Preserved cerebral microcirculation during cardiogenic shock*

Wan, Zhi; Ristagno, Giuseppe; Sun, Shijie; Li, Yongqin; Weil, Max Harry; Tang, Wanchun

doi:10.1097/ccm.0b013e3181a3a97b

Cited by 40 publications

(16 citation statements)

References 28 publications

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“…Interestingly, administration of inhibitors of inducible NO synthase (iNOS) prevented cerebral hyperemia [39] but not brain microvascular alterations [22], suggesting that other mechanisms are involved. On the other hand, in cardiogenic and in hemorrhagic shock, the cerebral microcirculation can be preserved even when peripheral microvascular disturbances are present [27,28]. However, the pathophysiology of microcirculatory dysfunction in sepsis may be different and more complex than in these conditions [40,41], and this could explain the cerebral microvascular impairment observed in our study.…”

Section: Discussionmentioning

confidence: 77%

“…We used the sidestream dark field (SDF) imaging technique, a modified orthogonal polarization spectral (OPS) technology [26], which has been successfully used to study the cerebral microcirculation in experimental models of cardiogenic and hemorrhagic shock [27,28] and cardiac arrest [29]. We hypothesized that the cerebral microcirculation may be impaired during sepsis and that these alterations would be unrelated to the global hemodynamic changes.…”

Section: Introductionmentioning

confidence: 99%

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Cerebral microcirculation is impaired during sepsis: an experimental study

et al. 2010

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IntroductionPathophysiology of brain dysfunction due to sepsis remains poorly understood. Cerebral microcirculatory alterations may play a role; however, experimental data are scarce. This study sought to investigate whether the cerebral microcirculation is altered in a clinically relevant animal model of septic shock.MethodsFifteen anesthetized, invasively monitored, and mechanically ventilated female sheep were allocated to a sham procedure (n = 5) or sepsis (n = 10), in which peritonitis was induced by intra-abdominal injection of autologous faeces. Animals were observed until spontaneous death or for a maximum of 20 hours. In addition to global hemodynamic assessment, the microcirculation of the cerebral cortex was evaluated using Sidestream Dark-Field (SDF) videomicroscopy at baseline, 6 hours, 12 hours and at shock onset. At least five images of 20 seconds each from separate areas were recorded at each time point and stored under a random number to be analyzed, using a semi-quantitative method, by an investigator blinded to time and condition.ResultsAll septic animals developed a hyperdynamic state associated with organ dysfunction and, ultimately, septic shock. In the septic animals, there was a progressive decrease in cerebral total perfused vessel density (from 5.9 ± 0.9 at baseline to 4.8 ± 0.7 n/mm at shock onset, P = 0.009), functional capillary density (from 2.8 ± 0.4 to 2.1 ± 0.7 n/mm, P = 0.049), the proportion of small perfused vessels (from 95 ± 3 to 85 ± 8%, P = 0.02), and the total number of perfused capillaries (from 22.7 ± 2.7 to 17.5 ± 5.2 n/mm, P = 0.04). There were no significant changes in microcirculatory flow index over time. In sham animals, the cerebral microcirculation was unaltered during the study period.ConclusionsIn this model of peritonitis, the cerebral microcirculation was impaired during sepsis, with a significant reduction in perfused small vessels at the onset of septic shock. These alterations may play a role in the pathogenesis of septic encephalopathy.

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Section: Discussionmentioning

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Cerebral microcirculation is impaired during sepsis: an experimental study

et al. 2010

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“…Finally, some studies suggest that sublingual microcirculation may not accurately correlate with other vital microvascular beds such as cerebral microcirculation. 35 On the other hand, the correlation between sublingual and intestinal microvascular beds have previously been validated. 36 …”

Section: Limitationsmentioning

confidence: 99%

Sublingual microcirculation is impaired in post-cardiac arrest patients

et al. 2013

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Aim We hypothesized that microcirculatory dysfunction, similar to that seen in sepsis, occurs in post-cardiac arrest patients and that better microcirculatory flow will be associated with improved outcome. We also assessed the association between microcirculatory dysfunction and inflammatory markers in the post-cardiac arrest state. Methods We prospectively evaluated the sublingual microcirculation in post-cardiac arrest patients, severe sepsis/septic shock patients, and healthy control patients using Sidestream Darkfield Microscopy. Microcirculatory flow was assessed using the Microcirculation flow index (MFI) at 6 and 24 hours in the cardiac arrest patients, and within 6 hours of Emergency Department admission in the sepsis and control patients. Results We evaluated 30 post-cardiac arrest patients, 16 severe sepsis/septic shock patients, and 9 healthy control patients. Sublingual microcirculatory blood flow was significantly impaired in post-cardiac arrest patients at 6 hours (MFI 2.6 [IQR: 2 - 2.9]) and 24 hours (2.7 [IQR: 2.3 - 2.9]) compared to controls (3.0 [IQR: 2.9 - 3.0]; p < 0.01 and 0.02, respectively). After adjustment for initial APACHE II score, post-cardiac arrest patients had significantly lower MFI at 6-hours compared to sepsis patients (p < 0.03). In the post-cardiac arrest group, patients with good neurologic outcome had better microcirculatory blood flow as compared to patients with poor neurologic outcome (2.9 [IQR: 2.4 – 3.0] vs. 2.6 [IQR: 1.9 – 2.8]; p < 0.03). There was a trend toward higher median MFI at 24 hours in survivors vs. non-survivors (2.8 [IQR: 2.4 – 3.0] vs. 2.6 [IQR: 2.1-2.8] respectively; p < 0.09). We found a negative correlation between MFI-6 and vascular endothelial growth factor (VEGF) (r= −0.49, P= 0.038). However, after Bonferroni adjustment for multiple comparisons, this correlation was statistically non-significant. Conclusion Microcirculatory dysfunction occurs early in post-cardiac arrest patients. Better microcirculatory function at 24 hours may be associated with good neurologic outcome.

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“…Rats were placed in the prone position, and cerebral microcirculation in the penumbra was visualized by using an SDF video microscope (MicroScan, MicroVision Medical, Amsterdam, the Netherlands) with a 5X optical probe [14,15] and monitored during re-flow. Images acquisitions and analyses were performed with the dedicated software analysis (Automated Vascular Analysis version 3.2; Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands), as previously described [16,17] .…”

Section: Sdf Imagingmentioning

confidence: 99%

Early Recruitment of Cerebral Microcirculation by Neuronal Nitric Oxide Synthase Inhibition in a Juvenile Ischemic Rat Model

et al. 2015

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Background: The development of collateral circulation is proposed as an inherent compensatory mechanism to restore impaired blood perfusion after ischemia, at least in the penumbra. We have studied the dynamic macro- and microcirculation after ischemia-reperfusion in the juvenile rat brain and evaluated the impact of neuronal nitric oxide synthase (nNOS) inhibition on the collateral flow. Methods: Fourteen-day-old (P14) rats were subjected to ischemia-reperfusion and treated with either PBS or 7-nitroindazole (7-NI, an nNOS inhibitor, 25 mg/kg). Arterial blood flow (BF) was measured using 2D-color-coded pulsed ultrasound imaging. Laser speckle contrast (LSC) imaging and sidestream dark-field videomicroscopy were used to measure cortical and microvascular BF, respectively. Results: In basal conditions, 7-NI reduced BF in the internal carotids (by ∼25%) and cortical (by ∼30%) BF, as compared to PBS. During ischemia, the increased mean BF velocity in the basilar trunk after both PBS and 7-NI demonstrated the establishment of collateral support and patency. Upon re-flow, BF immediately recovered to basal values in the internal carotid arteries under both conditions. The 7-NI group showed increased collateral flow in the penumbral tissue during early re-flow compared to PBS, as shown with both LSC imaging and side-stream dark-field videomicroscopy. The proportion of perfused capillaries was significantly increased under 7-NI as compared to PBS when given before ischemia (67.0 ± 3.9 vs. 46.8 ± 8.8, p < 0.01). Perfused capillaries (63.1 ± 17.7 vs. 81.1 ± 20.7, p < 0.001) and the BF index (2.4 ± 0.6 vs. 1.3 ± 0.1, p < 0.001) significantly increased under 7-NI given at the re-flow onset. Conclusions: Collateral support in the penumbra is initiated during ischemia, and may be increased during early re-flow by neuronal NOS inhibition (given in pre- and post-treatment), which may preserve brain tissue in juvenile rats.

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Preserved cerebral microcirculation during cardiogenic shock*

Cited by 40 publications

References 28 publications

Cerebral microcirculation is impaired during sepsis: an experimental study

Cerebral microcirculation is impaired during sepsis: an experimental study

Sublingual microcirculation is impaired in post-cardiac arrest patients

Early Recruitment of Cerebral Microcirculation by Neuronal Nitric Oxide Synthase Inhibition in a Juvenile Ischemic Rat Model

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