A comparison of peripheral vasoconstrictor responses and cardiovascular autonomic function tests in diabetic patients

Summary Venous occlusion plethysmography has been used to measure sympathetic vasoconstrictor responses in the feet and hands to a deep breath and body cooling and to assess blood flow variability. Measurements were made in 14 non-diabetic control subjects and 52 diabetic patients, 30 of whom had evidence of peripheral neuropathy. All the measurements were significantly reduced in the feet of patients with neuropathy. Vasoconstrictor responses were not significantly impaired in the hands of these patients. Cardiovascular autonomic function was assessed in the same subjects by standard tests of reflex heart rate responses and compared to sympathetic vasoconstrictor function as determined by the response to a deep breath. Eighteen of the 30 diabetic patients with peripheral neuropathy had impairment of both cardiovascular and sympathetic vasoconstrictor functon. Five had normal vasoconstrictor but impaired cardiovascular responses and two had normal cardiovascular but impaired vasoconstrictor function. It may therefore be important to assess both systems in diabetic patients.     

Vasodilatory effect of aerosol histamine during pulmonary vasoconstriction in unanesthetized sheep

The effects of aerosol histamine on pulmonary vascular resistance during pulmonary vasoconstriction were studied in 12 unanesthetized sheep. Sheep were chronically instrumented with Silastic catheters in the pulmonary artery and left atrium, thermodilution Swan-Ganz catheter in the main pulmonary artery for measurement of cardiac output, and tracheostomy for delivery of hypoxic gas and/or aerosol histamine. Seven minutes of isocapnic hypoxia (Fl_O2 = 0.12) caused pulmonary artery pressure (P_PA) to increase from 17.2 ± 0.4 to 27.0 ± 1.0 cm H₂O (X¯ ± SEM, P < 0.05) and pulmonary vascular resistance (PVR) to increase from 3.94 ± 0.33 to 4.71 ± 0.38 cm H₂O · L^?1. min (P < 0.05). When sheep breathed a combination of aerosol histamine (5 mg/ml) and 12% O₂, P_PA rose only to 21.3 ± 1.11 cm H₂O and PVR decreased to 3.51 ± 0.31 cm H₂O · L^?1. min. This was a significantly (P < 0.05) smaller response compared to hypoxia alone. Aerosol histamine alone had no significant effect on P_PA or PVR. Meclofenamate did not restore the histamine-induced loss of hypoxic vasoconstriction. Aerosol histamine significantly blunted the pulmonary vasoconstriction caused by intravenous serotonin (8 μg/kg/min) and intravenous prostaglandin H₂-analog (0.74 μg/kg/min). It was concluded that in the awake sheep aerosol histamine acted as a pulmonary vasodilator only in the presence of pulmonary vasoconstriction. Pediatr Pulmonol 1987; 3:94–100 .     

INHIBITION OF VASOCONSTRICTION BY PLATELET ACTIVATING FACTOR IN THE IN SITU BLOOD PERFUSED RAT MESENTERY

1. Perfusion pressure was measured in the in situ mesentery of anaesthetized rats perfused with blood at a constant 2 mL/min. 2. Increases in perfusion pressure were produced by mesenteric peri-arterial nerve stimulation at 10 Hz for 5 s at 2 min intervals and by bolus intra-arterial injections of the vasoconstrictors noradrenaline, angiotensin II and 5-hydroxytryptamine. 3. The intra-arterial infusion of platelet-activating factor (PAF) to produce a blood concentration of 3 X 10(-10) mol/L inhibited all responses to a similar extent. Intra-arterial prazosin (1-5 X 10(-9) mol/L), however, preferentially reduced responses to nerve stimulation and noradrenaline. 4. PAF at concentrations from 3 X 10(-11) to 10(-9) mol/L produced increasing inhibition of vasoconstrictor responses to nerve stimulation. The dose-response to PAF was shifted to the right by the concomitant intra-arterial infusion of the PAF antagonist SRI 63-441. 5. PAF at very low concentrations in vivo inhibits mesenteric vasoconstriction, produced by sympathetic nerve stimulation or various agonists, by a PAF-receptor mediated vasodilatation of the mesenteric vasculature.     

Optimal concentration of epinephrine for vasoconstriction in ear surgery.

OBJECTIVE: To determine the optimal concentration of epinephrine required for vasoconstriction in ear surgery by evaluating changes in laser doppler blood flow. STUDY DESIGN: Prospective, randomized, double-blinded. METHODS: Forty subjects undergoing surgical procedures under general anesthesia were injected in a standard posterior external auditory canal block with 1 mL of 1% lidocaine containing varying concentrations of epinephrine (nil, 1:50,000, 1:100,000, or 1:200,000) determined by randomization. Ear canal blood flow measurements were then made at 1-minute intervals for a 10-minute period using a laser doppler flow meter and compared with baseline blood flow. RESULTS: The control solution of 1% lidocaine had a significantly higher blood flow than the epinephrine-containing solutions with an actual 200% increase in blood flow for the first 5 minutes before returning to baseline. All epinephrine-containing solutions had an approximately 50% decrease in blood flow from baseline over the 10-minute period as compared with the control which was statistically significant (P < .0001). There was no significant difference between the blood flow reduction of 1:50,000, 1:100,000, and 1:200,000 epinephrine-containing solutions (P = .8875). CONCLUSIONS: One percent lidocaine control exhibited the expected initial vasodilatory effect for approximately 5 minutes. In this experimental model, using a lower concentration of 1:200,000 epinephrine would supply equivalent vasoconstriction in the ear compared with higher concentrations, thus reducing the possible systemic toxicity and related morbidity.     

Effects of NO inhalation on pulmonary leukocyte sequestration and blood volume in porcine endotoxaemia

Objective: Sequestration and migration of activated neutrophils plays a major role in the pulmonary injury typical of septic shock and the adult respiratory distress syndrome. Inhaled NO may counteract alveolar-capillary damage attributed to activated neutrophils. The present study describes a method to directly demonstrate the effects of NO inhalation on endotoxin-induced sequestration of ^{99 m}Tc-labelled leukocytes [A_s(t)] in the lungs of pigs.¶Design: Prospective controlled study.¶Setting: Laboratory for experimental surgery at a university medical centre.¶Subjects: Anaesthetised and ventilated pigs.¶Interventions: To induce inflammatory shock 26 animals received a continuous endotoxin infusion. Thirteen animals inhaled NO from the start of the experiments, while 13 served as controls. In 13 animals from both groups, leukocytes were labelled in vitro and reinjected, while in the 13 others erythrocytes were labelled in vivo to provide corrections for changes in blood volume.¶Measurements and results: The pulmonary distribution of ^{99 m}Tc-labelled leukocytes or erythrocytes was studied dynamically for 180 min. After correction for changes in pulmonary and heart blood volume (PBV, HBV), leukocyte sequestration curves were generated. Endotoxin induced pulmonary vasoconstriction, reduced PBV, impaired oxygenation, and caused a maximum increase in A_s(t) of 30 % in the lungs. NO inhalation attenuated pulmonary vasoconstriction and the reduction in PBV. The maximum increase in A_s(t) was reduced to 15 % of baseline.¶Conclusions: Inhaled NO exerts its main vascular effects in the pulmonary microvasculature, the primary site of physiological neutrophil margination and pathological adhesion of activated leukocytes. Early use of NO inhalation may offer protection against the development of more lasting pulmonary failure in septic shock by reducing leukocyte sequestration in the lungs.     

The venoarteriolar response of the skin in healthy legs measured at different depths

The venoarteriolar response (VAR) of the skin in healthy legs of 20 subjects was investigated. The laser Doppler flux (LDF), at an experimental venous hypertension of 30 mmHg, 45 mmHg and 60 mmHg, produced by a pneumatic cuff around the thigh in a recumbent position, was compared with the LDF in a sitting position. The LDF of the skin was measured simultaneously at the same site of the superficial capillary layer (with 543 nm) and of the deeper capillary layer (with 780 nm). At 543 nm the LDF did not differ significantly at any cuff pressure from the LDF recorded in a sitting position, whereas at 780 nm the LDF was significantly higher at the cuff pressure of 30 mmHg than the LDF in a sitting position (P = 0·002). The VAR was much weaker at 543 nm than at 780 nm, and the scatter of the VAR values was high. In a sitting position the VAR at 543 nm was 9·3% and at 780 nm 34·6% (P<0·001). The VAR at 543 nm at the cuff pressure of 30 mmHg did not differ significantly from the VAR caused by the sitting position, whereas at 780 nm the VAR at the cuff pressure of 30 mmHg was significantly less than the VAR caused by the sitting position (P = 0·001). Despite the high scatter of the VAR values, these findings suggest that the VAR in the superficial capillary layer is smaller, and that it reached maximum at lower venous hypertension, than the VAR in the deeper capillary layer.     

Reversible segmental cerebral vasoconstriction (Call-Fleming syndrome): are calcium channel inhibitors a potential treatment option?

The Call-Fleming syndrome is characterized by sudden onset of thunderclap-like headache and focal neurological deficits. The pathophysiological correlate is a reversible segmental cerebral vasoconstriction frequently associated with focal cerebral ischaemia. The syndrome has been described in a variety of clinical conditions, and recently an association between the syndrome and exposure to vasoactive drugs was observed. Effective treatment options are not known. A 63-year-old female developed sudden 'worst ever' headache. Initial neurological examination, laboratory blood tests, CSF examination and brain magnetic resonance imaging (MRI) were normal. Previous medical history was unremarkable and she did not take vasoactive drugs. Eleven days after the onset of headache she developed visual field impairment and a right-sided hemiparesis. Brain MRI revealed bilateral posterior and left parietal ischaemic strokes. Cerebral catheter angiography showed segmental arterial vasoconstriction. A vasodilative therapy with calcium channel inhibitors was started and serial transcranial Doppler ultrasonography demonstrated resolution of cerebral arterial vasoconstriction. The present case illustrates that calcium channel inhibitors may be an effective therapy for segmental cerebral arterial vasoconstriction. However, more clinical data are needed to prove this observation.     

The Typical Thunderclap Headache of Reversible Cerebral Vasoconstriction Syndrome and its Various Triggers

During the last 10 years, reversible cerebral vasoconstriction syndrome (RCVS) has emerged as the most frequent cause of thunderclap headache (TCH) in patients without aneurysmal subarachnoid hemorrhage, and as the most frequent cause of recurrent TCHs. The typical TCHs of RCVS are multiple, recurring over a few days to weeks, excruciating, short‐lived, and brought up by exertion, sexual activities, emotion, Valsalva maneuvers, or bathing, among other triggers. All these triggers induce sympathetic activation. In a minority of cases with RCVS, TCH heralds stroke and rarely death. Early diagnosis of RCVS in patients who present with isolated headache enables proper management and might reduce the risk of eventual stroke. This review describes the characteristics, triggers, diagnosis, and management of TCH in RCVS. One aim is to underline that the TCH pattern of RCVS is so typical that it enables, according to the 2013 revision of the International Classification of Headache Disorders, the diagnosis of “probable RCVS” in patients with such a headache pattern, normal cerebral angiography, and no other cause. Another objective is to discuss the role of physical and emotional stress in RCVS and in other related conditions involving similar triggers.     

Bath‐related thunderclap headache: Case report of a male patient

Bath‐related thunderclap headache (BRTH) is a rare entity, closed to reversible cerebral vasoconstriction syndrome. It is only described in middle‐aged women and mainly Asiatic ethnic origins. Role of estrogen is consequently discussed. We report here a case of a 36‐year‐old man, admitted for five episodes of thunderclap headaches, triggered by hot shower. This is the first male case of BRTH, opposing only a hormonal hypothesis. Furthermore, this African patient consolidates the non‐exclusivity of this affection to Asian ethnic origins.     

阻塞性黄疸大鼠离体胸主动脉收缩与舒张功能的变化

目的:研究阻塞性黄疸大鼠离体胸主动脉收缩及舒张功能的变化规律,探讨高胆红素血症导致阻塞性黄疸大鼠离体胸主动脉收缩及舒张功能变化的可能机制。方法:60只雄性SD大鼠随机分为胆总管结扎(BDL)组和假手术(SO)组,每组30只,术后3、7、14 d,取大鼠离体胸主动脉环,分别测定大鼠胸主动脉对高浓度钾离子(K+)诱发的最大收缩幅度、梯度浓度去甲肾上腺素(NE)和去氧肾上腺素(PE)引起的收缩反应以及硝普钠(SNP)引起的舒张反应。另取40只雄性SD大鼠,随机分为SO组、BDL 3 d组、BDL 7 d组、BDL 14 d组,每组10只。取大鼠的胸主动脉组织,利用Western印迹方法检测大鼠胸主动脉肾上腺素α1D受体亚型(α1D-AR)蛋白表达情况。结果:高钾离子、NE、PE 在BDL大鼠离体胸主动脉引起的收缩反应弱于SO组,而硝普钠引起的舒张反应强于SO组;BDL组大鼠α1D-AR蛋白表达较SO组减弱,并且随阻塞时间的延长,减弱更加明显。结论:BDL大鼠离体胸主动脉的收缩与舒张功能在高胆红素血症时发生改变,α1D-AR蛋白表达下降可能是收缩功能减弱的原因之一。