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Anesthesia and Analgesia Aug 2001We evaluated the vasomotor effects of clonidine in awake subjects with an intact central cardiovascular regulatory system. To determine the lower limit of the...
UNLABELLED
We evaluated the vasomotor effects of clonidine in awake subjects with an intact central cardiovascular regulatory system. To determine the lower limit of the vasoconstrictive effect of clonidine in awake volunteers, we blocked sympathetic innervation to the left arm by anesthetizing the brachial plexus. We then measured arterial blood pressure and vasoconstriction via finger volume plethysmography measuring infrared light transmitted through a fingertip (LTF). LTF values obtained from the left arm were compared with those from the neurally intact right arm during four progressively increasing IV doses of clonidine, targeting plasma clonidine concentrations of 0.3, 0.45, 0.68, and 1.0 ng/mL. Clonidine decreased systolic blood pressure (P < 0.004) from 135 +/- 8 mm Hg to 115 +/- 8 mm Hg and heart rate (P = 0.0017) from 68 +/- 7 mm Hg to 61 +/- 10 mm Hg. Clonidine decreased LTF by -12% +/- 11% (P < 0.0001) less than preinfusion values at the 0.68 ng/mL target concentration in the right hand. In contrast, in the left hand, clonidine increased LTF significantly more than (P < 0.0001) preinfusion values at all target concentrations, with a maximal increase of 30% +/- 7%. We conclude that IV clonidine, at doses that decrease arterial blood pressure, causes arterial vasoconstriction in awake subjects.
IMPLICATIONS
IV clonidine, at doses that decrease blood pressure, causes arterial vasoconstriction in awake subjects. These data suggest that an alpha-2 agonist with a high alpha-2a/alpha-2b selectivity should provide more profound sedative and analgesic effects with less undesirable vasoconstrictive effects.
Topics: Adrenergic alpha-Agonists; Adult; Blood Pressure; Clonidine; Female; Humans; Male; Skin; Skin Temperature; Vasoconstriction; Wakefulness
PubMed: 11473842
DOI: 10.1097/00000539-200108000-00006 -
Naunyn-Schmiedeberg's Archives of... Dec 2002Vasopressin is a potent renal vasoconstrictor in vitro which elicits relatively minor renal vascular effects in vivo. Efficient modulation might occur through shear...
Vasopressin is a potent renal vasoconstrictor in vitro which elicits relatively minor renal vascular effects in vivo. Efficient modulation might occur through shear stress-elicited release of vasodilator compounds from endothelial cells. The aim of this study was to evaluate in vitro, in the isolated perfused kidney, the influence of shear stress and related nitric oxide (NO) release on basal renal vascular tone and on vasopressin-induced renal vasoconstriction. Rat kidneys were perfused at a constant flow rate of 8 ml/min with Tyrode's solution (relative viscosity eta=1) or, in order to increase shear stress, with Tyrode's solution supplemented with 4.7% Ficoll 400 (Ficoll 400; eta=2.3), which is representative of the relative viscosity found in small vessels. Renal shear stress was further elevated during vasoconstriction elicited by vasopressin. Basal renal true vascular conductance, which reflects mean blood vessel radius, was 2.5-fold higher and overall wall shear stress doubled in Ficoll 400 - as compared to Tyrode-perfused kidneys. The decrease in vascular conductance elicited by NO synthase inhibition with N(omega)-nitro-L-arginine (L-NNA) increased with the viscosity of the perfusate. Shear stress was elevated during vasopressin-induced renal vasoconstriction, all the more kidneys were Ficoll 400-perfused. In these kidneys, the concentration-response curve to vasopressin was shifted to the right, giving evidence of hyporeactivity to the peptide. L-NNA potentiated vasoconstriction to vasopressin particularly in Ficoll 400-perfused kidneys, although additional inhibition of cyclooxygenase and/or cytochrome P(450) was without effect. These results provide in vitro evidence that shear stress enhanced by perfusate viscosity increases basal renal vascular conductance by an NO-dependent mechanism. Together with shear stress enhanced during vasoconstriction, it blunts vasopressin-induced renal vasoconstriction.
Topics: Animals; Dose-Response Relationship, Drug; In Vitro Techniques; Kidney; Male; Nitric Oxide; Perfusion; Rats; Rats, Sprague-Dawley; Shear Strength; Stress, Physiological; Vasoconstriction; Vasopressins
PubMed: 12444497
DOI: 10.1007/s00210-002-0638-7 -
Cerebrovascular Diseases (Basel,... 2013
Topics: Adult; Brain; Catha; Humans; Male; Phytotherapy; Plant Leaves; Subarachnoid Hemorrhage; Treatment Outcome; Vasoconstriction
PubMed: 24029701
DOI: 10.1159/000353664 -
Anesthesia and Analgesia May 1997Elderly patients become more hypothermic during surgery, shiver less postoperatively, and take longer to rewarm than younger patients. Similarly, the vasoconstriction...
Elderly patients become more hypothermic during surgery, shiver less postoperatively, and take longer to rewarm than younger patients. Similarly, the vasoconstriction threshold (triggering core temperature) is reduced approximately 1 degree C in elderly patients during nitrous oxide/isoflurane anesthesia. Accordingly, we tested the hypothesis that the vasoconstriction threshold in the elderly is also reduced approximately 1 degree C during nitrous oxide and sevoflurane anesthesia. Eleven young patients aged 30-50 yr and 14 elderly patients aged 60-80 yr were anesthetized with nitrous oxide (50%) and sevoflurane (1%). Mean skin temperature was calculated from four sites. Fingertip blood flow was estimated using forearm minus fingertip skin-temperature gradients, with a gradient of 0 degree C identifying onset of vasoconstriction. The distal esophageal temperature triggering onset of vasoconstriction identified the threshold for this thermoregulatory defense. The data from five patients who did not vasoconstrict at minimum core temperatures of 33-34 degrees C were eliminated, leaving 10 patients in each group. The vasoconstriction threshold was significantly less in the elderly (35.0 +/- 0.8 degrees C) than in younger patients (35.8 +/- 0.3 degrees C), despite similar mean skin temperatures (mean +/- SD, P < 0.01, Student's t-test). Age dependence of thermoregulatory vasoconstriction during nitrous oxide/sevoflurane anesthesia is similar to that previously observed during nitrous oxide/isoflurane anesthesia.
Topics: Adult; Aged; Aged, 80 and over; Aging; Anesthetics, Combined; Anesthetics, Inhalation; Body Temperature; Body Temperature Regulation; Ethers; Female; Humans; Male; Methyl Ethers; Middle Aged; Nitrous Oxide; Sevoflurane; Vasoconstriction
PubMed: 9141926
DOI: 10.1097/00000539-199705000-00014 -
British Journal of Pharmacology Jun 19921. The nature of the transmitter mediating vasoconstriction of guinea-pig submucosal arterioles following sympathetic nerve stimulation was studied. 2. Prazosin (0.1...
1. The nature of the transmitter mediating vasoconstriction of guinea-pig submucosal arterioles following sympathetic nerve stimulation was studied. 2. Prazosin (0.1 microM) abolished the response to exogenously applied phenylephrine (1 microM) but had no effect on constrictions of submucosal arterioles evoked by nerve stimulation (100 pulses at 10 Hz). 3. Vasoconstrictions and excitatory junction potentials elicited by nerve stimulation were potentiated by idazoxan (0.1 microM). 4. Following reserpine treatment, catecholamine fluorescence was absent in submucosal arterioles but nerve-evoked vasoconstrictions were unaltered. 5. Vasoconstrictions and excitatory junction potentials recorded in response to sympathetic nerve stimulation, as well as constrictions evoked by exogenously applied ATP (3 microM), were abolished by the P2-purinoceptor antagonist, suramin (100 microM). Suramin had no effect on the vasoconstriction in response to noradrenaline (3 microM), or the nicotinic excitatory postsynaptic potentials (e.p.s.ps) and noradrenergic inhibitory postsynaptic potentials (i.p.s.ps) recorded from submucosal neurones. 6. We conclude that postjunctional responses of submucosal arterioles following sympathetic nerve stimulation are mediated solely through the activation of P2X-purinoceptors by ATP or a related purine nucleotide. The function of neurally released noradrenaline is to act through prejunctional alpha 2-adrenoceptors to depress transmitter release.
Topics: Adenosine Triphosphate; Adrenergic alpha-Antagonists; Animals; Arterioles; Electric Stimulation; Evoked Potentials; Guanethidine; Guinea Pigs; In Vitro Techniques; Intestinal Mucosa; Muscle Contraction; Neuromuscular Junction; Prazosin; Receptors, Purinergic; Reserpine; Sympathetic Nervous System; Vasoconstriction
PubMed: 1356556
DOI: 10.1111/j.1476-5381.1992.tb14323.x -
Current Neurovascular Research 2018Delayed cerebral vasospasm (dCVS) following aneurysmal subarachnoid hemorrhage (aSAH) is (next to possible aneurysm rebleeding, cortical spreading depression and early...
BACKGROUND
Delayed cerebral vasospasm (dCVS) following aneurysmal subarachnoid hemorrhage (aSAH) is (next to possible aneurysm rebleeding, cortical spreading depression and early brain injury) one of the main factors contributing to poor overall patient outcome. Since decades, intensive research has been ongoing with the goal of improving our understanding of the pathophysiological principles underlying dCVS. Endothelin-1 (ET-1) and prostaglandin F2 alpha (PGF2a) seem to play a major role during dCVS. The synthesis of ET-1 is enhanced after subarachnoid hemorrhage (SAH) to mediate a long-lasting vasoconstriction, and PGF2a contributes to cerebral inflammation and vasoconstriction. Under physiological conditions, levosimendan (LS) demonstrates an antagonistic effect on PGF2a-induced cerebral vasoconstriction. Thus, the intention of the present study was to analyze potentially beneficial interactions in a pathophysiological situation.
METHODS
A modified double hemorrhage model was used. Functional interactions between the calcium-sensitizing action of LS and the vasoconstrictive properties of PGF2a were investigated.
RESULTS
After pre-incubation with LS, followed by application of PGF2a, a significant decrease in maximum contraction (Emax) for sham-operated animals was found (Emax 28% with LS, Emax 56% without LS). Using the same setting after SAH, the vessel segments did not reach a statistically significant contraction (but similar like the sham-operated vessels), neither for Emax nor pD2 (-log10EC50) nor EC50 (i.e., the concentration at which half of the maximal effect occurs). LS series in sham animals were performed by pre-incubation with PGF2a. The resultant Emax showed a statistically strong significance concerning a higher vasorelaxation compared with a solvent control group. Vessel segment relaxation was significantly stronger in the same experimental setup after SAH.
CONCLUSION
Under physiological and pathophysiological circumstances, LS reduced and dosedependently reversed PGF2a-induced vasoconstriction. These results can be applied to further developing methods to antagonize dCVS after aSAH.
Topics: Animals; Dinoprost; Dose-Response Relationship, Drug; Male; Organ Culture Techniques; Rats; Rats, Sprague-Dawley; Simendan; Subarachnoid Hemorrhage; Vasoconstriction; Vasodilator Agents
PubMed: 29595109
DOI: 10.2174/1567202615666180328121025 -
Orphanet Journal of Rare Diseases Apr 2015Reversible cerebral vasoconstriction syndrome (RCVS) is an infrequent disease characterized by severe headaches with or without focal neurological deficits or seizures...
BACKGROUND
Reversible cerebral vasoconstriction syndrome (RCVS) is an infrequent disease characterized by severe headaches with or without focal neurological deficits or seizures and a reversible vasoconstriction of cerebral arteries. The Orpha number for RCVS is ORPHA284388. However, RCVS triggered by blood transfusion is rare. Here we provided the clinical, neuroimaging and outcome data of patients diagnosed with RCVS resulting from red blood cells transfusion.
METHODS
We retrospectively identified 7 patients presenting with RCVS after red blood cells transfusion from January 2010 to May 2014. The information on clinical features, neuroimaging and outcome were collected and analyzed.
RESULTS
All 7 patients were Chinese women, with a mean age of 42 years (38-46). All the patients had severe anemia (Hb level < 6 g/dl) caused by primary menorrhagia due to uterine myoma (n = 5) or end-stage renal disease (n = 2) and severe anemia persisted for a average period of 4 months (2-6). Each patient received packed red blood cells transfusion (average: 1580 ml) over a period of 2-5 days. Blood transfusion increased the hemoglobin level by at least 4.5 g/dL from baseline. The neurological symptoms appeared a mean of 6.3 days (2-13) after the last blood transfusion. Headache was the most frequent symptom and seizure, transient or persistent neurological disorders were observed. Neuroimaging showed cortical subarachnoid hemorrhage (n = 2), focal intracerebral hemorrhage (n = 2), localized brain edema (n = 3), cerebral infarction (n = 1), and posterior reversible encephalopathy syndrome (n = 2). Cerebral vasoconstrictions were demonstrated by magnetic resonance angiography or cerebral angiography. Arterial constriction reversed in all patients within 1 to 3 months of follow-up after disease onset and no relapse was observed up to a mean of 17.1 ± 4.8 months of follow-up.
CONCLUSIONS
RCVS is a rare complication as a result of blood transfusion in patients with chronic severe anemia and should be considered in patients who show severe headache or neurologic deficits after transfusion.
Topics: Adult; Erythrocyte Transfusion; Female; Headache; Humans; Magnetic Resonance Angiography; Middle Aged; Retrospective Studies; Vasoconstriction; Vasospasm, Intracranial
PubMed: 25896868
DOI: 10.1186/s13023-015-0268-z -
BMC Neurology Oct 2023Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by sudden onset thunderclap headache and multiple segmental reversible cerebral vasoconstrictions...
A case report of reversible cerebral vasoconstriction syndrome with thunderclap headache significantly exacerbated in the supine position and alleviated in the standing position.
BACKGROUND
Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by sudden onset thunderclap headache and multiple segmental reversible cerebral vasoconstrictions that improve within 3 months. The postpartum period is a well-known precipitating factor for the onset of RCVS. Cerebral venous thrombosis (CVT) causes thunderclap headaches in the postpartum period. While headache in CVT is sometimes exacerbated in the supine position, the severity of the headache in RCVS is usually independent of body position. In this study, we report a case of RCVS with thunderclap headache exacerbated in the supine position, and headache attacks that resolved quickly in the standing position during the postpartum period.
CASE PRESENTATION
A 33-year-old woman presented with a sudden increase in blood pressure and thunderclap headache on the fifth postpartum day (day 1: the first sick day). The headache was severe and pulsatile, with onset in the supine position in bed, and peaked at approximately 10 s. It was accompanied by nausea and chills but there were no scintillating scotomas or ophthalmic symptoms. The headache resolved in the standing or sitting position but was exacerbated and became unbearable within a few seconds when the patient was in the supine position. Therefore, she was unable to lie supine at night. Computed tomography angiography (CTA) of the head on day 2 and magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) on day 3 showed no abnormalities. However, considering the possibility of RCVS, verapamil was initiated on day 3. The headache resolved the following day. MRA of the head on day 10 revealed diffuse and segmental stenoses in the bilateral middle and posterior cerebral arteries and basilar artery. Therefore, the patient was diagnosed with RCVS. The headache gradually resolved and disappeared completely on day 42. Cerebral vasoconstriction was also improved on MRA on day 43.
CONCLUSIONS
This postpartum RCVS case was notable for the exacerbation of headaches in the supine position. For the diagnosis of thunderclap headache in the postpartum period, RCVS should be considered in addition to CVT when the patient presents with a headache that is exacerbated in the supine position.
Topics: Female; Humans; Adult; Vasoconstriction; Standing Position; Supine Position; Cerebrovascular Disorders; Vasospasm, Intracranial; Headache Disorders, Primary; Headache
PubMed: 37789263
DOI: 10.1186/s12883-023-03381-6 -
Shock (Augusta, Ga.) 2000Previous studies indicate that cardiogenic shock (tamponade) in swine produces selective mesenteric ischemia due to disproportionate mesenteric vasospasm mediated...
Previous studies indicate that cardiogenic shock (tamponade) in swine produces selective mesenteric ischemia due to disproportionate mesenteric vasospasm mediated primarily by the renin-angiotensin axis. Here, we characterized the systemic and mesenteric hemodynamic responses to hypovolemic shock to better understand the neurohumoral mechanisms controlling this response. Varying degrees of hypovolemic shock were produced by graded levels of hemorrhage, from 12.5 to 50% of the calculated blood volume. Systemic and mesenteric pressures and blood flows were measured, and corresponding vascular resistances were calculated. The hemodynamic responses of the mesenteric vascular bed were compared with those of the systemic (nonmesenteric) vasculature. These experiments were then repeated after confirmed blockade either of the alpha-adrenergic nervous system (phenoxybenzamine), of vasopressin (Manning compound), or of the renin-angiotensin axis (enalapril). Graded levels of hemorrhage produced corresponding graded, reproducible, steady-state levels of systemic hypotension, hypoperfusion, and peripheral vasoconstriction, i.e., hemorrhagic shock. This was associated with disproportionate degrees of mesenteric ischemia due to disproportionate mesenteric vasoconstriction. The selective component of this mesenteric vasoconstrictive response was not attenuated by a-adrenergic blockade nor by vasopressin blockade but was blocked by ablation of the renin-angiotensin axis with enalapril. Like cardiogenic shock, hemorrhagic shock generates selective mesenteric ischemia by producing a disproportionate mesenteric vasospasm that is mediated primarily by the renin-angiotensin axis.
Topics: Animals; Blood Pressure; Enalapril; Female; Hemodynamics; Male; Phenoxybenzamine; Regional Blood Flow; Shock, Hemorrhagic; Splanchnic Circulation; Swine; Vasoconstriction
PubMed: 10774614
DOI: 10.1097/00024382-200004000-00003 -
Developmental Neuroscience 2009The pathophysiology of the effects of cocaine on fetal development has been described along 2 major pathways: neurochemical effects and vasoconstrictive effects.... (Review)
Review
The pathophysiology of the effects of cocaine on fetal development has been described along 2 major pathways: neurochemical effects and vasoconstrictive effects. Following a summary of these effects, we suggest a 'third pathophysiology' in which altered fetal programming affects the acute and long-term adverse effects of in utero cocaine exposure. We describe how cocaine as a stressor alters the expression of key candidate genes, increasing exposure to catecholamines and fetal cortisol-altering neuroendocrine (hypothalamic-pituitary-adrenal axis) activity, leading to infant behavioral dysregulation, poor behavioral control and emotion regulation during childhood and phenotypes that confer vulnerability to substance use in adolescence. This model is discussed in relation to follow-up studies of the effects of in utero cocaine exposure and maturational changes in brain development.
Topics: Animals; Behavior; Brain Chemistry; Cocaine-Related Disorders; Female; Fetus; Humans; Pregnancy; Prenatal Exposure Delayed Effects; Vasoconstriction
PubMed: 19372684
DOI: 10.1159/000207491