Acute Hypotension Research Articles

Does nicotinic acid (niacin) lower blood pressure?

Nicotinic acid (niacin) is a well-established treatment for dyslipidaemia – an important cardiovascular disease (CVD) risk factor. However, niacin may also reduce blood pressure (BP), which is another important CVD risk factor. This review examines the limited publicly available data on niacin’s BP effects. Acute administration of immediate-release niacin may lower BP because of niacin’s acute vasodilatory effects. Although not always supported by clinical trial data, the package insert of a prescription, extended-release niacin describes niacin-induced acute hypotension. From a chronic standpoint, larger studies, such as the Coronary Drug Project, suggest that niacin may lower BP when administered over a longer period of time. Post hoc analyses of some of the more recent niacin clinical trials also support a more chronic, dose-dependent, BP-lowering effect of niacin. Because laropiprant [a prostaglandin D2 (PGD2) type 1 (DP1) receptor antagonist] does not attenuate niacin’s BP-lowering effects, it is unlikely that any chronic lowering of BP by niacin is due to dilation of dermal vessels through activation of the DP1 receptor by PGD2. Further research is warranted to evaluate the extent and mechanisms of niacin’s effects on BP.

A patient with an uncommon complication from insertion of a central venous catheter: A case report

BackgroundA 72 year old male was admitted to the medical intensive care unit with septic shock.Case presentationA left subclavian central venous catheter was inserted on the day of admission whose tip was pushing against the wall of the vessel lumen. The patient's condition improved with treatment, but three days later had a new episode of acute hypotension. CT scan of the chest showed that the catheter had eroded through the superior vena cava wall.ConclusionThe catheter was pulled out and patient recovered from the complication with supportive therapy. Care should be taken that the tip of the catheter is in the center of the vessel lumen to avoid this rare, but potentially life threatening, complication.

Inspiratory resistance, cerebral blood flow velocity, and symptoms of acute hypotension

INTRODUCTION Symptoms of orthostatic intolerance, e.g., following prolonged bed rest and microgravity exposure, are associated with reductions in cerebral blood flow. We tested the hypothesis that spontaneously breathing through an impedance threshold device (ITD) would attenuate the fall in cerebral blood flow velocity (CBFV) during a hypotensive orthostatic challenge and reduce the severity of reported symptoms. METHODS While breathing through either an active ITD (-7 cm H2O inspiratory impedance) or a sham ITD (no impedance), 19 subjects performed a squat stand test (SST). Symptoms upon stand were recorded on a 5-point scale (1 = normal; 5 = faint) of subject-perceived rating (SPR). To address our hypothesis, only data from symptomatic subjects (SPR > 1 during the sham trial) were analyzed (N = 9). Mean arterial blood pressure (MAP) and mean CBFV were measured continuously throughout the SST and analyzed in time and frequency domains. RESULTS Breathing with the active ITD during the SST reduced the severity of orthostatic symptoms in eight of the nine symptomatic subjects (sham ITD SPR, 1.9 +/- 0.1; active ITD SPR, 1.1 +/- 0.1), but there was no statistically distinguishable difference in the reduction of mean CBFV between the two trials (sham ITD, -39 +/- 3% vs. active ITD, -44 +/- 3%). High frequency oscillations in mean CBFV, however, were greater during the active ITD trial (7.8 +/- 2.6 cm x s(-2)) compared with the sham ITD trial (2.5 +/- 0.9 cm x s(-2)). CONCLUSIONS Higher oscillations in CBFV while breathing with the active ITD may account for the reduction in symptom severity during orthostatic hypotension despite the same fall in absolute CBFV.

Traumatic dissection and rupture of the abdominal aorta as a complication of the Heimlich maneuver

Although the Heimlich maneuver is considered the best intervention for relieving acute upper airway obstruction, several complications have been reported in the literature. These complications can occur as a result of an increase in abdominal pressure leading to a variety of well-documented visceral injuries, including the great vessels. Acute abdominal aortic thrombosis after the Heimlich maneuver is a rare but recognized event; however, to date no case of traumatic dissection and rupture of the abdominal aorta has been described. We report the first known case, to our knowledge, of a traumatic dissection and rupture of the abdominal aorta after a forcefully applied Heimlich maneuver.

Effect of Prazosin on Dynamic Cerebral Autoregulation During Acute Hypotension in Healthy Human Subjects

To the Editor: Cerebral blood flow is excellently autoregulated when mean arterial pressure is between 65 and 140 mmHg.1 In the study by Ogoh et al,2 although the decrement in mean arterial pressure (MAP) in the 2 groups were similar, the MAP fell below the lower limits of cerebral autoregulation to an average of 57 mmHg when subjects took prazosin, and this would be …

The Effect of On-line High-flux Hemofiltration Versus Low-flux Hemodialysis on Mortality in Chronic Kidney Failure: A Small Randomized Controlled Trial

Given the paucity of prospective randomized controlled trials assessing comparative performances of different dialysis techniques, we compared on-line high-flux hemofiltration (HF) with ultrapure low-flux hemodialysis (HD), assessing survival and morbidity in patients with end-stage renal disease (ESRD). An investigator-driven, prospective, multicenter, 3-year-follow-up, centrally randomized study with no blinding and based on the intention-to-treat principle. Prevalent patients with ESRD (age, 16 to 80 years; vintage > 6 months) receiving renal replacement therapy at 20 Italian dialysis centers. Patients were centrally randomly assigned to HD (n = 32) or HF (n = 32). All-cause mortality, hospitalization rate for any cause, prevalence of dialysis hypotension, standard biochemical indexes, and nutritional status. Analyses were performed using the multivariate analysis of variance and Cox proportional hazard method. There was significant improvement in survival with HF compared with HD (78%, HF versus 57%, HD) at 3 years of follow-up after allowing for the effects of age (P = 0.05). End-of-treatment Kt/V was significantly higher with HD (1.42 +/- 0.06 versus 1.07 +/- 0.06 with HF), whereas beta(2)-microglobulin levels remained constant in HD patients (33.90 +/- 2.94 mg/dL at baseline and 36.90 +/- 5.06 mg/dL at 3 years), but decreased significantly in HF patients (30.02 +/- 3.54 mg/dL at baseline versus 23.9 +/- 1.77 mg/dL; P < 0.05). The number of hospitalization events for each patient was not significantly different (2.36 +/- 0.41 versus 1.94 +/- 0.33 events), whereas length of stay proved to be significantly shorter in HF patients compared with HD patients (P < 0.001). End-of-treatment body mass index decreased in HD patients, but increased in HF patients. Throughout the study period, the difference in trends of intradialytic acute hypotension was statistically significant, with a clear decrease in HF (P = 0.03). This is a small preliminary intervention study with a high dropout rate and problematic generalizability. On-line HF may improve survival independent of Kt/V in patients with ESRD, with a significant decrease in plasma beta(2)-microglobulin levels and increased body mass index. A larger study is required to confirm these results.

Signaling pathway of glutamate in the vestibular nuclei following acute hypotension in rats

Acute hypotension induces excitation of electrical activity and expression of c-Fos protein and phosphorylated extracellular signal-regulated kinase (pERK) in the vestibular nuclei. Expression of c-Fos protein and pERK is mediated by the excitatory neurotransmitter, glutamate. In this study, in order to investigate the signaling pathway of glutamate in the vestibular nuclei following acute hypotension, expression of the NR2B subunit of glutamate N-methyl- d-aspartate (NMDA) receptors and the GluR1 subunit of glutamate alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors was measured by Western blotting in the medial vestibular nucleus (MVN) following acute hypotension in bilateral labyrinthectomized (BL) rats. In intact labyrinthine animals, acute hypotension increased expression of pGluR1 and pNR2B in the MVN. Expression of pGluR1 Ser831 and Ser845 peaked at 5 and 30 min after acute hypotension and expression of pNR2B peaked at 60 min after acute hypotension, respectively. In BL animals, expression of pGluR1 Ser831, pGluR1 Ser845, and pNR2B was decreased significantly compared to intact labyrinthine animals following acute hypotension. These results suggest that excitatory afferent signals from the peripheral vestibular receptors, resulting from acute hypotension, release glutamate into postsynaptic neurons in the vestibular nuclei and the excitatory signals are transmitted through the GluR1 subunit of the AMPA receptors and the NR2B subunits of the NMDA receptors in the vestibular system.

Inspiratory Resistance, Cerebral Blood Flow Velocity, and Symptoms of Acute Hypotension

Symptoms of orthostatic intolerance, e.g., following prolonged bed rest and microgravity exposure, are associated with reductions in cerebral blood flow. We tested the hypothesis that spontaneously breathing through an impedance threshold device (ITD) would attenuate the fall in cerebral blood flow velocity (CBFV) during a hypotensive orthostatic challenge and reduce the severity of reported symptoms. While breathing through either an active ITD (-7 cm H2O inspiratory impedance) or a sham ITD (no impedance), 19 subjects performed a squat stand test (SST). Symptoms upon stand were recorded on a 5-point scale (1 = normal; 5 = faint) of subject-perceived rating (SPR). To address our hypothesis, only data from symptomatic subjects (SPR > 1 during the sham trial) were analyzed (N = 9). Mean arterial blood pressure (MAP) and mean CBFV were measured continuously throughout the SST and analyzed in time and frequency domains. Breathing with the active ITD during the SST reduced the severity of orthostatic symptoms in eight of the nine symptomatic subjects (sham ITD SPR, 1.9 +/- 0.1; active ITD SPR, 1.1 +/- 0.1), but there was no statistically distinguishable difference in the reduction of mean CBFV between the two trials (sham ITD, -39 +/- 3% vs. active ITD, -44 +/- 3%). High frequency oscillations in mean CBFV, however, were greater during the active ITD trial (7.8 +/- 2.6 cm x s(-2)) compared with the sham ITD trial (2.5 +/- 0.9 cm x s(-2)). Higher oscillations in CBFV while breathing with the active ITD may account for the reduction in symptom severity during orthostatic hypotension despite the same fall in absolute CBFV.

Multidisciplinary management of placenta percreta complicated by embolic phenomena

Hemorrhage and thrombosis are major causes of maternal mortality. This case discusses the management of a woman with placenta percreta complicated by intraoperative pulmonary embolism. A 39-year-old gravida 3 with two previous cesarean deliveries presented at 34 weeks of gestation with an antepartum hemorrhage. Magnetic resonance imaging confirmed placenta percreta. The multidisciplinary group including obstetricians, gynecological oncologists, interventional radiologists and anesthesiologists developed a delivery plan. Cesarean delivery was performed with internal iliac artery occlusion and embolization catheters in place. After the uterine incision our patient experienced acute hypotension and hypoxia associated with a drop in the end-tidal carbon dioxide and sinus tachycardia. She was resuscitated and the uterus closed with the placenta in situ. Postoperatively, uterine bleeding was arrested by immediate uterine artery embolization. With initiation of embolization, hypotension and hypoxia recurred. Oxygenation and hemodynamics slowly improved, the case continued and the patient was extubated uneventfully at the end of the procedure. Computed tomography revealed multiple pulmonary emboli. The patient was anticoagulated with low-molecular-weight heparin and returned six weeks later for hysterectomy. Placenta percreta with invasion into the bladder can be catastrophic if not recognized before delivery. The chronology of events suggests that this may have been amniotic fluid emboli. An intact placenta with abnormal architecture, such as placenta percreta, may increase the risk of amniotic fluid embolus. The clinical findings and co-existing filling defects on computed tomography may represent a spectrum of amniotic fluid embolism syndrome.

Autonomic Neural Control of the Cerebral Vasculature

The effect of antihypertensive drugs on autonomic neural control of the cerebral circulation remains unclear. This study was designed to compare middle cerebral artery mean blood velocity responses to acute hypotension with and without alpha(1)-adrenoreceptor blockade (Prazosin) in young, healthy humans. Acute hypotension was induced nonpharmacologically in 6 healthy subjects (mean+/-SE; 28+/-2 years) by releasing bilateral thigh cuffs after 9 minutes of suprasystolic resting ischemia before and after an oral dose of Prazosin (1 mg/20 kg body weight). Prazosin had no effect on thigh cuff release-induced reductions in mean arterial pressure and middle cerebral artery mean blood velocity. However, Prazosin attenuated the amount of peripheral vasoconstriction through the arterial baroreflex as evidenced by a slower return of mean arterial pressure to baseline (P=0.03). Immediately after cuff release, cerebral vascular conductance index increased through cerebral autoregulation and returned to resting values as a result of an increased perfusion pressure mediated through arterial baroreflex mechanisms. The rate of regulation, an index of cerebral autoregulation, was attenuated with Prazosin (control versus Prazosin; rate of regulation=0.204+/-0.020 versus 0.006+/-0.053/s, P=0.037). In addition, as mean arterial pressure was returning to resting values, the rate of change in cerebral vascular conductance index was decreased with Prazosin (0.005+/-0.006/s) compared with control (0.025+/-0.005/s; P=0.010). These data suggest that during recovery from acute hypotension, decreases in cerebral vascular conductance index were mediated by increases in arterial blood pressure and sympathetically mediated cerebral vasoconstriction.

High Risk of Hypopituitarism in Patients Who Recovered from Hemorrhagic Fever with Renal Syndrome

Hemorrhagic fever with renal syndrome (HFRS) caused by hantaviruses, is a severe systemic infection, with acute shock, vascular leakage, hypotension, and acute renal failure. Pituitary ischemia/infarction and necrosis are known causes of hypopituitarism, often remaining unrecognized due to subtle clinical manifestations. Cases of hypopituitarism after HFRS were previously only sporadically reported. The aim of this study was to determine, for the first time, the prevalence of hypopituitarism among HFRS survivors. In 60 adults (aged 35.8+/-1.3 yr) who recovered from HFRS 3.7 +/- 0.5 yr ago (median 2 yr), assessment of serum T(4), free T(4), TSH, IGF-I, prolactin, cortisol, and testosterone (in males) was followed by insulin tolerance test and/or GHRH+GH-releasing peptide-6 stimulation tests. Severe GH deficiency was confirmed in eight of 60 patients (13.3%): in five with multiple pituitary hormone deficiencies (MPHDs) and isolated in three. Thyroid axis deficiency was confirmed in five of 60 patients (8.3%), all with MPHD. Hypothalamus-pituitary-adrenal axis deficiency was observed in six of 60 (10.0%); in five with MPHD and isolated in one. Gonadal axis deficiency was confirmed in seven of 56 male subjects (12.5%): five with MPHD and isolated in two. Overall six patients (10.0%) had a single pituitary deficit (three GH, two gonadal, and one adrenal), and five (8.3%) had MPHD. The prevalence of patients having any endocrine deficiency was 18% (11 of 60). A high prevalence of hypopituitarism after recovery from HFRS is identified, with magnetic resonance imaging revealing atrophic pituitary and empty sella. Awareness is raised to neuroendocrine consequences of HFRS because unrecognized hypopituitarism significantly affects the physical and psychological well-being.

The Pulsed Doppler Predictors of Intra Dialysis Hypotension and Relationship between Doppler Indices and Net Fluid Loss after Dialysis in Patients with End Stage Renal Disease: Pulsed Doppler Study

Background: In patients with end stage renal disease (ESRD) on regular haemodialysis (HD), fluid status in the body has an important impact on the left ventricular (LV) filling and it can lead to intra-dialysis hypotension. The aim of the study is to study the pattern of diastolic pulsed Doppler filling in patients who had hypotension during HD and to correlate that with the net fluid loss at end of dialysis session. Material: Fifty two patients with (ESRD) on regular HD, 34 male, with mean age of 45.5 ± 13 year were studied. Each patient had pulsed Doppler study before and immediately after HD. Each patient was observed for the development of acute clinical events and hypotension defi ned as systolic blood pressure of less than 90 mmHg. Patients were divided into two groups according to the amount of net ultra fi ltrate loss after HD, group I (n = 25) with fluid loss of 2 litres. Results: The mean age was 45 ± 12 year for group I and 46 ± 11 year for group II. In the study group, 11 out of 52 (21%) patients developed systolic hypotension less than 90 mmHg during HD compared to those without, no patient necessitate HD discontinuation. The mean pre dialysis pulsed Doppler Early filling to late filling wave (E/A ratio) of those who developed hypotension was (0.7 ± 0.2 vs. 1.1 ± 0.2.1, p < 0.001) and the mean of Deceleration time of E wave (DT) (246 ± 40 vs. 224 ± 34 m.sec, p < 0.05) respectively. The mean difference between pre and post HD pulsed Doppler indices in group II compared with group I were as follow: the mean reduction of E wave velocity (32 ± 17 vs. 12 ± 15 m.sec, p < 0.01), the mean reduction of A wave velocity (13 ± 17 vs. 11 ± 16 m.sec, p = NS), E/A ratio reduced to 0.14 ± 0.03 vs. 0.01 ± 0.04, p < 0.05), the mean DT of E wave increase from (43 ± 51 vs. 16 ± 64 m.sec, p < 0.05). Conclusion: In patient ESRD on regular hemodialysis, the prolonged DT >246 m.sec of E wave and E/A ratio less than 0.7 both may be used as a predictors of asymptomatic hypotension during HD. The net fluid loss during HD is directly proportional to the reduction of left ventricle Doppler diastolic indices.

Amniotic fluid embolism managed with success during labour: report of a severe clinical case and review of literature

AFE (amniotic fluid embolism) is widely known as a disastrous rapid-progressing clinical entity. The incident ranges from 1:800 to 1:8,000. The mortality rate reaches 61-86%. Neonatal survival is reported at 70%. We describe the case of a healthy 29-year old primigravida developing amniotic fluid embolism during labour. Acute respiratory failure and hypotension combined with seizures were the initial symptoms. The patient under went an urgent caesarean section with extreme blood loss, complicated by disseminated coagulopathy. A total hysterectomy was performed due to profuse bleeding. Aggressive management was practiced with continuous transfusion of blood products and administration of vasocopressors. Amniotic fluid embolism or anaphylactoid syndrome of pregnancy is a life-threatening condition. Diagnosis is one of the exclusion. Its management is very difficult and requires quick management and cooperation of physicians from different specialties.

A 25-Year-Old Woman With Acute Pancreatitis and Hypotension Refractory to Aggressive Fluid Resuscitation

A 25-year-old woman with type II diabetes and hypertension presented to the emergency department complaining of abdominal pain and nonbloody, nonbilious emesis for 1 day. She denied fevers, chills, or dysuria. Due to mental status changes, she required intubation and transfer to the medical ICU.

S.23.01 Cardiovascular reflexes: physiological and pathophysiological influences from the brain

Effects of hepatoportal osmotic stimuli and changes in arterial blood pressure were studied on the neuronal activity of 24 thermosensitive and 47 thermally insensitive neurons of the preoptic and anterior hypothalamus (PO/AH) in the urethane-anesthetized rat. Infusion of hypertonic (3% NaCl, 9% mannitol) or hypotonie (water) solutions into the hepatic portal vein changes the activity in 59% of thermosensitive neurons and 13% of thermally insensitive neurons but the injection into the femoral vein did not. Changes in blood pressure induced by intravenous injection of vasoactive drugs altered the activity of thermosensitive neurons (75%) and thermally insensitive neurons (32%). Neurons having dual sensitivity to both osmotic and blood pressure were more frequently found among thermosensitive neurons (10/24) than among thermally insensitive neurons (4/47), x2(l)=11.03, p<0.001. The convergence of osmotic and baro/volaemic information on thermosensitive neurons may provide explanations for thermoregulatory changes observed during dehydration and acute hypotension.

Orthostatic Hypotension in the Elderly: Diagnosis and Treatment

Orthostatic hypotension is a common problem among elderly patients, associated with significant morbidity and mortality. While acute orthostatic hypotension is usually secondary to medication, fluid or blood loss, or adrenal insufficiency, chronic orthostatic hypotension is frequently due to altered blood pressure regulatory mechanisms and autonomic dysfunction. The diagnostic evaluation requires a comprehensive history including symptoms of autonomic nervous system dysfunction, careful blood pressure measurement at various times of the day and after meals or medications, and laboratory studies. Laboratory investigation and imaging studies should be based upon the initial findings with emphasis on excluding diagnoses of neurodegenerative diseases, amyloidosis, diabetes, anemia, and vitamin deficiency as the cause. Whereas asymptomatic patients usually need no treatment, those with symptoms often benefit from a stepped approach with initial nonpharmacological interventions, including avoidance of potentially hypotensive medications and use of physical counter maneuvers. If these measures prove inadequate and the patient remains persistently symptomatic, various pharmacotherapeutic agents can be added, including fludrocortisone, midodrine, and nonsteroidal anti-inflammatory drugs. The goals of treatment are to improve symptoms and to make the patient as ambulatory as possible rather then trying to achieve arbitrary blood pressure goals. With proper evaluation and management, the occurrence of adverse events, including falls, fracture, functional decline, and myocardial ischemia, can be significantly reduced.

Is the magnitude of acute post-exercise hypotension mediated by exercise intensity or total work done?

The purpose of this study was to investigate the effects of exercise intensity on the magnitude of acute post-exercise hypotension while controlling for total work done over the exercise bout. Seven normotensive physically active males aged 28 +/- 6 years (mean +/- SD) completed four experimental trials, a no exercise control, 30 min of semi-recumbent cycling at 70% VO2peak (INT), cycling for 30 min at 40% VO2peak (SMOD) and cycling at 40% VO2peak for a time which corresponded to the same total work done as in the intense trial (LMOD). Blood pressure (BP), heart rate, stroke volume, cardiac output, total peripheral resistance, core body temperature and forearm skin and limb blood flow were measured prior to and for 20 min following the exercise bout. Post-exercise summary statistics were compared between trials with a one-factor general linear model. The change in systolic BP, averaged over the 20-min post-exercise period was significantly lower only following the INT (-5 +/- 3 mm Hg) and LMOD exercise (-1 +/- 7 mm Hg) compared to values in control (P < 0.04). The changes in systolic BP and MAP following INT and LMOD were not significantly different from each other (P > 0.05). Similar results were obtained when the minimum values of these variables recorded during the post-exercise period were compared. Mean changes in cardiac output (1.9 +/- 0.3 l min(-1)) and total peripheral resistance (-3 +/- 1 mm Hg l(-1 )min(-1)) after INT exercise were also different from those in CON (P < 0.0005). The acute post-exercise reduction in BP was clinically similar following high intensity short duration exercise and moderate intensity longer duration exercise that was matched for total work done.

Functional limitation and right ventricular dysfunction at 6-month follow-up in patients with non-massive pulmonary embolism: useful outcomes for testing therapy of acute submassive pulmonary embolism?

Acute pulmonary embolism (PE) is a syndrome with a significant annual incidence, potentially associated with an elevated morality rate.1 Patients presenting with acute PE and persistent systemic hypotension, cardiogenic shock, or cardiac arrest are classified as having massive PE; in the absence of haemodynamic instability, PE is defined generically as non-massive. The latter, however, is classified as submassive acute PE in the presence of right ventricular (RV) dysfunction,1 to indicate that patients with normotensive acute PE and RV dysfunction may suddenly need escalation of therapy (vasopressor and/or inotropic support, rescue fibrinolysis, cardiopulmonary resuscitation).2–4 While clinical manifestation of acute PE may vary widely and significantly between patients, acute RV dysfunction is more quantifiable and uniform objective information in PE with relation to the severity of pulmonary vascular impairment.5 RV failure is the prominent cause of death in acute PE. This is further supported by the fact that in the setting of non-massive acute PE, RV dysfunction correlates with brain natriuretic peptide and troponins, which are in turn biomarkers of the severity of RV overload,6 providing additional information for risk stratification of the heterogeneous group of patients with normotensive PE.7–11 However, whether aggressive treatment (i.e. fibrinolysis or catheter-based pulmonary embolectomy) should be employed in acute submassive PE in addition to anticoagulation is controversial.1 In fact, while fibrinolysis or thromboembolectomy are associated with partial recovery of RV dysfunction,12 … *Corresponding author. Tel: +39 081 2543536; fax: +39 081 2543536. E-mail address : vpalmier{at}med.cornell.edu

Clinical and laboratory features of disseminated histoplasmosis in HIV patients from Brazil

To identify the main clinical and laboratory features of disseminated histoplasmosis (DH) in human immunodeficiency virus (HIV) patients and compare them with those of HIV patients with other opportunistic diseases. Retrospective study of HIV patients comparing the clinical and laboratory data of patients with and without DH. Univariate and multivariate analyses were performed to verify the risk factors related to DH. In total, 378 HIV patients were included, 164 with DH and 214 with other opportunistic diseases. Acute renal failure, respiratory insufficiency and septic shock were more frequent in DH patients, who also had a higher mortality (32%vs. 14%, P < 0.001). Independent risk factors for DH were: acute renal failure [odds ratio (OR) 5.2; 95% confidence interval (CI) 3.2-8.5; P < 0.001], splenomegaly (OR 3.4; 95% CI 1.19-9.9; P < 0.001), respiratory insufficiency (OR 2.7 95% CI 1.5-5.0; P < 0.001), proteinuria (OR 2.7; 95% CI 1.3-5.2; P = 0.03), hypotension (OR 2.5; 95% CI 1.2-5.0; P = 0.008), hepatomegaly (OR 2.4; 95% CI 1.2-4.8; P = 0.01), cutaneous lesions (OR, 1.9; 95% CI 1.0-3.3; P = 0.02) and weight loss (OR 1.8; 95% CI 1.0-3.1; P = 0.03). Our results suggest that DH is a severe opportunistic disease with high mortality rate, which should be promptly recognized in order to provide early specific treatment.

Hemodynamic and renal involvement of B1 and B2 kinin receptors during the acute phase of endotoxin shock in mice

B1 kinin receptor (B1R) is up-regulated by endotoxins and thus may represent a therapeutic target in sepsis. We investigated the expression and role of B1R and B2R in the acute phase of lipopolysaccharide (LPS)-induced endotoxin shock in C57BL/6 mice (WT) and B1R and B2R knock out mice (B1KO, B2KO). B1R mRNA was enhanced from 6 to 48 h after LPS while B2R mRNA was further increased in B1KO. Maximal hypotension was found 24 h after LPS, and was more pronounced in B1KO, but was reduced in B2KO. Glomerular filtration rate was more reduced by LPS in B1KO than in WT and B2KO. Glycemia was reduced by LPS and particularly in B1KO and B2KO mice. Mortality was increased by LPS in B1KO. These data suggest that the up-regulated B1R plays, at least transiently, a significant beneficial role in acute LPS-induced hypotension. Conversely, supra activation of B2R could be also involved in the increased mortality observed in B1KO mice.