Decrease of blood flow velocity in the middle cerebral artery after stellate ganglion block following aneurysmal subarachnoid hemorrhage: a potential vasospasm treatment?

OBJECTIVE: Cerebral vasospasm (CV) is a delayed, sustained contraction of the cerebral arteries that tends to occur 3-14 days after aneurysmal subarachnoid hemorrhage (aSAH) from a ruptured aneurysm. Vasospasm potentially leads to delayed cerebral ischemia, and despite medical treatment, 1 of 3 patients suffer a persistent neurological deficit. Bedside transcranial Doppler (TCD) ultrasonography is used to indirectly detect CV through recognition of an increase in cerebral blood flow velocity (CBFV). The present study aimed to use TCD ultrasonography to monitor how CBFV changes on both the ipsi- and contralateral sides of the brain in the first 24 hours after patients have received a stellate ganglion block (SGB) to treat CV that persists despite maximum standard therapy. METHODS: The data were culled from records of patients treated between 2013 and 2017. Patients were included if an SGB was administered following aSAH, whose CBFV was ≥ 120 cm/sec and who had either a focal neurological deficit or reduced consciousness despite having received medical treatment and blood pressure management. The SGB was performed on the side where the highest CBFV had been recorded with 8-10 ml ropivacaine 0.2%. The patient's CBFV was reassessed after 2 and 24 hours. RESULTS: Thirty-seven patients (male/female ratio 18:19), age 17-70 years (mean age 49.9 ± 11.1), who harbored 13 clipped and 22 coiled aneurysms (1 patient received both a coil and a clip, and 3 patients had 3 untreated aneurysms) had at least one SGB. Patients received up to 4 SGBs, and thus the study comprised a total of 76 SGBs.After the first SGB, CBFV decreased in 80.5% of patients after 2 hours, from a mean of 160.3 ± 28.2 cm/sec to 127.5 ± 34.3 cm/sec (p < 0.001), and it further decreased in 63.4% after 24 hours to 137.2 ± 38.2 cm/sec (p = 0.007). A similar significant effect was found for the subsequent SGB. Adding clonidine showed no significant effect on either the onset or the duration of the SGB. Contralateral middle cerebral artery (MCA) blood flow was not reduced by the SGB. CONCLUSIONS: To the authors' knowledge, this is the largest study on the effects of administering an SGB to aSAH patients after aneurysm rupture. The data showed a significant reduction in ipsilateral CBFV (MCA 20.5%) after SGB, lasting in about two-thirds of cases for over 24 hours with no major complications resulting from the SGB.

Vancomycin and to lesser extent tobramycin have vasomodulatory effects in experimental endotoxemia in the rat.

BACKGROUND: Antibiotic treatment represents a key component of therapy for severe sepsis. Apart from their antimicrobial efficacy, when choosing antibiotics in septic conditions, vasomodulatory effects should also be taken into account. OBJECTIVES: Aim of this study was to evaluate the vasomodulatory effects of vancomycin (VANCO) and tobramycin (TOBRA) in experimental endotoxemia by using intravital microscopy (IVM) of the intestinal microcirculation and measurements of the arterial contractility in vitro. METHODS: Endotoxemia was induced in rats by intravenous administration of lipopolysaccharide (LPS). VANCO or TOBRA were given immediately after LPS administration. Intestinal functional capillary density (FCD) and leukocyte-endothelial interactions were evaluated by IVM 2 hrs after LPS challenge. The effects of the antibiotics on the motility of aortal rings were examined in vitro. RESULTS: Leukocyte adhesion was significantly potentiated in the LPS group and in both antibiotic groups as compared to control group. Roller flow in V1 and V3 venules increased in antibiotic treated groups as compared to untreated LPS animals. FCD in the longitudinal muscular and mucosal layers decreased significantly in either endotoxemia or antibiotics treated rats. However, administration of VANCO ameliorated FCD in endotoxemic rats. Both antibiotics, in higher concentration, produced moderate relaxation of the arterial smooth muscle. CONCLUSION: Tobramycin and vancomycin did not affect the interaction between leukocytes and microvascular endothelium while vancomycin increased functional capillary density in the intestinal wall. Both antibiotics had direct relaxing effects on the vascular smooth muscle. Therefore, vancomycin and to lesser extent tobramycin may influence vascular tone and thereby affect microcirculation in endotoxemia and sepsis.

Effects of activated protein C on the mesenteric microcirculation and cytokine release during experimental endotoxemia.

PURPOSE: Activated protein C (APC) is the first anti-inflammatory drug to be approved for the treatment of severe sepsis. However, the underlying mechanisms are not completely elucidated. Therefore, the aim of our study was to evaluate the effects of APC on the microcirculation (mesenteric leukocyte-endothelial interaction, plasma extravasation) using intravital microscopy (IVM) and on cytokine release during experimental endotoxemia in rats. METHODS: We divided forty, male, Lewis rats into four groups (n = 10 per group): Controls, LPS (15 mg x kg(-1) lipopolysaccharide iv), APC (2 mg x kg(-1) APC iv), and LPS+APC. We determined mesenteric leukocyte-endothelial interactions and plasma extravasation at zero, one and two hours following administration of LPS and APC by IVM. Plasma levels of tumour necrosis factor-alpha, IL-1beta, interleukin (IL)-6, and IL-10 were measured at zero and at two hours. RESULTS: Leukocyte adherence (-74%) and plasma extravasation (-28%) during endotoxemia were diminished significantly following APC treatment, compared to untreated LPS animals (P = 0.0001 and P = 0.0004, respectively). Interleukin-1ss release was also significantly reduced by APC treatment (2567.4 +/- 320.9 pg x mL(-1) in the LPS group vs 1626.1 +/- 427.2 pg x mL(-1) in the LPS+APC group; P = 0.001). CONCLUSION: These rodent experiments showed that APC treatment significantly attenuated deterioration of the mesenteric microcirculation and systemic IL-1ss release caused by endotoxin challenge. Because of the crucial role of the microcirculation in ongoing sepsis pathogenesis and multiple organ dysfunction syndrome, these effects may be of clinical importance.