Effect of T-2 toxin on regional blood flow and vascular resistance in the conscious rat

Abstract

Effect of T-2 Toxin on Regional Blood Aow and Vascular Resistance in the Conscious Rat. SIREN, A.-L.. AND FEUERSTEIN, G. (1986). Toxico/. App/. Pharmaco/. 83, 438-444. The acute effect ofT-2 toxemia on local blood flow and vascular resistance in hindquarter. mesenteric. and renal vascular beds was continuously measured by the directional pulsed Doppler technique in conscious, male Sprague-Dawley rats. Intravenous injection ofT-2 toxin (I mg/kg) in the conscious rat reduced blood flow and increased vascular resistance in all blood vessels studied but had no significant effect on mean arterial pressure or heart rate. The blood flow in hindquarters gradually decreased to a minimum of -77 ± 9% (mean ±SE) 6 hr after the toxin injection. The hindquarter vascular resistance concomitantly increased to a maximum value of + 323 ± 69% above thc resistance before toxin administration. Mesenteric and renal blood flow initially increased (slightly) and then gradually decreased. The maximum drop of blood flow, -90 ± 13% and -76 ± 13%for the mesenteric and renal vascular beds, respectively, was achieved 4 hr after T-2 toxin injection and the blood flow values remained low for up to 6 hr. Simultaneously with the impairment of blood flow the mesenteric and renal vascular resistance increased to reach the maximal values of +404 ± 99% and +556 ± 15%, respectively. ln addition, plasma renin activity was markedly elevated (+653 ± 160%) at the time of reduced renal blood flow. lntravenous injection of the same value ofvehicle ( 10% ethano1 in saline) had no significant effect on any ofthe cardiovascular variables studied. Two of five rats in the T-2 toxin-treated group died within 5 hr after the T-2 toxin injection and only one animal survived 24 hr while all the control animals survived over 24 hr. The results suggest that strong vasoconstriction in skeletal muscle. mesenteric, and renal vascular beds Ieads to impairment oflocal blood flow. The ischemia in vital argans tagether with the earlier reported decrease in cardiac output by T -2 toxin might then be the cause of rapid death in acute T-2 toxemia.

Cardiovascular effects of anatoxin-A in the conscious rat

“…Vascular resistance was calculated by dividing the mean arterial pressure by blood velocity (Doppler shift in kilohertz) as earlier described (Haywood et a/.. 1981;Siren et al. 1988;Siren and Feuerstein, 1986). Changes in blood flow and vascular resistance are expressed as a percentage of control values.…”

Effects of T-2 mycotoxin on gastrointestinal tissues: A Review ofin vivo andin vitro models

“…Prostaglandins are known to act peripherally to accelerate gastric emptying and small intestine transit (Ruvcart and Rush 1984), and to stimulate intestinal motility (Fargeas et al 1984). Disturbances of gastrointestinal motility by T-2 mycotoxin may be in part due to changes in mesenteric blood flow (Lundeen et al 1986;Siren and Feuerstein 1986). Another trichothecene, fusarenon-X, has been found to increase small intestinal propulsion and to inhibit spontaneous peristalsis (Matsuoka et al 1979).…”

Acute T-2 Intoxication: Physiologic Consequences and New Therapeutic Approaches.

“….... -stimulation of the sympatho-adrenomedullary system was evidenced by TA8 elevated circulating levels of norepinephrine, epinephrine and dopamine. ,.iced Furthermore, significant neuroendocrine derangements were noted by elevated circulating levels of vasopressin and selected prostanoids (e.g., prostacyclin but not LTC 4 or TXA 2 ).…”