Regional blood flow responses to vasodilators and inotropes in congestive heart failure.
Regional blood flow and the distribution of cardiac output is an important aspect of the pathophysiology and pharmacology of human congestive heart failure. This study presents the cumulative experience and data from our laboratories with specific reference to (1) the regional blood flow responses, some rather unique, to various vasodilators and inotropes in patients with congestive heart failure (CHF), and (2) the pharmacophysiologic conclusions and concepts that have evolved from these data. Certain drugs and drug groups evoke rather consistent changes in the blood flow of certain organ systems in CHF. Renal blood flow is augmented by hydralazine, an effect that persists with chronic administration. The converting enzyme inhibitors, captopril and enalapril, increase renal blood flow; this implies that the renin-angiotensin II-aldosterone axis plays a major role in modifying renal blood flow and regional blood flow distribution in human CHF. Nitrates either reduce or do not change renal blood flow. Augmentation of hepatic-splanchnic blood flow occurs after first-dose alpha 1-adrenoceptor blockade suggesting that alpha-adrenergic agonism plays an important role in modifying hepatic-splanchnic flow and the regional distribution of cardiac output in CHF. A number of drugs and drug groups increase limb blood flow (e.g., dobutamine, dopexamine, intravenous nitrates, nitroprusside, hydralazine and nifedipine). With respect to regional blood flow and the distribution of cardiac output in CHF, major differences have been shown to exist between drug groups, between drugs within a group and between different doses of a drug. Certain agents can cause a redistribution of systemic flow without changing cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001775:Blood Circulation / Q000187:drug effects*; D002302:Cardiac Output / Q000187:drug effects; D002316:Cardiotonic Agents / Q000494:pharmacology*; D002395:Catecholamines / Q000494:pharmacology; D002396:Catechols / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology / Q000502:physiology; D005121:Extremities / Q000187:drug effects; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D008102:Liver Circulation / Q000187:drug effects; D009566:Nitrates / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D012079:Renal Circulation / Q000187:drug effects; D013152:Splanchnic Circulation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology*
D000317:Adrenergic alpha-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002316:Cardiotonic Agents; D002395:Catecholamines; D002396:Catechols; D009566:Nitrates; D010726:Phosphodiesterase Inhibitors; D014665:Vasodilator Agents; D009599:Nitroprusside; D004298:Dopamine