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Biomedical subjects

J D Coffman

Publications and source records attributed to J D Coffman.

At least 55 records · Page 3Linked to original sources
PubMed1982

Peripheral arterial and venous responses to acetylstrophanthidin in patients with acute myocardial infarction.

The peripheral arterial and venous responses to rapidly active acetylstrophanthidin (rather than the much slower digitalis) were studied in patients with acute myocardial infarction without congestive heart failure. In eight control patients placebo did not change mean blood pressure (BP), calf blood flow (CBF), calf vascular resistance (CVR), or calf venous volume (CVV). Seventeen patients received 10 mg IV acetylstrophanthidin. In these patients BP increased 5.3%, CBF decreased 18.2%, and CVR increased 29.2%. Venous capacitance was not changed. Acetylstrophanthidin induced no significant change in cardiac output, systemic vascular, resistance, pulmonary capillary wedge pressure, or right atrial pressure. In patients with acute myocardial infarction not complicated by congestive heart failure, digitalis may promote limb vasoconstriction and increase blood pressure, but it does not adversely affect cardiac function.

Electrocardiography↗
PubMed1981

Effect of morphine on limb capacitance and resistance vessels.

1. The actions of 15 mg of intravenous morphine on hand and forearm capacitance and resistance vessels were studied with venous occlusion plethysmography. 2. In contrast to a 5% increase in forearm venous volume, intravenous morphine caused a 26% decrease in hand venous volume. This hand venoconstriction was confirmed by finding an increase in hand venous tone. The effects of morphine on hand veins were attenuated by intraarterial phentolamine and blocked by intravenous naloxone. 3. Whereas morphine had no significant effect on forearm resistance vessels, it caused a 70% reduction in hand vascular resistance. 4. Intra-arterial morphine had no local action on hand capacitance or resistance vessels. 5. Though the contrasting actions of morphine on hand and forearm capacitance vessels resulted in no important change in limb venous capacitance, the large reduction of cutaneous vascular resistance may contribute to haemodynamic benefit in patients with pulmonary oedema.

Adult↗
PubMed1981

Beta-adrenergic vasodilator mechanism in the finger.

The digital vasospastic phenomena, which are induced by beta-adrenergic-blocking agents, suggest a beta-adrenergic finger vasodilator mechanism. We measured fingertip total blood flow with venous occlusion plethysmography and studied nutritional blood flow with Na131I clearance. During fingertip vasoconstriction caused by branchial artery infusion of norepinephrine or angiotensin, intra-arterial isoproterenol caused a sustained increase in fingertip total blood flow. Furthermore, propranolol significantly potentiated the vasoconstriction caused by intra-arterial norepinephrine and attenuated the vasodilator action of isoproterenol. No change in branchial artery blood pressure occurred to explain the changes in fingertip blood flow. Isoproterenol did not change nutritional flow, implying beta-adrenergic vasodilation solely of the fingertip arteriovenous shunts. When fingertip vasoconstriction was induced by reflex sympathetic nerve action during environmental cooling and mental stress, or by norepinephrine release from sympathetic nerves caused by intra-arterial tyramine infusion, isoproterenol and propranolol had no effect on fingertip total blood flow. This effect is probably specific for the beta-receptor agonist, since intra-arterial histamine caused a large increase in finger blood flow during environmental cooling. We conclude that there is a beta-adrenergic vasodilator mechanism in human digital arteriovenous shunts that may be humorally activated, but which has no apparent functional role in modulating sympathetic vasoconstriction. Our results suggest a spatial dissociation of the effector sites for vasoactive humoral agents and sympathetic vasoconstrictor nerves.

Adrenergic beta-Antagonists↗
PubMed1980

Naloxone reversal of morphine-induced peripheral vasodilatation.

Naloxone is used to reverse the central nervous system amd respiratory depressant effects of morphine, but it is not known whether the narcotic antagonists also reverses the peripheral vasodilatation. Since the cutaneous vasodilatation induced by morphine may be hemodynamically important in cardiac patients, we studied the effect of naloxone on the morphine-induced vasodilatation in the cutaneous vascular bed of the hand using venous occlusion plethysmography. Morphine, 15 mg intravenously, caused a 70% reduction in hand vascular resistance. Given 18 min after morphine, naloxone, 0.8 mg intravenously, completely reversed the vasodilatation in 12 to 17 min. Saline placebo given 18 min after morphine induced no reversal; the vasodilatation lasted at least 35 min. Naloxone acts as a pure antagonist to these actions of morphine, since it has no actions on blood flow in the hand when given alone.

Adult↗
PubMed1975

Venous flow velocity, venous volume and arterial blood flow.

The relationship of arterial blood flow and venous volume to venous flow velocity was studied in normal subjects. The effects of current modes of treatment in venous thrombosis and of a vasodilator drug on venous flow velocity were also investigated. Total calf flow and venous volume were measured by venous occlusion plethysmography while venous flow axial velocity was determined by the transit time of 131-I albumin from calf to inguinal region. Local intravenous epinephrine administration induced venoconstriction and increased venous flow velocity. Intra-arterial isoproterenol and angiotensin increased and decreased arterial flow, respectively, with no change in venous flow velocity of volume, but local heat increased arterial flow and venous flow velocity with no change in venous volume. Local cold, despite venoconstriction, decreased venous flow velocity accompanied by a decreased arterial flow. Intravenous heparin did not affect venous flow velocity. Intravenous but not oral nylidrin increased venous flow velocity. Therefore venous flow velocity can be significantly increased by venocontriction, by large increases in arterial flow (local heat), and by a parenteral vasodilator drug. These experiements indicate that there is a basis for applying heat but not cold in the prevention and treatment of venous thrombosis.

Adult↗
PubMed1975

Vasodilator drugs in peripheral vascular disease.

The use of vasodilator drugs in peripheral vascular disease is reviewed. Discussed are actions and efficacy of direct-acting drugs such as isoxsuprine, papaverinek niacin and cyclandelate; the beta-receptor stimulating drug, nylidrin; and drugs which affect the sympathetic nervous system, such as tolazoline, reserpine, guanethidine, methyldopa, ergot alkaloids and alcohol. Both animal and clinical studies reveal little evidence of the effectiveness of vasodilator drugs in the treatment of obstructive arterial disease. In some patients with vasospastic diseases, vasodilators which act upon the sympathetic nervous system (reserpine and guanethidine) may have an ameliorating effect by increasing cutaneous capillary blood flow.

Arterial Occlusive Diseases↗