters per second) was monitored in the middle cerebral artery using transcranial Doppler sonography, and SjO2 (expressed as a percentage) was measured using a fiberoptic thermodilution catheter placed in the right jugular bulb. Data were recorded before, during, and for 4 min after laser injection. After laser injection, intraventricular echogenic contrast was seen in transesophageal-sonography, and 2-4 s later high-intensity signals (microemboli) appeared in the transcranial Doppler sonography spectra. As long as mean arterial pressure remained stable during the observation period, Vmean and SjO2 did not change. These data show that microemboli can be detected after laser injection in the middle cerebral artery, although they do not effect Vmean and SjO2. The results suggest that these microemboli do not induce a global oxygen imbalance.

The Effects of Varying Volumes of Crystalloid Administration Before Cesarean Delivery on Maternal Hemodynamics and Colloid Osmotic Pressure

The value of intravenous crystalloid administration in preventing spinal-induced hypotension in the parturient has recently been questioned. Also, the association between increasing crystalloid volume and decreasing postpartum colloid osmotic pressure (COP) raises concern regarding the risk of maternal and fetal pulmonary edema. To study the dose-response effect of varying amounts of crystalloid volume prior to spinal anesthesia, we measured maternal hemodynamic variables and maternal and fetal COP in three groups of healthy parturients receiving spinal anesthesia for elective cesarean delivery. Fifty-five parturients were randomized in a double-blind fashion to receive one of 10, 20, or 30 mL/kg of crystalloid volumes prior to induction of spinal anesthesia. Measurements included mean arterial blood pressure (MAP), cardiac index (CI), and systemic vascular resistance index (SVRI) recorded using noninvasive thoracic impedance monitoring until delivery. Maternal and neonatal COP were measured. All groups showed declines in MAP and SVRI from baseline at 5 min after spinal anesthesia, but the amount of decline did not differ among groups. Total ephedrine and additional intravenous (i.v.) fluid administered did not differ among groups. The 20- and 30- mL/kg groups showed a larger decline in maternal COP than the 10-mL/kg group; no differences in neonatal COP were seen with varying preload. We conclude that increasing the amount of i.v. crystalloid administered to 30 mL/kg in the healthy parturient does not significantly alter maternal hemodynamics or ephedrine requirements after spinal anesthesia and has no apparent benefit.

Thoracic epidural clonidine and morphine for postoperative pain relief

This study was undertaken to evaluate the potentiation of the postoperative analgesic effect of thoracic epidural morphine by coadministration of thoracic epidural clonidine in a randomized double-blinded design. Twenty patients underwent radical gastrectomy under combined general anaesthesia (enflurane and nitrous oxide/oxygen) and epidural anaesthesia with local anaesthetics. They received a thoracic epidural bolus injection of either 0.05 mg.kg-1 morphine plus 3 micrograms.kg-1 clonidine (M+C group; n = 10) or 0.05 mg.kg-1 morphine alone (M group; n = 10) immediately before completion of surgery. All patients received iv morphine via patient-controlled analgesia (PCA) equipment for 24 hr postoperative period, and the PCA iv consumption of morphine was the primary variable of efficacy of the analgesic regimen. In addition, data analyses included mean arterial blood pressure, heart rate, respiratory rate, arterial blood gas measurement, sedation score, and visual analogue pain scale score (VAS). The cumulative number of iv morphine injections via PCA was less in the M+C group than in the M group at each hour for 24 hr postoperative period (P < 0.05), while the numbers of PCA morphine injections per hour beyond nine hours after surgery were higher in the M group than in the M+C group (P < 0.05). Sedation score was higher, and VAS and mean blood pressure were lower in the M+C group only at one hour after surgery compared with the M group. We conclude that the combined single thoracic epidural administration of morphine plus clonidine produces a more potent and longer lasting analgesia than does morphine alone.

Development of hypertension in animals with reduced total peripheral resistance.

The object of the present study was to determine whether deoxycorticosterone acetate (DOCA)-salt hypertension can be produced in rats in the presence of low total peripheral resistance (TPR) induced by long-term administration of minoxidil, a vasodilator. The rats were divided into four groups: sham-control, DOCA-salt, minoxidil, and DOCA-salt with minoxidil. The rats in both DOCA groups had DOCA pellets implanted subcutaneously and were given saline to drink. The rats in both minoxidil groups were given minoxidil (3 mg/day) in the drinking water throughout the experiment. Final measurements, including mean arterial blood pressure, cardiac index, and renal blood flow were made after 4-6 weeks. Flow measurements were made using radioactive microspheres. Cardiac index (ml.min-1.100 g-1) in sham-control rats averaged 18 +/- 2 and was higher in the other groups: 23 +/- 4 (DOCA-salt), 25 +/- 2 (minoxidil), and 30 +/- 2 (DOCA-salt plus minoxidil). Mean arterial pressure (mm Hg) was increased in both DOCA-salt rats (160 +/- 8) and DOCA-salt plus minoxidil rats (153 +/- 5) as compared with sham-control (116 +/- 2) and minoxidil (113 +/- 3) rats. There was no significant difference in TPR between the sham-control and DOCA-salt rats, but TPR in minoxidil and DOCA-salt plus minoxidil rats was 30% and 28% lower than that in untreated sham-control and DOCA-salt hypertensive rats, respectively. In contrast, renal vascular resistance was significantly increased in both DOCA-salt groups as compared with non-DOCA-salt groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Impact of metabolic control in progression of clinical diabetic nephropathy.

Renal clearance of 51Cr-EDTA as a measure of glomerular filtration rate was followed prospectively for 21 months in 18 Type 1 (insulin-dependent) patients with juvenile-onset diabetes and nephropathy. Hypertension was treated aggressively, attaining a mean blood pressure of 154/88 mmHg in the supine and 126/82 mmHg in the standing position. The mean glycosylated haemoglobin value (HbA1c) during the observation period was found to correlate well with the mean of random blood glucose values (r = 0.72). It also correlated to the rate of glomerular filtration rate decline over time, whether the latter was calculated as slope coefficient for all available data (r = -0.52, p less than 0.05) or based on the first and last observations only (r = -0.57, p less than 0.05). In a multiple linear stepwise regression analysis also including mean arterial blood pressure, the correlation between glomerular filtration rate decline and HbA1c was significant at p less than 0.01; this explained one-third of the progression, while mean arterial pressure could not be shown to contribute. It is concluded that hyperglycaemia, contrary to the general belief, is a risk factor for the progression of clinical diabetic nephropathy with reduced glomerular filtration rate.

Endotoxemic acute renal failure in awake rats.

The sequence of changes in renal function in endotoxemic acute renal failure (ARF) and the role of hypotension and systemic hemodynamics were evaluated in awake female Sprague-Dawley rats given an intravenous bolus of Escherichia coli endotoxin (20-40 mg/kg). After endotoxin ARF was abrupt in onset as glomerular filtration rate (GFR) fell promptly and progressively by 53% within 3.5 h, whereas renal blood flow decreased by 42% and renal vascular resistance nearly doubled. Systemic hemodynamics remained stable, including mean arterial blood pressure, cardiac output, and total peripheral resistance. Early endotoxemic ARF was associated with oliguria and sodium retention, a finding consistent with intact tubular function. Three and one-half hours after endotoxin, however, fractional water and sodium excretion were significantly increased. Ultrastructural studies then demonstrated sequestration of phagocytic leukocytes and intracellular edema in the peritubular capillaries with normal glomeruli. The decrease in GFR was spontaneously reversible within 7-9 days. Extracellular fluid volume expansion with saline either before or 24 h after administration of endotoxin failed to prevent the decrease in GFR or to normalize renal function. The data suggest that endotoxin has direct renal effects. The endothelial cells may be the primary target of endotoxin in the kidney.