Transient vasodilation

In the vascular system, endothelial ETB receptors mediate a transient vasodilation, whereas ETA receptors cause a long-lasting vasoconstriction. The role of ETb receptors expressed on smooth muscle cells... 

Alcohol can affect the metabolism of trichloroethylene. This is noted in both toxicity and pharmacokinetic studies. In toxicity studies, simultaneous exposure to ethanol and trichloroethylene increased the concentration of trichloroethylene in the blood and breath of male volunteers (Stewart et al. 1974c). These people also showed "degreaser s flush"—a transient vasodilation of superficial skin vessels. In rats, depressant effects in the central nervous system are exacerbated by coadministration of ethanol and trichloroethylene (Utesch et al. 1981). 

ET-1 stimulates cyclooxygenase (COX) which catalyzes the formation of prostacyclin from arachidonic acid. Prostacyclin then binds to and activates the isoprostanoid receptor (IP) on VSM. ET-1 also activates ET-B which stimulates endothelial nitric oxide synthease (eNOS) to produce NO from L-arginine. Both prostacyclin and NO are potent vasodilators of VSM (relaxation). Additionally, ET-1 binds to the ETb receptors on the endothelium of pulmonary smooth muscle and stimulate the formation of NO, which produces vasodilation in the absence of smooth muscle ETa and ETb receptor activation. This receptor distribution helps to explain the phenomenon that ET-1 administration causes transient vasodilation (initial endothelial ETb activation) and hypotension, followed by prolonged vasoconstriction (smooth muscle ETa and ETb activation) and hypertension. 

Excessive nicotinic acid can cause transient vasodilation with hypotension... 

Royal jelly exhibited a transient vasodilating effect on dog femoral artery, which was due to its acetylcholine constituent. Peptides present in royal jelly were found to possess antihypertensive effect when orally administered in hypertensive rats for 28 days. A similar effect was observed in rats administered a royal jelly protein hydrolysate, and the antihypertensive effect was attributed to the inhibition of ACE. " ... 

In low doses, inhaled NO may have a beneficial therapeutic effect, since NO in the inspired air leads to pulmonary vasodilation. In persistent pulmonary hypertension of the newborn, NO inhalation has already been used with some success. NO inhalation as the treatment for acute respiratory distress syndrome, however, has been disappointing. Only transient improvements of oxygenation were detected and the outcome of placebo-controlled trials did not show any improvement... 

The majority of patients treated for primary and secondary syphilis experience the Jarisch-Herxheimer reaction after treatment, characterized by flu-like symptoms such as transient headache, fever, chills, malaise, arthralgia, myalgia, tachypnea, peripheral vasodilation, and aggravation of syphilitic lesions. 

Advise patients that initiation of treatment and (to a lesser extent) dosage increases may be associated with transient symptoms of dizziness or lightheadedness (and rarely syncope) within the first hour after dosing. Thus, during these periods, avoid situations such as driving or hazardous tasks, where symptoms could result in injury. In addition, vasodilatory symptoms often do not require treatment, but it may be useful to separate the time of dosing of carvedilol from that of the ACE inhibitor or to temporarily reduce the dose of the ACE inhibitor. Do not increase the dose of carvedilol until symptoms of worsening heart failure or vasodilation have been established. 

Antiadrenergic] Uses HTN Action Centrally acting antihypCTtensive Dose Adults. 250-500 mg PO bid-tid (max 2-3 g/d) or 250 mg-1 g IV q6-8h Peds. 10 mg/kg/24 h PO in 2-3 doses (max 40 mg/kg/24 h q6-12h) or 5-10 mg/kg/dose IV q6-8h to total dose of 20 0 mg/kg/24 h X in renal insuff/elderly Caution [B (PO), C (IV), +] Contra Liver Dz MAOIs Disp Tabs, inj SE Discolors urine initial transient sedation/drowsiness frequent, edema, hemolytic anemia, hepatic disorders Interactions T Effects W/ anesthetics, diuretics, levodopa, Li, methotrimeprazine, thioxanthenes, vasodilators, verapamil T effects OF haloperidol, Li, tolbutamide effects W/amphetamines, Fe, phenothiazine, TCAs ... 

The effects of phenytoin on the cardiovascular system vary with the dose, the mode and rate of administration, and any cardiovascular pathology. Rapid administration can produce transient hypotension that is the combined result of peripheral vasodilation and depression of myocardial contractility. These effects are due to direct actions of phenytoin on the vascular bed and ventricular myocardium. If large doses are given slowly, dose-related decreases in left ventricular force, rate of force development, and cardiac output can be observed, along with an increase in left ventricular end-diastolic pressure. 

The hemodynamic effects of diazoxide are similar to those of hydralazine and minoxidil. It produces direct relaxation of arteriolar smooth muscle with little effect on capacitance beds. Since it does not impair cardiovascular reflexes, orthostasis is not a problem. Its administration is, however, associated with a reflex increase in cardiac output that partially counters its antihypertensive effects. Propranolol and other -blockers potentiate the vasodilating properties of the drug. Diazoxide has no direct action on the heart. Although renal blood flow and glomerular filtration may fall transiently, they generally return to predrug levels within an hour. 

Isoflurane (Forane) is a structural isomer of enflurane and produces similar pharmacological properties some analgesia, some neuromuscular blockade, and depressed respiration. In contrast, however, isoflurane is considered a particularly safe anesthetic in patients with ischemic heart disease, since cardiac output is maintained, the coronary arteries are dilated, and the myocardium does not appear to be sensitized to the effects of catecholamines. Also, blood pressure falls as a result of vasodilation, which preserves tissue blood flow. Isoflurane causes transient and mUd tachycardia by direct sympathetic stimulation this is particularly important in the management of patients with myocardial ischemia. 

The salicylates are also potent antipyretic agents, with the exception of diflunisal, which is only weakly active. Aspirin acts at two distinct but related sites. It decreases prostaglandin-induced fever in response to pyrogens and induces a decrease in interleukin-1 modulation of the hypothalamic control of body temperature. Thus, the hypothalamic control of body temperature returns, vasodilation occurs, heat dissipates, and fever decreases. Other uses of aspirin include inhibition of platelet aggregation via inhibition of thromboxanes, which has been shown to decrease the incidence of blood clots, myocardial infarction, and transient ischemic attacks. 

Arthralgia, vasodilation, anxiety, hypertonia, nausea, transient chest pain, dyspnea, flu-like symptoms, rash, pruritus Occasional (17%-10%)... 

A characteristic triphasic response is observed after intravenous injection. The early transient fall in blood pressure is due to stimulation of chemoreceptors. The second phase, pressor effect is due to vasoconstriction. The final depressor phase is due to vasodilator action on the skeletal muscle. 

Organic kallikrein has been used to induce peripheral vasodilation and itfrrfa in blood pressure. However, in therapeutic use these drugs did not succeed because the enzyme administered as well as the Idnin formed is relatively quickly inactivated in the circulation whereby the action becomes transient. 

The antiplatelet/antithrombotic activity of dipyridamole has been demonstrated in laboratory and in animal models, and has been shown to inhibit platelet aggregation and vessel-wall thrombogenesis [9-11]. Dipyridamole has been given either alone or with aspirin in the management of myocardial infarction and stroke. For the secondary prevention of stroke or transient ischemic attack, the drug may be given as a modified-release preparation in a dose of 200 mg twice daily. Dipyridamole administered intravenously results in a marked coronary vasodilation and is used in stress testing in patients with ischemic heart disease [5]. 

Q7 The mechanisms which trigger migraine remain controversial. The underlying pathophysiology could be due to vasoconstriction of the cerebral arteries, causing transient ischaemia. This would be followed by compensatory vasodilation of the cerebral blood vessels to protect the ischaemic areas. This vasodilation may lead to an increase in intracranial pressure, which causes a severe headache. These events may be followed by changes in nerve activity and neurotransmitter levels. Inflammatory components are also likely to be involved in the pathology of this condition. 

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