Vasoconstrictor drugs

Complex 101 has been shown to reverse the poor response of the artery to vasoconstrictor drugs (508), which is a major clinical problem in the treatment of patients with septic shock. The excessive production of NO appears to be a major contributory factor not only in... 

Autonomic and hormonal control of cardiovascular function. Note that two feedback loops are present the autonomic nervous system loop and the hormonal loop. The sympathetic nervous system directly influences four major variables peripheral vascular resistance, heart rate, force, and venous tone. It also directly modulates renin production (not shown). The parasympathetic nervous system directly influences heart rate. In addition to its role in stimulating aldosterone secretion, angiotensin II directly increases peripheral vascular resistance and facilitates sympathetic effects (not shown). The net feedback effect of each loop is to compensate for changes in arterial blood pressure. Thus, decreased blood pressure due to blood loss would evoke increased sympathetic outflow and renin release. Conversely, elevated pressure due to the administration of a vasoconstrictor drug would cause reduced sympathetic outflow, reduced renin release, and increased parasympathetic (vagal) outflow. 

Albumin is used in combination with vasoconstrictor drugs, such as terlipressin and octreotide, in treating hepatorenal syndrome. Adverse events were reported in four trials, but it was not clear which drug had caused them [l , 2 ]. 

Gluud LL, Christensen K, Christensen E, Krag A. Systematic review of randomized trials on vasoconstrictor drugs for hepatorenal syndrome. Hepatology 201(>, 51(2) 576-84. 

A major use of butyric acid is in the manufacture of cellulose acetate butyrate plastics. They are used as textile fibers and in situations where resistance to heat and sunlight is essential. Calcium butyrate has been used in some leather tanning processes. Butyric acid esters are added as flavors in some soft drinks and chewing gums. Various derivatives of butyric acid are used as vasoconstrictor drugs, in anesthetics, and as antioxidants (Playne 1985). 

Vasoconstrictor. A drug that causes a contraction of the vascular smooth muscle, thus increasing the resistance to blood flow. 

Vasoconstrictors are drugs which increase the tone of smooth muscle cells in the vasculature. They include sympathomimetic amines and certain eicosanoids and peptides (angiotensin, vasopressin, urotensin or en-dothelin). 

Vasopressin is a peptide hormone produced by the hypothalamus and secreted by the posterior pituitary in response to stimulation. Normal stimuli for vasopressin release are hyperosmolarity and hypovolemia, with thresholds for secretion of greater than 280 mOsm/kg and greater than 20% plasma volume depletion. A number of other stimuli, such as pain, nausea, epinephrine, and numerous drugs, induce release of vasopressin. Vasopressin release is inhibited by volume expansion, ethanol, and norepinephrine. The physiological effect of vasopressin is to promote free water clearence by altering the permeability of the renal collecting duct to water. In addition, it has a direct vasoconstrictor effect. Consequently, vasopressin results in water retention and volume restoration. In patients with septic shock, vasopressin is appropriately secreted in response to hypovolemia and to elevated serum osmolarity (R14). 

Another vasoactive substance produced by the endothelium is thromboxane A2 (TxA2). Normally, small amounts of TxA2 are released continuously however, increased synthesis appears to be associated with some cardiac diseases. Synthesized from arachidonic acid, a plasma membrane phospholipid, TxA2 is a potent vasoconstrictor. Furthermore, this substance stimulates platelet aggregation, suggesting that it plays a role in thrombotic events such as myocardial infarction (heart attack). Nonsteroidal anti-inflammatory drugs such as aspirin and ibuprofen block formation of TxA2 and reduce formation of blood clots. 

The answer is d. (Hardman, p T36J The addition of a vasoconstrictor, such as epinephrine or phenylephrine, to certain short-acting, local anesthetics is a common practice in order to prevent the rapid systemic absorption of the local anesthetics, to prolong the local action, and to decrease the potential systemic reactions. Some local anesthetics cause vasodilation, which allows more compound to escape the tissue and enter the blood. Procaine is an ester-type local anesthetic with a short duration of action due to rather rapid biotransformation in the plasma by cholinesterases. The duration of action of the drug during infiltration anesthesia is greatly increased by the addition of epinephrine, which reduces the vasodilation caused by procaine. 

Subcutaneous Route. Drugs given by the SC route are forced into spaces between connective tissues, as with IM injections. Vasoconstrictors and drugs that cause local... 

Cocaine readily penetrates mucous membranes and is an effective topical local anaesthetic that demonstrates intensive vasoconstrictor action. It has stimulant effects on the central nervous system and is a drug of addiction. It causes agitation, dilated pupils, tachycardia, hypertension, hallucinations, hyperthermia, hypertonia, hyperreflexia and cardiac effects. 

Wound healing Because of the inhibitory effect of corticosteroids on wound healing in patients who have experienced recent nasal septal ulcers, recurrent epistaxis, nasal surgery, or trauma, use nasal steroids with caution until healing has occurred. Vasoconstrictors In the presence of excessive nasal mucosa secretion or edema of the nasal mucosa, the drug may fail to reach the site of intended action. In such cases, use a nasal vasoconstrictor during the first 2 to 3 days of therapy. 

Drugs that may be affected by ergot alkaloids include nitrates, 5HTireceptor agonists, and vasoconstrictors. 

Intramuscular and subcutaneous injections are by far the most common means of parenteral drug administration. Because of the high tissue blood flow and the ability of the injected solution to diffuse laterally, drug absorption generally is more rapid after intramuscular than after subcutaneous injection. Drug absorption from intramuscular and subcutaneous sites depends on the quantity and composition of the connective tissue, the capillary density, and the rate of vascular perfusion of the area. These factors can be influenced by the coinjection of agents that alter local blood flow (e.g., vasoconstrictors or vasodilators) or by substances that decrease tissue resistance to lateral diffusion (e.g., hyaluronidase). 

The injection of a vasoconstrictor, which causes an increase in mean arterial blood pressure, results in activation of the baroreceptors and increased neural input to the cardiovascular centers in the medulla oblongata. The reflex compensation for the drug-induced hypertension includes an increase in parasympathetic nerve activity and a decrease in sympathetic nerve activity. This combined alteration in neural firing reduces cardiac rate and force and the tone of vascular smooth muscle. As a consequence of the altered neural control of both the heart and the blood vessels, the rise in blood pressure induced by the drug is opposed and blunted. 

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