Vasomotion in rat diaphragm microcirculation at rest and during stepwise arterial pressure reduction

The effect of haemorrhagic hypotension on the incidence, frequency and relative amplitude of vasomotion in rat diaphragm microcirculation was assessed by laser Doppler flowmetry (LDF). Graded bleeding to four hypotension levels (80, 60, 40 and 30% of the control state) were performed in 24 Sprague–Dawley rats. The incidence of vasomotion was 83% in the control state, 96% at the 80% level, 100% at the 60% level, 96% at the 40% level, and 46% at the 30% level. The median fundamental frequency of vasomotion determined manually during the control state and at the hypotension levels (in descending order) was 4.11 (range, 3.29–5.58) cycles min^?1 (cpm), 4.48 (3.21–5.92) cpm, 4.20 (3.5–5.56) cpm, 4.01 (3.33–5.36) cpm, 3.71 (3.25–4.49) cpm (P < 0.01 from the fundamental frequency at 80 and 60% hypotension levels). The median relative amplitudes determined manually during the control state and descending hypotension levels were 44.5% (range, 24.9–135.9%), 69.4% (26.6–147.2%), 84.0% (40.3–177.1%) (P < 0.01 from resting and last stage of bleeding), 90.40% (26.2–189.6%) (P < 0.01 from resting and last stage of bleeding), 69.2% (35.6–93.2%). We concluded first that during the resting condition, vasomotion was frequently present in diaphragm microcirculation, which is distinct from other vascular beds of skeletal muscles. Second, the relative amplitude of vasomotion during haemorrhagic hypotension plotted against decreasing blood pressure exhibited a reverse U-shaped curve with a maximum at 40–60% of the control blood pressure, while the frequency of vasomotion remained relatively constant until the last stage of haemorrhage and centred around 3–5 cpm.     

The forgotten lumbar puncture

Lumbar puncture is crucial in two distinct clinical situations in the diagnosis of the headache patient. The first is the patient who is suspected of having a symptomatic headache; the second is the patient with a chronic intractable or atypical headache disorder. This review discusses the usefulness of the lumbar puncture in the diagnosis of headache secondary to subarachnoid hemorrhage, meningitis, and intracranial hypotension and hypertension. The value of lumbar puncture in the presence of a normal CT/MRI scan is discussed.     

甘露醇治疗颅内高压症36例临床分析

本文收集36例各种病因引起的颅内高压病例，依据脑CT提示脑出血量及脑积水程度，脑脊液压力及患者生命体征的特征，分为经、中、重三种类型进行脱水治疗。治愈率86％，病死率13．8％。治疗中应注意防止肾衰、糖尿病以及低颅内压综合征的出现。     

Effects of sodium nitroprusside (MR7S1) and nitroglycerin on the systemic,renal, cerebral,and coronary circulation of dogs anesthetized with enflurane

Summary In beagle dogs anesthetized with enfluranenitrous oxide, effects of sodium nitroprusside (SNP; MR7S1) and nitroglycerin (NTG) on hemodynamics and main organ circulation were studied to evaluate their effectiveness and safety as hypotensive agents during anesthesia. SNP (MR7S1) infusion (1–10 g/kg/min) decreased arterial blood pressure in a dose-dependent manner. The hypotension was stable during the infusion. After discontinuation of infusion, the blood pressure rapidly returned to the initial level. The hypotension was associated with decreases in cardiac output and total peripheral resistance. NTG infusion (3–10 g/kg/min) decreased arterial blood pressure, too, but the hypotension was less marked and not dose dependent, and the recovery was slower. Neither drug changed the heart rate. Infusion of SNP (MR7S1) and NTG did not change the hypotension induced by the injection of adenosine, SNP, and NTG. Furthermore, cerebral blood flow, cerebral oxygen consumption, and renal blood flow were unchanged during the hypotension produced by either drug. Coronary blood flow was decreased, but this was due to decreases in cardiac oxygen consumption. In conclusion, SNP (MR7S1) is superior to NTG as a hypotensive agent during anesthesia in efficacy, clear dose dependency, and rapid recovery. The hypotension induced by NTG as well as SNP (MR7S1) seems to have no undesirable effects on the circulation of important organs.     

Diastolic Blood Pressure and Heart Rate Biofeedback Training During Orthostatic Stress

Forty male college student volunteers were asked either to increase their diastolic pressure or their heart rate while sitting and during orthostatic stress (going from a sitting to a standing position), and half of them were also given second- to-second visual feedback for the target variable. Systolic blood pressure was also continuously recorded. Comparisons were made between baseline and voluntary control conditions, and test trials were included to examine immediate carry-over effects. With voluntary control instructions, substantial increases in tonic levels were obtained for the three cardiovascular variables in both sitting and postural change conditions. In general, the increases were significantly greater for feedback than for no-feedback conditions. Phasic effects of feedback were also observed during postural change conditions: the blood pressure troughs and the heart rate peak occurred earlier with feedback than for instructions only. Immediate transfer effects were obtained in feedback conditions only. The results were discussed in terms of concomitant effects of somatic and cognitive activities. The distinctive feedback effects on the time course of the responses suggest that a precise analysis of response patterns is needed in selecting appropriate feedback methods in the management of orthostatic hypotension.     

Near-infrared spectrophotometry determined brain oxygenation during fainting

During orthostatic hypotension we evaluated whether presyncopal symptoms relate to a reduced brain oxygenation. Nine subjects performed 50° head-up tilt for 1 h and eight subjects were followed during 2 h of supine rest and during 1 h of 10° head-down tilt. Cerebral perfusion was assessed by transcranial Doppler determined middle cerebral artery blood velocity (MCA v_mean), while brain blood oxygenation was assessed by near-infrared spectrophotometry determined concentration changes for oxygenated (ΔHbO₂) and deoxygenated haemoglobin and brain cell oxygenation by the oxidized cytochrome c concentration (ΔCytO₂). During head-up tilt, six volunteers developed presyncopal symptoms and mean arterial pressure (88 (78–103) to 68 (57–79) mmHg; median and range), heart rate (96 (72–111) to 65 (50–107) beats min^?1), MCA v_mean (59 (51–82) to 41 (29–56) cm s^?1), ΔHbO₂ (by ?5.3 (?3.0 to ?14.8) μmol l^?1) and ΔCytO₂ were reduced (by ?0.2 (?0.1 to ?0.4) μmol l^?1; P < 0.05). During tilt down the cardiovascular variables recovered immediately and ΔHbO₂ increased to 2.2 (?0.9–12.0) mmol L^?1 above the resting value and also ΔCytO₂ recovered. In the nonsyncopal head-up tilted subjects as in the controls, blood pressure, heart rate, MCA v_mean and brain oxygenation indices remained stable. The results suggest that during orthostasis, presyncopal symptoms relate not only to cerebral hypoperfusion but also to reduced brain oxygenation.     

Oxygen-dependent mechanisms in cerebral autoregulation

Autoregulatory adjustments in the caliber of cerebral arterioles were studied in anesthetized cats equipped with cranial windows for the direct observation of the pial microcirculation. Increased venous pressure caused slight, but consistent, arteriolar dilation, at normal and at reduced arterial blood pressure and irrespective of whether or not intracranial pressure was kept constant or allowed to increase. Arterial hypotension caused arteriolar dilation which was inhibited partially by perfusion of the space under the cranial window with artificial CSF equilibrated with high concentrations of oxygen. This vasodilation was inhibited to a greater extent by perfusion of the space under the cranial window with fluorocarbon FC-80, equilibrated with high concentrations of oxygen. CSF or fluorocarbon equilibrated with nitrogen did not influence the vasodilation in response to arterial hypotension. The response to increased venous pressure was converted to vasoconstriction when fluorocarbon equilibrated with high concentrations of oxygen was flowing under the cranial window. The vasodilation in response to arterial hypotension was inhibited by topical application of adenosine deaminase. The results show that both metabolic and myogenic mechanisms play a role in cerebral arteriolar autoregulation. Under normal conditions, the metabolic mechanisms predominate. The presence of the myogenic mechanisms may be unmasked by preventing the operation of the metabolic mechanisms. The major metabolic mechanism seems to be dependent on changes in PO₂ within the brain with secondary release of adenosine.     

Hyperglycemic and Hyperosmolar Responses to Graded Hemorrhage

Changes of the arterial plasma osmolality and of the glucose concentration were followed during a 30 min period of graded hemorrhagic hypotension (80, 50, and 30 mmHg) in the cat. Bleeding evoked a significant plasma hyperosmolality at all three hypotension levels and the responses were quantitatively related to the degree of hypotension. An approximate steady state increase in the arterial plasma osmolality was reached about 20 min after the start of the bleeding and it then averaged 8, 20, and 25 mOsm/kg H₂O at 80, 50, and 30 mmHg, respectively. Bleeding also evoked an increase in the plasma glucose concentration, which almost entirely accounted for the observed hyperosmolality, especially at 80 and 50 mmHg. In late stages of hypotension at 30 mmHg, elevated plasma lactate and potassium concentrations contributed to the overall hyperosmolality. — Previous hemorrhagic hypotension experiments at 50 mmHg (Järhult 1975 b) have shown that hyperosmolality serves as an important regulator of the plasma and extracellular fluid volumes during bleeding. The present results indicate that such an osmolar compensatory mechanism is operating over wide ranges of hemorrhagic hypotension.     

Effect of Transmural Pressure on Constrictor Reactions of Caudal Artery in Hypotensive and Hypertensive Rats

Clipping of the abdominal aorta distally to the renal arteries produces a persistent decrease in blood pressure in hindquarter vessels by 35-40%. On week 6-7 postoperation, the reactions of the caudal artery perfused in vitro under constant pressure to norepinephrine were studied. At transmural pressure of 150 mm Hg, the vascular responses in hypotensive rats were reduced compared to those in normotensive control. By contrast, the responses of hypertensive vessels were more pronounced at 75 mm Hg even after deendothelization.     

前部增生性玻璃体视网膜病变引起慢性低眼压房水生成率的测定

目的：探讨前部增生性玻璃体视网膜病变（anterior prolieferative vitreoretinopathy,aPVR)低眼压状态下房水生成率变化,从房水动力学的角度揭示aPVR引起慢性低眼压的发病机制。方法：利用培养的同种兔皮肤成纤维细胞制作aPVR引起慢性低眼的动物模型。于术前及术后不同时间点分别观测眼压、术后14d,28d,56d分别以高效液相色谱仪测量房水荧光素清除率,进一步计算房水生成率。结果：术后2周、4周、8周实验组平均眼压、房水生成率明显低于对照组（P＜0．05或P＜0．01）。结论：在aPVR病理状态下,低眼压的形成与房水生成率下降有关。