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At least 199 records · Page 11Linked to original sources
PubMed1976

Sodium nitroprusside: pharmacology, toxicology and therapeutics.

Sodium nitroprusside is a potent, effective, and readily reversible direct vasodilating agent. It is broken down by hemoglobin into cyanide, which is in part detoxified by liver and kidney to thiocyanate. Some cyanide, especially in nitroprusside- "resistant" individuals who need large amounts of the drug, appears to remain free to cause cyanide poisoning. Patients requiring inordinate amounts probably should not continue to receive the drug, although maximum dosage limits for long-term therapy are not established. Blood thiocyanate levels do not indicate the extent to which free cyanide is limiting oxygen utilization in essential tissue, nor do blood cyanide levels. Metabolic acidosis, elevated lactate levels, elevated lactate/pyruvate ratios, and elevated mixed venous blood oxygen content are at present the best indications of the presence of cyanide poisoning during nitroprusside administration. Nitroprusside appears useful for induction of hypotension during surgery, and for treatment of hypertensive emergencies from all causes, although continuance for more than a few days is probably unwise. The reductions of cardiac afterload and ventricular filling pressure by nitroprusside appear useful in treatment of severe myocardial failure or infarction, but studies of myocardial cyanide toxicity are needed before complete acceptance of this therapy is warranted. Initial dose rates between 0.5 and 1.5 mug/kg/min are recommended only as starting points for very careful titration. Total projected intra-operative dosage should be calculated as quickly as possible and should not exceed 3-3.5 mg/kg. It is hoped that future studies will reveal the maximum dose of nitroprusside that can safely be metabolized in a 24-hour period, and may indicate that cofactors of rhodanase such as thiosulfate, or cobalamins such as hydroxocobalamin, can be administered with nitroprusside to prevent cyanide poisoning.

Anesthesia, General↗
PubMed1998

[Raynaud's phenomena: diagnostic and treatment study].

Raynaud's phenomenon is a common paroxystic vasomotor disorder. Diagnosis is easily made based on white fingers caused by cold. Aetiological evaluation must distinguish between functional disorders (primary Raynaud's phenomenon or Raynaud's disease) and secondary Raynaud's phenomenon. Initially, physical examination as well as nailfold capillary microscopy are sufficient for the diagnosis of bilateral Raynaud's phenomenon. Prescription of other investigations is guided by the results of this first evaluation. Progressive systemic sclerosis is the first hypothesis if the bilateral vasomotor disorder does not satisfy the criteria for primary Raynaud's phenomenon. Unilateral Raynaud's phenomenon is much less common and always secondary to local or regional vascular disease. Treatment of Raynaud's phenomenon must be adapted to the level of discomfort and to the cause of the vasomotor disorder. Prescription of drugs must be restricted to the most serious cases.

Capillaries↗
PubMed1999

In vitro response of large colon arterial and venous rings to vasodilating drugs in horses.

OBJECTIVE: To determine in vitro vasomotor response of equine large colon arterial and venous rings with and without endothelium to vasodilator drugs, including dopamine (DOP), dopexamine (DPX), acepromazine (ACE), isoxsuprine (ISX), and nifedipine (NFP). ANIMALS: 7 adult horses. PROCEDURE: Relaxation of large colon arteries and veins in response to vasodilating drugs was determined by measuring the change in tension of vessel rings when exposed to a cumulative concentration range (10(-8) to 10(-4)M) of each drug. Vessel rings, with and without endothelium, were mounted in organ baths, attached to a transducer, and contracted with norepinephrine (NE). Cumulative concentration-response relationships, percentage maximal relaxation, and EC50 (concentration of drug required to relax the NE-induced contracted tissue to 50% of its contracted state) values were calculated. RESULTS: There were significant differences among drugs for EC50 (ACE = ISX < NFP) and percentage maximal relaxation (ACE = ISX > NFP = DPX > DOP) values in veins. Endothelium removal from veins had no significant effect. There were no differences in EC50 values for arteries; however, percentage maximal relaxation was significantly different among drugs (ACE = ISX = NFP > DPX = DOP). Endothelial removal resulted in higher EC50 and lower percentage maximal relaxation values, compared with endothelium-intact arteries. CONCLUSION AND CLINICAL RELEVANCE: ACE and ISX were the most potent and efficacious drugs evaluated and could potentially be used to improve blood flow after correction of large-colon volvulus. Dopamine cannot be recommended because of its biphasic response and potential to further decrease blood flow. Endothelium removal altered the vasodilatory responses of colonic arterial rings, but did not affect venous rings.

Acepromazine↗
PubMed1982

The effects of progestins on vasomotor flushes.

For patients with severe vasomotor flushes who require therapy but for whom estrogens are contraindicated, progestins can be tried. These drugs appear to offer the benefit of a reduction of vasomotor flushes without such unwanted side effects as the increased risk of contracting endometrial cancer. However, progestins cannot replace estrogens universally since there is no evidence that they prove effective against osteoporosis-related fractures and genital atrophy. Nonetheless, as more physicians begin to add medroxyprogesterone acetate to the estrogen regimen to reduce the risk of endometrial hyperplasia, it might be that a lower dose of estrogen will be necessary to relieve flushes. We hope that this additive effect exists, although it has not yet been shown. Whether or not the addition of medroxyprogesterone will carry risks or counteract the beneficial effects of estrogens on such disorders as osteoporosis remains to be elucidated. What is clear from the medroxyprogesterone and estrogen studies is that whenever these drugs are discontinued, the vasomotor flushes can recur, albeit with less intensity and less frequency.

Administration, Oral↗
PubMed1985

[Hyperreflectoric rhinopathy].

Research in molecular biology in the past few years offers new views on vasomotor rhinitis. The key role of mediator substances which contain the mast cell and which, after degranulation, are active immediately by histamine release or act in a delayed manner (eg. leucotriene), is discussed, as well as the "liberofunction" of the neurotransmitter acetylcholine. The contribution to vasomotor rhinitis of other humoral systems, the kinine system and complement factors are also taken into account. The biopharmacological actions of the effector systems of the nasal mucosa (vessels, exocrine glands, nociceptors) are also analyzed. Using clinical examples the differentiation between humoral or neural reflex mediated hyperreflexia is worked out related to the classic triad of sneezing, profuse nasal discharge, nasal obstruction. The causes of vasomotor rhinitis (exogenous endogenous and drugs) are examined in the light of their pathophysiological importance. The differential diagnosis must cover allergic rhinopathy as well as the different kinds of rhinitis medicamentosa, the most important of which are discussed. Drugs which can help are discussed as well as continuous physical therapy.

Acetylcholine↗
PubMed2001

Does it make sense to develop new centrally acting cardiovascular drugs?

1. The autonomic nervous system plays a pivotal role in modulating all the components of the cardiovascular regulation. Therefore, one can assume that drugs targeting this system may be useful in the management of several cardiovascular diseases. 2. Drugs acting on central nervous system centres seem to be modulators rather than blockers; as such, they are expected to preserve the contraregulatory processes and to generate only a few side effects. 3. Because the sympathetic nervous system is largely involved in the regulation of vasomotor tone, centrally acting antihypertensive drugs were developed first. 4. Recently, new leader compounds selective for non- adrenergic imidazoline recepetors have been synthetized. Although such drugs have no capacity to activate alpha2-adrenoceptors, they have been proven to be hypotensive. These drugs are expected to be even better tolerated than the currently available centrally active drugs. They may also have additional beneficial effects. 5. Here, the experimental evidence suggesting that such drugs may be useful in the management of some cardiac arrhythmias and/or left ventricular dysfunction will be reviewed.

Animals↗
PubMed1995

[Drug-induced iatrogenic arterial diseases].

Several drugs have been shown to cause vasomotor troubles such as Raynaud's phenomenon, erythromelalgia, vasculitis, livedo reticularis, or acrocyanosis. Vascular symptoms may develop a few weeks or more after drug initiation, particularly when other drugs are associated than can potentiate vascular side effects. In this review, the authors described the main characteristics of drug-induced vasculopathy, particularly those associated with ergotamine derivates, beta blocking agents or antineoplastic chemotherapy.

Arteries↗