Biomedical subjects

F Kozma

Publications and source records attributed to F Kozma.

5 recordsLinked to original sources

PubMed1999

Contribution of endogenous carbon monoxide to regulation of diameter in resistance vessels.

Endogenous carbon monoxide was proposed to subserve vasodepressor functions. If so, inhibition of heme oxygenase may be expected to promote vascular contraction. This hypothesis was examined in large and small arteries and in isolated first-order gracilis muscle arterioles of rat. The heme oxygenase inhibitors chromium mesoporphyrin (CrMP) and cobalt protoporphyrin (0.175-102 micromol/l) decreased the diameter of pressurized (80 mmHg) gracilis muscle arterioles, whereas magnesium protoporphyrin, a weak heme oxygenase inhibitor, did not. CrMP also elicited development of isometric tension in the muscular branch of the femoral artery but not in the aorta or femoral artery. Arteriolar constrictor responses to CrMP varied in relation to the intravascular pressure, were blunted in preparations exposed to exogenous carbon monoxide (100 micromol/l), and were unaffected by an endothelin receptor antagonist. Importantly, CrMP amplified the constrictor response to increases of pressure in gracilis arterioles. Accordingly, the constrictor effect of heme oxygenase inhibitors is attributable to magnification of myogenic tone due to withdrawal of a vasodilatory mechanism mediated by endogenous carbon monoxide. The study suggests that the vascular carbon monoxide system plays a role in the regulation of basal tone in resistance vessels.

Animals↗

PubMed1999

Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions.

Carbon monoxide (CO) is a pollutant commonly recognized for its toxicological attributes, including CNS and cardiovascular effects. But CO is also formed endogenously in mammalian tissues. Endogenously formed CO normally arises from heme degradation in a reaction catalyzed by heme oxygenase. While inhibitors of endogenous CO production can raise arterial pressure, heme loading can enhance CO production and lead to vasodepression. Both central and peripheral tissues possess heme oxygenases and generate CO from heme, but the inability of heme substrate to cross the blood brain barrier suggests the CNS heme-heme oxygenase-CO system may be independent of the periphery. In the CNS, CO apparently acts in the nucleus tractus solitarii (NTS) promoting changes in glutamatergic neurotransmission and lowering blood pressure. At the periphery, the heme-heme oxygenase-CO system can affect cardiovascular functions in a two-fold manner; specifically: 1) heme-derived CO generated within vascular smooth muscle (VSM) can promote vasodilation, but 2) its actions on the endothelium apparently can promote vasoconstriction. Thus, it seems reasonable that the CNS-, VSM- and endothelial-dependent actions of the heme-heme oxygenase-CO system may all affect cardiac output and vascular resistance, and subsequently blood pressure.

Blood Pressure↗

PubMed1997

Role of carbon monoxide in heme-induced vasodilation.

We investigated the effects of carbon monoxide and heme-L-lysinate on the diameter of isolated, pressurized gracilis muscle arterioles. Both agents increased arteriolar diameter. The vasodilatory effect of heme-L-lysinate, but not of carbon monoxide was prevented by an inhibitor of heme oxygenase. Hence, heme-L-lysinate-induced vasodilation appears to be mediated by a product of vascular heme metabolism, presumably carbon monoxide. This implies that vascular formation of carbon monoxide may subserve a vasodilatory function.

Animals↗

PubMed1967

Behavioral control by an imprinted stimulus: long-term effects.

Newly hatched ducklings were exposed to imprinting procedures and subsequently trained to peck a key by presenting the imprinting stimulus as the reinforcing (response-contingent) event. Individual ducklings then lived in the apparatus under an arrangement in which each peck produced a 15-sec stimulus presentation. For all ducklings, key-pecks tended to occur in bursts, and as the duckling matured, burst length decreased and the interval between bursts increased. However, even when subjects were 60 days old, some responses still occurred.

Animals↗

PubMed1966

Behavioral control by an imprinted stimulus.

Newly hatched ducklings were exposed to imprinting procedures and subsequently trained to peck a key by presenting the imprinting stimulus as the reinforcing (response contingent) event. It was found that the key peck was learned only when imprinting procedures were initiated during the first 6 to 8 hr after hatch. Additional studies revealed that: (1) the duckling's distress vocalizations were reduced in the presence of the imprinting stimulus and enhanced in its absence; (2) when the ducklings had constant access to the imprinted stimulus (via a key peck), pecking responses occurred in bursts and relatively few distress vocalizations occurred; (3) the initial effect of extinction procedures was an increase in key peck rate. When, however, repeated key pecks failed to produce the imprinted stimulus, distress vocalization ensued and peck rate declined; (4) both the presentation of an unfamiliar mechanical figure and delivery of electrical shock enhanced distress vocalization and key pecks; (5) for some ducklings, certain familiar objects in the environment influenced distress calls in a manner comparable to the imprinted stimulus in that distress calls increased when these objects were removed.

Journal Article↗