mmHg Mean Arterial Blood Pressure Research Articles

Treatment effects of blood pressure targets and hemodynamics according to initial blood lactate levels in comatose out-of-hospital cardiac arrest patients – A sub study of the BOX trial

BackgroundOut-of-hospital cardiac arrest (OHCA) survivors remaining comatose are often circulatory unstable with high mortality in the first days following resuscitation. Elevated lactate will reflect the severity and duration of hypoperfusion in cardiac arrest. Further, the severity of hypoperfusion could modify the effect on survival of different mean arterial blood pressure (MAP) targets. MethodsIn this sub-study of the BOX trial, adult successfully resuscitated comatose OHCA patients (n = 789) with a presumed cardiac cause were randomized to a MAP target of 63 mmHg vs. 77 mmHg. Patients were arbitrarily grouped in low-lactate: <25% of sample, medium-lactate: 25%–75%, and high >75 percentile according to blood lactate levels at hospital arrival as a surrogate of the severity of hypoperfusion. Invasive hemodynamic evaluations were performed using an arterial catheter and pulmonary artery catheter (PAC), and data from admission to 48 hours (h) were recorded. Logistic regression analysis evaluated whether lactate levels (as continuous and categorical) modify the effect of MAP targets on mortality at 365 days. ResultsThe three lactate groups had initial lactate levels of low-lactate: <2.9 mmol/L, medium-lactate: 2.9–7.9 mmol/L, and high-lactate > 7.9 mmol/L. All patients were randomized to a 63 mmHg or 77 mmHg MAP target. The proportion of patients in the high-MAP target group was 100/201 (50%), 178/388 (46%), and 114/197 (58%) for low, medium, and high-lactate groups respectively. At admission, the high-lactate groups had a lower MAP compared to the medium-lactate (2.6 mmHg (95% CI: 0.1–5.0 mmHg, p = 0.02), and the low-lactate group, (3.6 mmHg (95% CI: 0.8–6.5 mmHg, p < 0.01). Accordingly, the vasoactive inotropic score was 79% (95%CI: 42%–124%%) higher with increasing initial lactate level (High-lactate vs. low-lactate) with the largest difference at 6 hours (110.6% (95%CI: 54.4%–187.2%) higher in high-lactate patients). No difference in the cardiac index or systemic vascular resistance was observed between lactate groups. The initial lactate level (continuous) modified the effect of the two MAP targets (p = 0.04). In the highest lactate group, the mortality was 100/197 (51%), and with an odds ratio (OR): 1.7 (95%CI: 0.9–3.0) if randomized to MAP 77 mmHg compared to MAP 63 mmHg. In the lowest lactate group, the mortality was 35/201(17%) and similar if randomized to a MAP target of 77 mmHg (OR: 1.1 (95% CI: 0.5–2.3)). ConclusionComatose OHCA patients with high initial lactate levels required more vasoactive drugs on the first two days of ICU admission to meet the blood pressure target and had a poorer prognosis. No indication that aiming for a higher MAP target is beneficial in patients with an initial high lactate level was found, however, given the post-hoc nature of this study, these results should be considered hypothesis-generating

Blood Pressure Changes During Mechanical Thrombectomy for Acute Ischemic Stroke Are Associated With Serious Early Treatment Complications: Symptomatic Intracerebral Hemorrhage and Malignant Brain Edema.

BackgroundSymptomatic intracranial hemorrhage (sICH) and malignant brain edema (MBE) are well-known deleterious endovascular treatment (EVT) complications that some studies found to be associated with postprocedural blood pressure (BP) variability. We aimed to evaluate their association with periprocedural BP changes, including its intraprocedural decrease.MethodsWe retrospectively analyzed the data of 132 consecutive patients that underwent EVT between 1 December 2018 and 31 December 2019, for anterior circulation ischemic stroke. Analyzed predictors of sICH and MBE included non-invasively obtained BP before and 5-min after treatment, intraprocedural relative decreases of BP from baseline, and its post-treatment increases. SICH was defined in accordance with the Safe Implementation of Thrombolysis in Stroke-Monitoring Study (SITS-MOST) criteria and MBE as brain edema with midline shift on the follow-up imaging. We used binary logistic regression analysis to investigate the association of BP parameters and the incidence of sICH and MBE.ResultsAmong the included patients, 11 (8.3%) developed sICH and 31 (23.5%) MBE. The intraprocedural decrease of mean arterial blood pressure (MAP) was independently associated with MBE occurrence (aOR per 10 mmHg drop from baseline 1.27; 95% CI 1.01–1.60; P = 0.040). Over 40% MAP drop was associated with a higher risk of sICH in the entire cohort (aOR 4.24; 95% CI 1.33–13.51; P = 0.015), but not in the subgroup with successful reperfusion (aOR 2.81; 95% CI 0.64–12.23; P = 0.169). Post-treatment systolic blood pressure (SBP) and MAP elevation above their minimal values during MT are significantly associated with the development of sICH (aOR per 10 mmHg SBP increase 1.78; 95% CI 1.15–2.76; P = 0.010 and aOR per 10 mmHg MAP increase 1.78; 95% CI 1.04–3.03; P = 0.035).ConclusionsIn the anterior circulation ischemic stroke patients relative MAP decrease during EVT is associated with a higher risk of MBE occurrence, and over 40% MAP drop with a higher incidence of both MBE and sICH. Post-treatment elevation of SBP and MAP increased the risk of sICH.

Impact of chronic hyperleptinemia on placental ischemia‐induced hypertension in pregnant rats

Obesity is a risk factor for preeclampsia, which is new‐onset hypertension during pregnancy. The mechanisms linking obesity and preeclampsia are poorly understood. The adipokine, leptin, is elevated in the circulation in proportion to fat mass and elicits hypertension when infused into non‐pregnant animals. However, less is studied about how hyperleptinemia impacts blood pressure regulation during pregnancy. A contributing factor to hypertension during preeclampsia is placental ischemia. Therefore, we tested the hypothesis that chronic hyperleptinemia exaggerates placental ischemia‐induced hypertension. On gestational day 14, timed‐pregnant Sprague‐Dawley rats were implanted with osmotic pumps to intravenously deliver recombinant rat leptin at 1.0 ug/kg per min or vehicle and placental ischemia was produced by the reduced uterine perfusion pressure (RUPP) procedure or Sham surgery. By day 19, leptin levels were elevated (P&lt;0.05) in Sham (leptin‐infused, N=9: 41.0±2.8 ng/mL vs vehicle, N=23: 0.8±0.1 ng/mL) and RUPP (leptin‐infused, N=9: 29.7±7.2 ng/mL vs vehicle, N=17: 1.0±0.1 ng/mL). RUPP elicited hypertension (Sham+vehicle: 100±1 mmHg vs RUPP+vehicle: 122±3 mmHg mean arterial blood pressure, P&lt;0.05). In contrast to our hypothesis, hyperleptinemia attenuated RUPP hypertension (RUPP+leptin: 109±4 mmHg, P&lt;0.05 vs RUPP+vehicle) and did not alter blood pressure in Sham rats (Sham+leptin: 100±6 mmHg vs Sham+vehicle). Therefore, we examined whether hyperleptinemia was vasoprotective by promoting vasorelaxation during pregnancy in isolated third‐order mesenteric arteries. Although endothelial‐dependent vasorelaxation to acetylcholine (measured as logEC50 sensitivity) was similar within Sham (vehicle: −6.8±0.1 M vs leptin: −6.9±0.2 M) and RUPP (vehicle: −7.0±0.2 M vs leptin: −7.0±0.3 M) groups, endothelial‐independent vasorelaxation to the nitric oxide (NO)‐donor, sodium nitroprusside, was increased (P&lt;0.05) in both Sham (vehicle: −6.0±0.2 M vs leptin: −6.8±0.3 M) and RUPP (vehicle: −6.9±0.2 M vs leptin: −7.6±0.01 M) groups. This suggested that NO‐cyclic guanosine monophosphate (cGMP) signaling was increased. Plasma levels of cGMP were elevated (P&lt;0.05) within Sham (vehicle: 1.6±0.3 pmol/mL vs leptin: 3.9±0.6 pmol/mL) and RUPP (vehicle: 3.6±0.8 pmol/mL vs leptin: 5.8±1.1 pmol/mL) groups. In contrast to our original hypothesis, chronic hyperleptinemia does not produce hypertension during pregnancy likely via promoting vascular NO‐cGMP signaling.Support or Funding InformationHL130577

Muscle membrane properties in A pig sepsis model: Effect of norepinephrine.

Sepsis-induced myopathy and critical illness myopathy are common causes of muscle weakness in intensive care patients. This study investigated the effect of different mean arterial blood pressure (MAP) levels on muscle membrane properties following experimental sepsis. Sepsis was induced with fecal peritonitis in 12 of 18 anesthetized and mechanically ventilated pigs. Seven were treated with a high (75-85 mmHg) and 5 were treated with a low (≥60 mmHg) MAP target for resuscitation. In septic animals, resuscitation was started 12 h after peritonitis induction, and muscle velocity recovery cycles were recorded 30 h later. Muscles in the sepsis/high MAP group showed an increased relative refractory period and reduced early supernormality compared with the remaining septic animals and the control group, indicating membrane depolarization and/or sodium channel inactivation. The membrane abnormalities correlated positively with norepinephrine dose. Norepinephrine may contribute to sepsis-induced abnormalities in muscle by impairing microcirculation. Muscle Nerve 57: 808-813, 2018.

Cigarette smoke extract inhibits fluid and HCO3− secretion and CFTR activity in guinea pig pancreatic ductal cells

Spontaneous depolarizations around the core are a consistent feature of focal cerebral ischemia, but the associated regional hemodynamic changes are heterogeneous. We determined how the features of depolarizations relate to subsequent cerebral blood flow (CBF) changes in global forebrain ischemia.Forebrain ischemia was produced in halothane-anesthetized rats (n = 13) by common carotid artery occlusion and hypovolemic hypotension. Mean arterial blood pressure (MABP) was monitored via a femoral catheter. Specific illuminations allowed the capture of image sequences through a cranial window to visualize: changes in membrane potential (voltage-sensitive dye method); CBF (laser speckle contrast imaging); cerebral blood volume (intrinsic optical signal, IOS at 540–550 nm); and hemoglobin deoxygenation (IOS at 620–640 nm).A depolarization occurred (n = 9) when CBF fell below 43.4 ± 5% of control (41 ± 4 mmHg MABP), and propagated with a distinct wave front at a rate of 2.8 mm/min. Depolarizations were either persistent (n = 4), intermediate (n = 3) or short, transient depolarization (n = 2). Persistent and intermediate depolarizations were associated with sustained hypoperfusion (−11.7 ± 5.1%) and transient hypoperfusion (−17.4 ± 5.2, relative to CBF before depolarization). Short, transient depolarizations did not generate clear CBF responses.Depolarizations during incomplete global ischemia occurred at the lower limit of CBF autoregulation, propagated similar to spreading depolarization (SD), and the hemodynamic responses indicated inverse neurovascular coupling. Similar to SDs associated with focal stroke, the propagating event can be persistent or transient.

Effects of fever on haemodynamic parameters in neurosurgical intensive care unit patients

To investigate the effects of fever on the haemodynamic parameters (pulse rate, arterial oxygen saturation, systolic blood pressure, diastolic blood pressure and mean arterial blood pressure) of patients in a neurosurgical intensive care unit. A prospective, repeated-measures study. This study was performed in the neurosurgical intensive care unit of a University Hospital in the West of Turkey. The research sample included all patients with at least two occurrences of fever in the postoperative period. Body temperature and haemodynamic parameters of patients were measured on admission, one hour before the onset of fever and during fever (peak temperature). Increase of body temperature during fever episodes was followed by a significant increase in pulse rate (p = 0.001) with significant decreases in systolic blood pressure (p = 0.002) and arterial oxygen saturation (p = 0.001). Furthermore fever episodes were followed by a non-significant increase in diastolic blood pressure (p = 0.074) and a non-significant decrease in mean arterial blood pressure (p = 0.097). In this study, a degree celsius (1 °C) increase in body temperature, was associated with a decline of 4.43 mmHg in systolic blood pressure, 0.166 mmHg mean arterial blood pressure and 0.64% arterial oxygen saturation, respectively. It was also associated with an increase of 1.61 mmHg in diastolic arterial blood pressure and 7.46 beats/per minute pulse rate, respectively. The findings from this research have demonstrated the effects that fever can have on haemodynamic parameters of patients in one neurosurgical intensive care unit. Hence the study highlights the importance for intensive care unit (ICU) nurses to appreciate the physiological effects of fever which have the potential to cause complications in febrile patients. Increasing knowledge about the effects of fever on haemodynamic parameters can therefore be of benefit to nurses in terms of quality and efficacy of patient care.

Ideal resuscitation pressure for uncontrolled hemorrhagic shock in different ages and sexes of rats.

IntroductionOur previous studies demonstrated that 50-60 mmHg mean arterial blood pressure was the ideal target hypotension for uncontrolled hemorrhagic shock during the active hemorrhage in sexually mature rats. The ideal target resuscitation pressure for immature and older rats has not been determined.MethodsTo elucidate this issue, using uncontrolled hemorrhagic-shock rats of different ages and sexes (6 weeks, 14 weeks and 1.5 years representing pre-adult, adult and older rats, respectively), the resuscitation effects of different target pressures (40, 50, 60, 70 and 80 mmHg) on uncontrolled hemorrhagic shock during active hemorrhage and the age and sex differences were observed.ResultsDifferent target resuscitation pressures had different resuscitation outcomes for the same age and sex of rats. The optimal target resuscitation pressures for 6-week-old, 14-week-old and 1.5-year-old rats were 40 to 50 mmHg, 50 to 60 mmHg and 70 mmHg respectively. Ideal target resuscitation pressures were significantly superior to other resuscitation pressures in improving the hemodynamics, blood perfusion, organ function and animal survival of uncontrolled hemorrhagic-shock rats (P < 0.01). For same target resuscitation pressures, the beneficial effect on hemorrhagic shock had a significant age difference (P < 0.01) but no sex difference (P > 0.05). Different resuscitation pressures had no effect on coagulation function.ConclusionHemorrhagic-shock rats at different ages have different target resuscitation pressures during active hemorrhage. The ideal target resuscitation hypotension for 6-week-old, 14-week-old and 1.5-year-old rats was 40 to 50 mmHg, 50 to 60 mmHg and 70 mmHg, respectively. Their resuscitation effects have significant age difference but had no sex difference.

Comparison of direct and Doppler arterial blood pressure measurements in rabbits during isoflurane anaesthesia

ObjectiveTo measure the level of agreement between Doppler measured (DOP) arterial blood pressure (ABP) in the forelimb and directly measured (DIR) auricular systolic ABP (SAP) and mean ABP (MAP) in isoflurane-anaesthetized rabbits. Study designProspective clinical study. AnimalsData were analysed from 17 of 24 healthy rabbits, weighing 1.3–2.8 kg. MethodsRabbits were anaesthetized for neutering using a standardized protocol. A 26G catheter placed in an auricular artery was connected via heparinised saline filled non-compliant tubing (regularly flushed) to a calibrated pressure transducer (zeroed level with the thoracic inlet) to obtain DIR ABP. A cuff was placed proximal to the carpus (approximately level with the thoracic inlet) and a Doppler transducer sited over the dorsal carpal branch of the radial artery to obtain DOP ABP. Simultaneous DIR and DOP ABP recordings were made every 5–10 minutes during anaesthesia. Agreement was assessed as described by Bland JM & Altman (2007). ResultsMean ± SD cuff width: limb circumference ratio was 0.50 ± 0.04. Mean between-method differences ± SD, DIR SAP- DOP and DIR MAP- DOP, were +1 ± 8 and −13 ± 8 mmHg respectively. The 95% limits of agreement between DIR SAP and DOP and between DIR MAP and DOP were −14 to +17 and −28 to +2 mmHg respectively. Differences between DIR SAP and DOP were ≤10 mmHg 85% of the time. Defining hypotension as either DIR SAP < 80 mmHg or DIR MAP < 60 mmHg, and taking DOP ABP of <80 mmHg to indicate hypotension, sensitivity and specificity were 92% and 67% respectively. ConclusionsGood agreement was found between DIR SAP and DOP. Doppler measurements below 80 mmHg are a reliable indicator of arterial hypotension. Clinical relevanceDOP is acceptable for monitoring ABP in isoflurane-anaesthetized rabbits and is useful for detection of hypotension.

Determination of the Optimal Mean Arterial Pressure for Postbleeding Resuscitation after Hemorrhagic Shock in Rats

The authors previously found that 50-60 mmHg mean arterial blood pressure (MAP) was an optimal target resuscitation pressure for hemorrhagic shock before bleeding was controlled in rats. However, the optimal target resuscitation pressure for hemorrhagic shock after bleeding has been controlled has not been determined. A model of uncontrolled hemorrhagic shock was initiated in anesthetized Wistar rats. After 1-h hypotensive resuscitation and bleeding was stopped, rats received fluid resuscitation to different target MAPs (50, 70, or 90 mmHg) with lactated Ringer's solution (LR), 6% hydroxyethyl starch (HES), LR+HES (2:1) or LR+whole blood (2:1) for 2 h. Animal survival, hemodynamic parameters, and vital organ functions were observed. After bleeding had been controlled, mildly hypotensive resuscitation at a target MAP of 70 mmHg increased the survival time and survival rate compared with a target MAP of 50 mmHg and 90 mmHg (P < 0.05 or 0.01). Hemodynamic parameters, cardiac output, oxygen delivery, and vital organ function (including mitochondrial function) in 70 mmHg target MAP groups were better than in other two-target pressure groups (P < 0.05 or 0.01). Among the fluids tested, LR+whole blood (2:1) or LR+HES130 (2:1) had better effects than LR or HES alone at each level of target blood pressure. Mildly hypotensive resuscitation is also needed for hemorrhagic shock after bleeding has been controlled, irrespective of whether crystalloids or colloids are used. The optimal target pressure was 70 mmHg in our rat model. A resuscitation pressure that is too low or too high cannot produce a good resuscitative effect.

Human adult mesenchymal stem cells improve rat spatial cognitive function after systemic hemorrhagic shock

The aim of the present study was to examine whether a single infusion of human adult mesenchymal stem cells (hMSC) has protective effects on rat cognitive functions after systemic hemorrhagic shock. Systemic hemorrhagic rat shock model of pronounced (30 min) systemic hypotension [30–40 mmHg mean arterial blood pressure (MABP) reduction] was used to induce cerebral oligemia. Immediately after the experimental transient hypotension period ended, human processed lipoaspirate-derived mesenchymal stem cells (hMSC, 1 × 10 6) were administered via the femoral vein. Rats were tested in relation to their cognitive spatial abilities using the Morris water maze before and 3 days after transient oligemia and with/without hMSC transplantation. Immunohistological investigations were performed with respect to apoptosis and BrdU staining. A clear functional improvement was observed in the rats’ spatial cognitive abilities after hypotension and subsequent hMSC transplantation. In the hypotension group, hMSC infusion reduced the mortality from 50% to 25%. Six days after hMSC administration and hypotension, we did not detect any BrdU-labeled cells in rat brain, lung, and liver; however, BrdU-positive cells were found in spleen. No signs of cerebral apoptosis were observed. We conclude from this study that hMSCs derived from peripheral blood could be an important cell source to improve functional outcome after transient cerebral oligemia. Identifying the underlying mechanism for this, however, should be the subject of further investigations.

Blood Pressure Effects on Retinal Vessel Diameter and Flicker Response: A 1.5-Year Follow-Up

The study examined the influence of individual blood pressure changes overtime on retinal vessel diameter and the latter's response to flicker light. The diameter of a retinal arterial and venous segment was measured continuously on-line with a Dynamic Vessel Analyzer in 20 patients twice (mean interval between examinations of 24 months). Eleven patients had no cardiovascular disease. Nine patients had arterial hypertension and were untreated at the time of the first measurement; at the time of the second measurement they were undergoing various antihypertensive therapies. Each test consisted of a 50-s baseline plus three 20-s periods of flicker stimulation followed by an 80-s period of observation. During the examinations the blood pressure was measured at 1-minute intervals. In the hypertension group changes in the mean arterial blood pressure (MAP) correlated significantly with changes in the arterial baseline diameter (y = -0.1 - 0.37x, r =0.74, p (increase) <0.03). A comparison of the two measurements showed no such relationship in the group of cardiovascularly healthy subjects. The venous baseline and the arterial and venous flicker response did not change significantly in either group between the two measurements and showed no relationship to blood pressure changes. In hypertensive subjects, long-term therapy-related changes in blood pressure induced a change in the arterial baseline by approximately +3.7 microm/-10 mmHg MAP. An influence of lowering MAP to the arterial flicker response could not be detected.

ARTERIAL HYPOTENSION (AH) AND THE DYNAMICS OF IRON NITROSYL HEMOGLOBIN (HBNO) IN A RAT MODEL OF BLAST-INDUCED INJURY

Cardio-pulmonary contusion and hemorrhage followed by AH are the common features of polytruma produced by blast shock waves (SW). Presumably vascular resistance and AH are associated with effects of neuro-humoral factors such as nitric oxide (NO). To address these NO effects in blast polytrauma we compared two models (1) pulmonary injury produced by experimental SW combined with isobaric hemorrhage (H), and (2) AH produced by exogenous NO. To this goal, Sprague-Dawley rats were exposed to SW at peak overpressure ~120 kPa. At ~50 min after SW impact, exposed animals were subjected to H (40 mmHg MAP for 100 min). Vascular consumption of the released NO was induced by iv administration of (MGD)2Fe2+, a NO-trapping agent. SIN-1 and DEA NONOate (NO release with half-time 40 min and 2 min respectively) were administered through trachea with dose 6 mg/kg and 4.5 mg/kg respectively. Electron paramagnetic resonance was used to measure levels of NO-adducts with hemoglobin (HbNO) in blood collected from femoral artery. Exposure to SW led to a decrease in the both of the mean arterial blood pressure (MAP) (~30%) and heart rate (HR) (~25%). These alteration were accompanied by 2-fold increase in the blood HbNO levels. H led to further decrease in MAP and HR (respectively ~65% and ~45%) and 8-fold increase in blood HbNO adducts. MAP and HR were restored by administration of (MGD)2Fe2+ and, in part, by administration of lactated Ringer's saline. These effects induced by SW and H were simulated by SIN-1 and DEA NONOate. The dynamic of alterations induced by these NO-donors was in accordance with their rates of NO release. We speculate that the AH of blast is caused in part by the vasodilatory action of NO and in part by effects of NO in the autonomic regulation of HR. Supported by DoD PRMRG 033201.

SUBCLASS OPIOID RECEPTORS ASSOCIATED WITH THE CARDIOVASCULAR DEPRESSION AFTER TRAUMATIC SHOCK AND THE ANTISHOCK EFFECTS OF ITS SPECIFIC RECEPTOR ANTAGONISTS

The present available opioid receptor antagonists such as naloxone and naltrexone are not highly receptor selective. They may antagonize mu opioid receptors to affect the pain threshold of the patients with traumatic shock while they exert antishock effects. Therefore, they are not suitable for traumatic shock. It is very important to elucidate the subclass of opioid receptors that are closely associated with cardiovascular depression of traumatic shock and then choose their specific receptor antagonists to treat it. Traumatic shock was used in pentobarbital-anesthetized Wistar rats by right femur fracture plus hemorrhage (fixed hemorrhage at a rate of 20 mL/kg in experiment 1 or hemorrhage to 40 mmHg mean arterial blood pressure for 60 min in experiments 2 and 3), and the changes of myocardial and brain opioid receptors after traumatic shock, the antagonizing effects of mu, delta, and kappa opioid receptor antagonists on the cardiovascular depression of traumatic shock and the antishock effects of delta and kappa opioid receptor antagonists ICI174,864 and Nor-binaltorphimine (Nor-BNI) were observed. The results indicate that after traumatic shock, the number of myocardial and brain delta and kappa opioid receptors were significantly increased that were significantly associated with the decreased cardiovascular functions. mu Opioid receptors in the heart and brain did not change significantly. Intracerebral ventricular administration of ICI174,864 and Nor-BNI significantly antagonized the decreased cardiovascular function after traumatic shock and increased the survival rate of traumatic shock rats, but mu opioid receptor antagonist beta-funaltrexamine did not. Meanwhile, intravenous administration of delta and kappa opioid receptor antagonists ICI174,864 and Nor-BNI also significantly increased the mean arterial blood pressure, improved the hemodynamic parameters, and prolonged the survival rate of traumatic shock rats. These findings suggest that opioid receptors are involved in the cardiovascular depression of traumatic shock, and the subclass receptors are mainly delta and kappa opioid receptors. delta and kappa opioid receptor antagonists have good beneficial effects on traumatic shock.

The effect of hospitalisation on ambulatory blood pressure in pregnancy.

Twenty-four-hour ambulatory blood pressure monitoring was performed on 40 women (20 hypertensive, 20 normotensive) on a hospitalised and non-hospitalised day. Mean blood pressure differences were calculated for the awake, sleeping and 24-hour periods on both days. Mean heart rate was higher at home (1.79, p = 0.04) than in hospital, but there were no significant differences in mean systolic (1.30 mmHg, p = 0.06), diastolic (0.78 mmHg, p = 0.21) or mean arterial blood pressure (0.81 mmHg, p = 0.19) between the hospitalised and non hospitalised day for the group overall. Nevertheless, the range of individual responses was wide (-8.5 mmHg to 15.4 mmHg mean arterial blood pressure). Hypertensive women receiving antihypertensive therapy had significantly greater differences in mean arterial blood pressure between the hospital and non-hospital day when compared to the rest of the group (5.8 mmHg, compared to 3.3 mm Hg, p = 0.02). Although hospitalisation does not significantly lower blood pressure in pregnant women as a group, women receiving antihypertensive therapy demonstrate significant differences in blood pressure between hospital and home. Based on conventional blood pressure measurements alone, these women may be at risk of either under treatment, or over treatment, of blood pressure.

Ischemic Brain Injury Caused by Interrupted Versus Uninterrupted Occlusion in Hypotensive Rats with Subarachnoid Hemorrhage: Neuroprotective Effects of Citicoline

This study investigated the neuroprotection provided by cytidine 5'-diphosphocholine (citicoline) during interrupted and uninterrupted occlusion of the basilar artery after subarachnoid hemorrhage (SAH) in 121 hypotensive rats. Animals were anesthetized and the basilar artery was exposed through a transclival approach. Baseline local cerebral blood flow (LCBF) values were recorded, and then the basilar artery was punctured, causing SAH. Blood was drawn to induce hypotension [60–70 mmHg mean arterial blood pressure (MABP)]. Control rats received intraperitoneal (i.p.) injections of 0.5 ml saline immediately after SAH before hypotension induction and after 60 min of occlusion. Experimental rats received 400-mg/kg citicoline i.p. at the same time points. Control group I and treatment group III were subjected to 60 min of interrupted occlusion (5 min of reperfusion after each 10 min of occlusion). Control group II and treatment group IV were subjected to 60 min of uninterrupted occlusion. MABP and LCBF were recorded every 5 minutes. Brain edema was evaluated in seven rats from each group at 24 hours after ischemic injury. At 3 days after occlusion, another set of 28 rats was killed and coronal brain slices were stained to assess infarct volume. The groups' physiological and edema findings were similar. In all groups, LCBF fell immediately after SAH and remained below baseline throughout the experiment. In the citicoline-treated rats, arterial pressure increased significantly after 30–40 min of occlusion, and brain slices showed significantly smaller infarct volumes compared to control slices (p < 0.05). Mortality was significantly lower in the citicoline-treated animals (p < 0.001). The results suggest that citicoline provides significant neuroprotection during cerebral ischemia, and that it significantly reduces mortality. Part of the neuroprotective effect may be mediated by recovery of arterial pressure.

Vasopressin and oxytocin: modulators of neurohypophysial blood flow

We examined the role of arginine vasopressin (AVP) as a mediator of neurohypophysial (NH) blood flow regulation in anesthetized dogs. First, we evaluated the NH hyperemia that occurs during hemorrhagic hypotension in the presence (n = 7) and absence (n = 7) of the selective AVP-V1 receptor antagonist [d(CH2)5Tyr(Me)]AVP. AVP-V1 blockade did not alter NH transient or steady-state flow responses to a standardized decrease to 80 mmHg mean arterial blood pressure. We then determined whether exogenous AVP alters NH and regional cerebral blood flow (CBF) (n = 8). Sequential intracarotid infusions resulted in sagittal sinus blood AVP concentrations ranging from 6.97 +/- 3.3 x 10(3) to 2.45 +/- 0.47 x 10(6) pg/ml. No change in NH blood flow (control 428 +/- 162 vs. 487 +/- 75 ml.min-1.100 g-1) was observed even at the highest blood level. However, CBF at the highest AVP level increased from a control value of 20 +/- 3 to 40 +/- 4 ml.min-1.100 g-1, while cerebral oxygen consumption remained unchanged. Administration of a selective AVP-V1 receptor antagonist, [d(CH2)5Tyr(Me)]AVP, blocked AVP-induced elevation in CBF in a third set of dogs (n = 5). Oxytocin was also given by intracarotid infusion at a constant rate (1-200 micrograms/ml) in a final group (n = 5). NH blood flow was unchanged at all doses, whereas CBF increased from control (24 +/- 2 to 38 +/- 5 ml.min-1.100 g-1) at the highest dose. (ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic regulation of renin secretion and renal hemodynamics during deliberate hypotension in humans.

To assess the relative contributions of neural and nonneural stimuli of renin secretion, the effects of an alpha 1-agonist, phenylephrine (Phe), or a beta-agonist, epinephrine (Epi), on plasma renin activity (PRA), renal blood flow (RBF), and glomerular filtration rate (GFR) were compared during sympathetic blockade with epidural hypotensive anesthesia [mean arterial blood pressure (MAP) = 60 and 50 mmHg]. Controls (NaCl) received saline alone to maintain MAP at 50 mmHg. Epi increased PRA (ng.ml-1.h-1) from 0.9 +/- 0.6 to 3.0 +/- 1.5 at 60 mmHg MAP and 4.7 +/- 1.8 at 50 mmHg MAP, with associated decreases in RBF (-33 and -60%, respectively) and GFR (-27 and -53%, respectively). During hypotension with Phe and NaCl, PRA and RBF were unchanged from baseline but GFR decreased. Urinary Na secretion decreased comparably in all three groups. In conclusion, during sympathetic blockade with epidural anesthesia, marked reductions in both renal perfusion pressure and distal nephron Na delivery were insufficient to increase renin secretion. beta-Adrenergic stimulation (e.g., Epi) was required to increase PRA. Epi decreased RBF suggesting an angiotensin II-mediated effect.

破裂脳動脈瘤症例の予後に影響を及ぼす術中因子の分析

Induced hypotension has commonly been used during intracranial aneurysm surgery in order to facilitate dissection and reduce the risk of intraoperative rupture. It is not known for certain, however, whether this procedure is appropriate or not. We analyzed intraoperative prognostic factors, including induced hypotension below 60 mmHg mean arterial blood pressure (MABP) using trimetaphan camsylate, in 90 patients who underwent clipping of intracranial aneurysms. The intraoperative factors were temporary clipping, low density areas and brain swelling on postoperative CT scan, and intraoperative rupture. In addition, we investigated the Hunt & Kosnik grade, CT grade, and past history of hypertension as preoperative factors, and delayed ischemic neurological deficits (DIND) as a postoperative factor. The data were evaluated using methods of multivariate statistical analysis (quantification theory 2nd family).These factors affected the prognosis in the following order according to their relative influence strengths: preoperative factors, postoperative factor, and intraoperative factors. In all cases induced hypotension below 60 mmHg MABP had a little influence on prognosis, but in patients with a past history of hypertension or in Hunt & Kosnik grade III and IV patients, induced hypotension had an adverse effect on outcome. These patients have a high probability of developing reduced cerebral blood flow and impaired autoregulation after subarachnoid hemorrhage. Especially when extended for over 30 minutes, induced hypotension below 60 mg MABP was more harmful. It is concluded that, in order to facilitate dissection during intracranial aneurysm surgery, temporary clipping is superior to prolonged induced hypotension.

Electrical correlates of brain injury resulting from severe hypotension and hemodilution in monkeys.

The effects of hypotension, hemodilution, and their combination on the relationship between concurrent brain electrical activity and resulting brain injury were studied in anesthetized monkeys. The authors compared changes in the electroencephalogram and somatosensory and auditory evoked potentials with eventual neuropathologic outcome. Our goals were: 1) to define the margin of safety for the monkey brain during hemodilution and hypotension under several simulated clinical conditions; and 2) to determine whether noninvasive measurements of brain electrical activity can predict ischemic brain cell damage. Forty-one monkeys were anesthetized with halothane (0.8 vol % inspired) and ventilated mechanically. Arterial hypotension was induced with trimethaphan (25 +/- 8 mmHg mean arterial blood pressure [MABP] for 30 min). Hemodilution was induced by replacing blood with lactated Ringer's solution (14 +/- 2% hematocrit for 1 h). Combined hemodilution and hypotension consisted of 30 min of hemodilution alone followed by superimposing hypotension for 30 min (16 +/- 3% hematocrit and 29 +/- 5 mmHg MABP). Ten monkeys died following severe hypotension alone or combined hemodilution and hypertension as a consequence of cardiac arrest or undetermined (possibly neurologic) causes. No histologic evidence of ischemic brain cell injury was found in surviving monkeys subjected to hemodilution or hypotension alone. Neuropathologic alterations in the cerebral cortex, cerebellum, hippocampus and globus pallidus as well as neurologic and behavioral deficits were found in seven of 16 surviving monkeys subjected to both hemodilution and hypotension. These findings resulted from combinations of hematocrit less than 20% and MABP below 40 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoregulation of cortical blood flow and oxygen tension in the rabbit.

The relationship between cerebral blood flow autoregulation and oxygen tension of cerebral tissue is not fully known. We have examined the autoregulation of local cortical blood flow (CoBF) and cortical oxygen tension (bPO2) in the rabbit. CoBF was measured continuously by using the heated thermocouple technique and bPo2 was monitored by the polarographic method. Intravenous injection of phenylephrine hydrochloride or trimethaphan camsylate was used to test for autoregulation by increasing or decreasing perfusion pressure. The mean values of CoBF and bPO2 were 36 +/- 5 ml/100g/min and 32 +/- 12 mmHg respectively at 90 mmHg mean arterial blood pressure (MABP). The changes in both CoBF and bPO2 with changing perfusion pressure were often relatively small at near baseline blood pressure and became more pronounced with large increases or decreases in MAPB. On returning from high MABP to baseline blood pressure, a hysteresis effect on CoBF was observed in 20 out of 22 cases. The autoregulation of CoBF was maintained in the range between 80 and 100 mmHg MABP. On the other hand, bPO2 was maintained constant in the range between 75 and 110 mmHg. This range is significantly wider than that of CoBF. We conclude that autoregulation of CoBF limits changes in local CoBF to maintain constant oxygen tension in brain tissue.