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The contribution of carbon monoxide (CO) to the acute cardiovascular effects of smoking is not clear. Using a double-blind, randomized, vehicle-controlled study design, we examined the sympathetic and vascular responses to modest increases in carboxyhemoglobin in 10 healthy humans. We measured muscle sympathetic nerve activity (microneurography), forearm blood flow (plethysmography), heart rate, blood pressure, and minute ventilation at baseline and during 60 minutes of CO inhalation (1000 ppm during the first 30 minutes and 100 ppm during the last 30 minutes). The same measurements were made in a vehicle session (room air inhalation) on a separate day. During the first 30 minutes of CO inhalation, carboxyhemoglobin levels increased progressively from 0.2 +/- 0.1% to 8.3 +/- 0.5% and were maintained at about this level for a further 30 minutes. Forearm vascular resistance did not change with CO but increased slightly with vehicle; the effects of CO on muscle sympathetic nerve activity, forearm blood flow, blood pressure, heart rate, and minute ventilation were not significantly different from the effects of vehicle. Modest increases in carboxyhemoglobin levels equivalent to those resulting from cigarette smoking are unlikely to contribute to the acute sympathetic and hemodynamic effects of smoking in healthy humans.

Acute increases in plasma insulin produce both sympathoexcitation and vasodilation in normal young adults. Aging is associated with insulin resistance and may alter the sympathetic or the vascular responses to insulin. Therefore, we assessed sympathetic and vascular responses to acute physiological increases in plasma insulin levels in 10 healthy, normotensive elderly (65+/-2 years) and 12 normal young (27+/-1 years) subjects matched for body mass index (25+/-1 kg/m2 in both groups). We measured muscle sympathetic nerve activity (microneurography), FBF (plethysmography), heart rate, and blood pressure and calculated forearm vascular resistance and insulin sensitivity (M value) during a 90-minute hyperinsulinemic/euglycemic clamp. M values were 4.3+/-0.4 mg x kg(-1) x min(-1) in the elderly and 8.4+/-1.4 mg x kg(-1) x min(-1) in the young subjects (P<.05). Baseline muscle sympathetic nerve activity was higher in the elderly subjects (33+/-3 versus 15+/-2 bursts per minute, P<.05); however, the absolute and percent increases in muscle sympathetic nerve activity were smaller in the elderly than in the young subjects (+10+/-1 versus +15+/-1 bursts per minute, or +37+/-11% versus +110+/-16%, P<.05). Forearm vascular resistance decreased with insulin from 46+/-2 to 31+/-3 units in the young but increased with insulin in the elderly subjects from 37+/-3 to 47+/-7 units (P<.05). Heart rate increased in young but not in elderly subjects. Insulin did not change blood pressure in either group. In conclusion, as opposed to vasodilation in young adults, insulin caused vasoconstriction in healthy elderly individuals. The failure of the vasodilator action of insulin in the elderly may permit even modest insulin-induced sympathoexcitation to elicit vasoconstriction. We speculate that the vasoconstrictor response to insulin may further potentiate insulin resistance in the elderly.

Objective: To determine sympathetic and vascular responses to modest increases in plasma insulin level., Background: Most studies of sympathetic and vascular actions of insulin have evaluated high plasma insulin levels ( > 50 microU/ml). Those levels increase sympathetic nerve activity but also cause vasodilation. Hypertension and obesity are associated with only modestly elevated fasting insulin levels., Methods: We investigated the effects of a 90 min low-dose hyperinsulinemic euglycemic clamp on muscle sympathetic nerve activity (microneurography), forearm vascular resistance (plethysmography), heart rate, blood pressure and central venous pressure. Insulin and vehicle sessions were performed in 12 normal subjects., Results: Plasma insulin levels were elevated from values of 10 +/- 2 in the fasting state to 25 +/- 3 microU/ml during insulin infusion. Insulin levels did not change during vehicle administration. Muscle sympathetic nerve activity increased from 16 +/- 2 to 25 +/- 3 burst/min during the insulin session and did not change during vehicle administration. In contrast to muscle sympathetic nerve activity, forearm vascular resistance did not change during insulin administration (from 50 +/- 3 to 51 +/- 4 U). Forearm vascular resistance tended to fall during vehicle administration (from 45 +/- 2 to 37 +/- 3 U). There were no changes in heart rate, blood pressure and central venous pressure that could be attributed to insulin., Conclusions: Modest elevations of plasma insulin levels produce sympathetic activation similar to that caused by high levels, but, in contrast to high levels modest elevations in plasma insulin level do not decrease forearm vascular resistance. The present findings suggest a dissociation between sympathoexcitatory and vascular actions of insulin at low plasma levels.

This is a case report of heparin-associated thrombocytopenia syndrome (white clot syndrome). An 81-Year-old patient was treated with sodium-heparin for proximal deep-venous thrombosis and pulmonary embolism. During administration of heparin, the platelet count decreased to a nadir of 27/nl on day 14 after initiation of this therapy. We also observed a recurrence of pulmonary embolism as well as arterial thromboembolism in the right arm and the right leg. After immediate discontinuation of heparin therapy and change of anticoagulation to oral anticoagulants with overlapping administration of a low molecular weight heparin and application of immunoglobulins, we observed total recanalization of the arterial occlusions, normalization of lung-perfusion scan and rapid recovery of the platelet count.