Amanda Roberta de Almeida

Importance Of Anesthesia For The Genesis Of Neurogenic Pulmonary Edema In Spinal Cord Injury.

There are reports describing both provocation and inhibition of neurogenic pulmonary edema by anesthetic drugs. Therefore, we compared the effect of two types of anesthesia on the formation of neurogenic pulmonary edema in rats with balloon-induced acute spinal cord injury. Animals with sham procedure (group 1) were anesthesized by intraperitoneal sodium pentobarbital. In the experimental groups, rats were submitted to acute spinal cord lesion by insufflations of a balloon in the epidural space at T8 for 1 min (group 3 under i.p. sodium pentobarbital and group 2 under i.p. xylazine-ketamine anesthesia). In rats with pentobarbital anesthesia, systolic blood pressure doubled the baseline value during compression, whereas this effect was less pronounced in the ketamine-xylazine group. The pulmonary index (100 x wet lung weight/body weight) was 0.395 (+/-0.018) in sham-operated rats, rose to 0.499 (+/-0.060) in group 2, and was maximum under pentobarbital anesthesia (0.639+/-0.14; p=0.0018). Histologic examination of the spinal cord showed parenchymal ruptures and acute hemorrhage. Comparison of the pulmonary index with histologic slides of lung parenchyma revealed that relevant intra-alveolar edema occurred only for index values above 0.55. On electron microscopy, endothelial alterations, and damage of the alveolar lining cells were found. Our study indicates that neurogenic pulmonary edema caused by spinal cord injury is less pronounced in rats under xylazine-ketamine anesthesia, when compared with pentobarbital.

Hemodynamic parameters and neurogenic pulmonary edema following spinal cord injury: an experimental model

Neurogenic pulmonary edema is a serious and always life-threatening complication following several lesions of the central nervous system. We report an experiment with 58 Wistar-Hanover adult male rats. Two groups were formed: control (n=4) and experimental (n=54). The experimental group sustained acute midthoracic spinal cord injury by Fogartys balloon-compression technique containing 20 microL of saline for 5, 15, 30 or 60 seconds. The rats were anesthetized by intraperitoneal (i.p.) sodium pentobarbital (s.p.) 60 mg/Kg. The quantitative neurological outcome was presented at 4, 24 and 48 hours from compression to characterize the injury graduation in different groups. Poor outcome occurred with 60 seconds of compression. Six animals died suddenly with pulmonary edema. Using the procedure to investigate the pulmonary edema during 60 seconds of compression, followed by decompression and time-course of 60 seconds, 20 rats were randomly assigned to one of the following groups: control (1, n=4, anesthetized by i.p. s.p., 60 mg/Kg but without compression) and experimental (2, n=7, anesthetized by i.p. xylazine 10 mg/Kg and ketamine 75 mg/Kg) and (3, n=9, anesthetized by i.p. s.p., 60 mg/Kg). The pulmonary index (100 x wet lung weight/body weight) was 0.395 +/- 0.018 in control group, rose to 0.499 +/- 0.060 in group 2, and was 0.639 +/- 0.14 in group 3. Histologic examination of the spinal cord showed parenchymal ruptures and acute hemorrhage. Comparison of the pulmonary index with morphometric evaluation of edema fluid-filled alveoli by light microscopy showed that relevant intra-alveolar edema occurred only for index values above 0.55. The results suggest that the pulmonary edema induced by spinal compression is of neurogenic nature and that the type of anesthesia used might be important for the genesis of lung edema.

Long-term effects of intracerebroventricular insulin microinjection on renal sodium handling and arterial blood pressure in rats

The role of the central nervous system (CNS) in the control of hydrosaline homeostasis has been strikingly demonstrated by several studies. Our laboratory recently showed that centrally administered insulin produced a dose-related increase in the urinary output of sodium, which was abolished by bilateral renal denervation, nitric oxide synthase inhibition and cerebroventricular streptozotocin administration in rats. Recent studies have shown that hyperinsulinemia induces subtle derangements of intracellular insulin-insulin receptor trafficking and insulin metabolism, which are associated with an impairment of insulin signaling. The long-term effect of high insulin levels on the periventricular region could alter insulin signaling, which in turn, may modify the central natriuretic and cardiovascular effects of this peptide. In order to evaluate this hypothesis, we investigated the effects of 7-day i.c.v. insulin administration on tubular handling and blood pressure in conscious, unrestrained rats and their controls, randomly assigned to one of two separate groups: (a) i.c.v. 0.15M NaCl-injected (n=7) and (b) i.c.v. 126.0 ng insulin-injected rats (n=7). In the current study, there were no significant differences between the blood pressure, daily tap water intake and serum sodium, potassium, lithium and creatinine levels in control i.c.v. 0.15M NaCl-injected rats, compared with the insulin-treated group. Conversely, there was a significant decrease in the daily solid rat chow intake (Co: 16.4+/-3.5 g vs. Ins: 10.3+/-2.6g, P=0.003) in 7-day long-term insulin-treated rats, compared with the control group. We confirmed that centrally administered insulin produced a substantial increase in the urinary output of Na+, Li+ and K+, and that the response was significantly enhanced in long-term i.c.v. insulin pre-treated animals, when compared with controls (fractional sodium excretion (FE(Na)) from basal: 0.047+/-0.18% to Ins-treated: 0.111+/-0.035%, P=0.001). Additionally, we demonstrated that insulin-induced natriuresis occurred by increasing fractional proximal (FEP(Na)) from basal (16.8+/-2.6% to Ins-treated: 26.7+/-2.8%, P=0.001) and post-proximal sodium excretion (FEPP(Na)) from basal (0.37+/-0.03% to Ins-treated: 0.42+/-0.05%, P=0.043), despite a decreased Na(+) filtered load and rat food intake. The current data suggest that centrally injected insulin maintain its CNS ability to amplify neuronal hypotensive and natriuretic pathways that counteract the known peripheral antinatriuretic effects of insulin.

Bartonella henselae transmission by blood transfusion in mice.

Bartonella spp. are neglected fastidious Gram‐negative bacilli. We isolated Bartonella henselae from 1.2% of 500 studied blood donors and demonstrated that the bacteria remain viable in red blood cell units after 35 days of experimental infection. Now, we aim to evaluate the possibility of B. henselae transmission by blood transfusion in a mouse model.

Development of hypertension in a pyelonephritis-induced model : The effect of salt intake and inability of renal sodium handling

The role of the kidney in the control of blood pressure has been convincingly demonstrated by several studies. Recent evidence has suggested that subtle acquired tubulointerstitial injury may cause a defect in sodium excretion function, thus leading to salt-sensitive hypertension. There are no reports, however, examining the effect of experimental chronic pyelonephritis on renal sodium handling and arterial pressure. Thus, to examine the influence of salt intake and unilateral nephrectomy, unanesthetized, unrestrained rats were randomly assigned to one of two separate groups: sham-operated rats (CO) or chronic unilateral pyelonephritic rats (CP). After twenty one days, the pyelonephritic group was subdivided in two: one subgroup continued with water intake (CPw), while the other was changed to 0.9% NaCl intake (CPs), like the control group (COs). After seven days, all rats were submitted to unilateral nephrectomy of the left normal kidney. Data presented herein show that chronic pyelonephritis produced an increase in mean arterial pressure (CO: 121.4 ± 1.0 mmHg to CP: 127.0 ± 0.9 mmHg, p = 0.000) that was enhanced by saline ingestion (COs: 121.6 ± 1.4 mmHg; CPw: 127.0 ± 1.8 mmHg; CPs: 132.1 ± 1.2 mmHg, p = 0.000) and further aggravated by unilateral nephrectomy (CO: 125.2 ± 2.6 mmHg; CPw: 127.5 ± 0.9 mmHg; CPs: 139.2 ± 1.1 mmHg, p = 0.000). Unchanged blood pressure measurements (120.2 ± 2.3 mmHg) were observed beyond 21 days in control rats maintained on water regimen when compared with saline-drinking groups. These changes in mean arterial pressure were observed despite an increased fractional sodium excretion in the CPs group compared to the other groups before uninephrectomy (COs: 0.125 ± 0.025%; CPw: 0.045 ± 0.013%; CPs: 0.292 ± 0.046%; p = 0.000), as compared to CPw after uninephrectomy (COs: 0.249 ± 0.077%; CPw: 0.062 ± 0.011%; CPs: 0.363 ± 0.195%, p = 0.019). In addition, it was shown that daily liquid intake was higher in CPs than in CPw but similar to COs, both before uninephrectomy (COs: 42.8 ± 2.6 ml/d; CPw: 34.3 ± 3.5 ml/d; CPs: 51.8 ± 3.7 ml/d, p = 0.006) and after uninephrectomy (COs: 40.9 ± 5.5 ml/d; CPw: 33.8 ± 1.4 ml/d; CPs: 53.0 ± 3.5 ml/d, p = 0.004). The current data suggest that chronic pyelonephritis promotes an inability of renal tubules to handle sodium excretion when exposed to sodium overload and aggravated by uninephrectomy, thus constituting a model for salt-sensitive hypertension.The role of the kidney in the control of blood pressure has been convincingly demonstrated by several studies. Recent evidence has suggested that subtle acquired tubulointerstitial injury may cause a defect in sodium excretion function, thus leading to salt-sensitive hypertension. There are no reports, however, examining the effect of experimental chronic pyelonephritis on renal sodium handling and arterial pressure. Thus, to examine the influence of salt intake and unilateral nephrectomy, unanesthetized, unrestrained rats were randomly assigned to one of two separate groups: sham-operated rats (CO) or chronic unilateral pyelonephritic rats (CP). After twenty one days, the pyelonephritic group was subdivided in two: one subgroup continued with water intake (CPw), while the other was changed to 0.9% NaCl intake (CPs), like the control group (COs). After seven days, all rats were submitted to unilateral nephrectomy of the left normal kidney. Data presented herein show that chronic pyelonephritis produced an increase in mean arterial pressure (CO: 121.4 ± 1.0 mmHg to CP: 127.0 ± 0.9 mmHg, p=0.000) that was enhanced by saline ingestion (COs: 121.6 ± 1.4 mmHg; CPw: 127.0 ± 1.8 mmHg; CPs: 132.1 ± 1.2 mmHg, p=0.000) and further aggravated by unilateral nephrectomy (CO: 125.2 ± 2.6 mmHg; CPw: 127.5 ± 0.9 mmHg; CPs: 139.2 ± 1.1 mmHg, p=0.000). Unchanged blood pressure measurements (120.2 ± 2.3 mmHg) were observed beyond 21 days in control rats maintained on water regimen when compared with saline-drinking groups. These changes in mean arterial pressure were observed despite an increased fractional sodium excretion in the CPs group compared to the other groups before uninephrectomy (COs: 0.125 ± 0.025%; CPw: 0.045 ± 0.013%; CPs: 0.292 ± 0.046%; p=0.000), as compared to CPw after uninephrectomy (COs: 0.249 ± 0.077%; CPw: 0.062 ± 0.011%; CPs: 0.363 ± 0.195%, p=0.019). In addition, it was shown that daily liquid intake was higher in CPs than in CPw but similar to COs, both before uninephrectomy (COs: 42.8 ± 2.6 ml/d; CPw: 34.3 ± 3.5 ml/d; CPs: 51.8 ± 3.7 ml/d, p=0.006) and after uninephrectomy (COs: 40.9 ± 5.5 ml/d; CPw: 33.8 ± 1.4 ml/d; CPs: 53.0 ± 3.5 ml/d, p=0.004). The current data suggest that chronic pyelonephritis promotes an inability of renal tubules to handle sodium excretion when exposed to sodium overload and aggravated by uninephrectomy, thus constituting a model for salt-sensitive hypertension.

Bartonella henselae Infection in Sickle Cell Disease Mice Is Associated with Hyperalgesia

BACKGROUND Sickle cell disease (SCD) is the most prevalent hematologic genetic disorder. Acute vaso-occlusive painful crisis is the hallmark of the disease and may be related to subclinical infections. Bartonellosis, a rare and neglected infection, is caused by Bartonella spp., which can be found in donated blood. These bacteria cause intraerythrocytic and endothelial infection and pain, all of which occur in SCD. It is likely that this infection is transmitted to SCD patients during transfusion from donated blood, leading to pain. We, therefore, evaluated whether Bartonella henselae infection would cause hyperalgesia in mice with SCD. MATERIALS AND METHODS SCD mice were generated by transplantation of nucleated bone marrow cells harvested from transgenic Berkeley sickle mice into 2-month-old irradiated C57BL/6 mice. We infected four SCD mice by intraperitoneal inoculation with B. henselae, and inoculated four other mice with the same volume of saline. Mechanical hyperalgesia was determined using von Frey monofilaments by two blinded observers. Thereafter, the animals were anesthetized and euthanized to collect blood, liver, and spleen samples to seek B. henselae infection by PCR. FINDINGS We confirmed the experimental infection in all animals by PCR. Tremors and mechanical hypersensitivity were demonstrated by SCD mice infected with B. henselae infection but not in those receiving saline. CONCLUSION B. henselae infection may be related to pain and other symptoms in SCD.

Acute and Late Bartonella henselae Murine Model Infection

Bartonella spp. are fastidious gram-negative neglected bacilli with worldwide distribution. They are able to cause intraerythrocytic and potentially fatal infection. Cats and dogs are reservoirs of some species of these agents. Blood-sucking arthropods are potential vectors. Our aim was to evaluate the blood, skin, liver, and spleen in BALB/c mice by using molecular tests and confocal microscopy to demonstrate Bartonella henselae infection in the bloodstream and organs after 4 and 21 days of intraperitoneally injected bacterial suspension. We demonstrate that the occurrence of infection in organs precedes the detectable infection in blood. Therefore, late manifestation in blood may be another challenge in early detection and diagnosis of B. henselae infection.

Topical use and systemic action of green and roasted coffee oils and ground oils in a cutaneous incision model in rats (Rattus norvegicus albinus)

Introduction Wounds are a common health problem. Coffee is widely consumed and its oil contains essential fatty acids. We evaluated the local (skin) and systemic effects associated with the topical use of coffee oils in rats. Methods Punch skin wounds (6 mm) incisions were generated on the backs of 75 rats. Saline (SS), mineral oil (MO), green coffee oil (GCO), roasted coffee oil (RCO), green coffee ground oil (GCGO) or roasted coffee ground oil (RCGO) were topically applied to the wounds. Healing was evaluated by visual and histological/morphometric optical microscopy examination; second harmonics generation (SHG) microscopy, wound tissue q-PCR (values in fold-change) and blood serum (ELISA, values in pg/mL). Results RCO treated animals presented faster wound healing (0.986 vs. 0.422), higher mRNA expression of IGF-1 (2.78 vs. 1.00, p = 0.01), IL-6 (10.72 vs. 1.00, p = 0.001) and IL-23 (4.10 vs. 1.2, p = 0.05) in early stages of wound healing; higher IL-12 (3.32 vs. 1.00, p = 0.05) in the later stages; and lower serum levels of IFN-γ (11.97 vs. 196.45, p = 0.01). GCO treatment led to higher mRNA expression of IL-6 (day 2: 7.94 vs. 1.00, p = 0.001 and day 4: 6.90 vs. 1.00, p = 0.01) and IL-23 (7.93 vs. 1.20, p = 0.001) in the early stages. The RCO treatment also produced higher serum IFN-α levels throughout the experiment (day 2: 52.53 vs. 21.20; day 4: 46.98 vs.21.56; day 10: 83.61 vs. 25.69, p = 0.05) and lower levels of IL-4 (day 4: 0.9 vs.13.36, p = 0.01), adiponectin (day 10: 8,367.47 vs. 16,526.38, p = 0.001) and IFN-γ (day 4: 43.03 vs.196.45, p = 0.05). The SHG analysis showed a higher collagen density in the RCO and GCO treatments (p = 0.05). Conclusion Topical treatment with coffee oils led to systemic actions and faster wound healing in rats. Further studies should be performed are necessary to assess the safety of topical vegetal oil use for skin lesions.