scholarly journals STUDIES UPON THE PHYSIOLOGICAL ACTION OF HEMATOPORPHYRIN

1928 ◽  
Vol 47 (4) ◽  
pp. 593-610 ◽  
Author(s):  
Hans Smetana

The results of these observations may be briefly summarized as follows: Feeding of hematoporphyrin to white mice over long periods of time produced no apparent changes in these animals and had no effect upon their sensitivity to light. Albino and slightly pigmented mice and rats injected with hematoporphyrin were protected from the rays of the sun by staining them a blue-black color with Verhoeff's hematoxylin. The dioxyphenylalanine (Dopa) reaction revealed no changes in the cutaneous pigment of animals injected with hematoporphyrin and exposed to sunlight, kept in the dark or diffused daylight. It was therefore assumed that the natural pigment of the skin plays only a physical rôle in protecting animals injected with hematoporphyrin from sunlight. Exposure to sunlight of only the intestine and mesentery of a cat under ether anesthesia, which had been injected with hematoporphyrin, was followed by death of the animal. Repeated injections into white mice of large amounts of blood from guinea pigs in hematoporphyrin shock failed to produce symptoms of hematoporphyrin shock. In a parabiosis experiment, one of a pair of white rats promptly developed characteristic symptoms and died when injected with hematoporphyrin and exposed to sunlight, while the other animal, which was protected from light, but whose circulation had been demonstrated to connect freely with that of its partner, showed no changes during the entire procedure. It has, therefore, been impossible, so far, to demonstrate any substance present in the blood of animals in hematoporphyrin shock which is capable of reproducing this condition in other animals when introduced into the circulation. Injection of hematoporphyrin followed by exposure of the entire animal to sunlight has been found to produce physiological changes in cats similar to those observed in traumatic shock. There promptly occurred a rapid fall of blood pressure to a very low level and marked lowering of body temperature. The venous blood was found to be poor in oxygen, rich in carbon dioxide and to show low carbon dioxide-combining power. The respiration, which first was accelerated, later on became deep and irregular. The reflexes and typical blood pressure responses to cutaneous and vagal stimulation could always be obtained until death. Marked diminution of oxygen and increase of carbon dioxide content were found to occur in mixtures of blood and hematoporphyrin exposed in vitro to sunlight. These changes in the blood, identical with those occurring in vivo during hematoporphyrin shock, support Gaffron's views regarding the effect produced by the combined action of hematoporphyrin and light, but do not further elucidate the nature of the manner in which such alterations take place. Unsuccessful attempts were made to produce, in both cats and dogs, physiological changes similar to those observed in hematoporphyrin shock by exposing only the blood flowing through a quartz glass cannula, connecting the femoral artery and vein, to strong arclight and sunlight. In another series of animals, which were first injected with hematoporphyrin, exposure of the circulating blood alone to arclight or sunlight did not produce hematoporphyrin shock, although the blood pressure did fall to an unusually low level in one instance. No changes were found to occur in the amount of non-protein nitrogen, sugar or creatinine of the blood of animals in hematoporphyrin shock.

1913 ◽  
Vol 18 (1) ◽  
pp. 7-17 ◽  
Author(s):  
Francis W. Peabody

In most cases of uncomplicated lobar pneumonia the decrease of respiratory surface is completely compensated for, and the oxygen content of the blood is within normal limits. Occasional cases of uncomplicated pneumonia have an oxygen content of the venous blood which is below normal. In the two cases reported here, this was associated with a carbon dioxide content of the blood which was higher than normally, and the condition was apparently due to an interference with the respiratory exchange of gases. In the terminal stage of the fatal cases of pneumonia in which death does not occur with great suddenness, there is often a progressive diminution in the oxygen content of the blood. Synchronous with this is a progressive decrease in the oxygen-combining capacity of the blood. These changes are usually seen in patients in whom an intense bacteremia has developed and are analogous to those found in the arterial blood of infected rabbits, and to those resulting from the growth of the pneumococcus in blood in vitro. In all three conditions there is probably a change of oxyhemoglobin to methemoglobin. This change of the hemoglobin molecule, so that it no longer takes up and gives off oxygen readily, is probably a factor in the immediate cause of death in many cases of pneumonia.


1981 ◽  
Author(s):  
J M Fisher ◽  
A L Willis ◽  
D L Smith ◽  
D Donegan

Under light ether anesthesia, blood of male guinea pigs (Hartley strain, 330-410 g, Simonsen, Gilroy, CA) or rats (Sprague-Dawley, 230-575 g, Simonsen) was withdrawn into sodiun citrate (0.38% w/v). Platelet rich plasm (PRP) was then prepared by a rapid centrifugation procedure. Aggregation induced by ADP (1.6 μg/ml) was then examined in 0.15 or 0.25 ml aliquots of PRP at various time intervals from 5-60 min after blood withdrawal. A spontaneous time-dependent rise in aggregation response occurred that was similar to that observed when PGI2 (0.5-3ng) was added to PRP in vitro. In both species, intraperitoneal ackninistration of indanethacin (100 mg/kg, 1h previously) failed to interfere with the spontaneous rise in aggregation although vascular PGI2 formation was shown to be virtually abolished. Similar results were seen in essential fatty acid (EFA) deficient rats that had been chronically maintained on a fat free diet. In these animals, vascular PGI2 product ion was less than 15% that of controls. These results clearly indicate that any basal levels of PGI2 present in the arterial circulation are less than those (0.3-1ng/ml) necessary to appreciably inhibit aggregation. This conclusion coincides with that of Steer, et al. (Nature, 283, 194, 1980) who failed to detect biologically active amounts of PGI2 in hiimn venous blood and of several other groups who have failed to detect significant blood levels of the PGI2 breakdown product, 6-keto-PGF1α.


1964 ◽  
Vol 206 (6) ◽  
pp. 1281-1284 ◽  
Author(s):  
Thomas D. Darby ◽  
Daniel T. Watts

Dogs were anesthetized with pentobarbital 30 mg/kg. Cannulas were placed for measurement of arterial and central venous blood pressures. The left femoral artery was cannulated and attachment was made to a reservoir set to maintain arterial blood pressure at 40 mm Hg. Blood pH, pCO2, and pO2 were obtained concomitantly with measurements of blood epinephrine levels utilizing the rat uterus assay method. Rapid hemorrhage to 40 mm Hg blood pressure elicited increments in blood epinephrine levels that closely followed the development of uncompensated acidosis. Correction of the acidosis by intravenous administration of tromethamine or sodium bicarbonate at a blood pressure of 40 mm Hg reduced the blood epinephrine levels by at least 50%, markedly improved cardiac function, increased hemorrhage volume, reduced respiratory rate, and, paradoxically, increased arterial pO2. In vitro studies showed that acidosis did not inhibit destruction of epinephrine added to blood. It was concluded that the adrenal gland is stimulated by acidosis to secrete epinephrine. This stimulation is an important source of blood epinephrine during periods of hypotension associated with shock.


1912 ◽  
Vol 16 (5) ◽  
pp. 701-718 ◽  
Author(s):  
Francis W. Peabody

A diminution in the carbon dioxide content of the blood is a constant feature in pneumonia. Occasional cases, however, may fail to show low carbon dioxide. The carbon dioxide in the blood bears little definite relation to the severity of the disease, except that it tends to be lowest in severe cases and in the terminal stages of the disease. There is less deviation from the normal in short or mild cases. The diminution in the carbon dioxide in the blood bears no immediate relation to temperature, as it may persist for some days after the patient is afebrile. The diminution in carbon dioxide corresponds to the other evidences of metabolic changes in infection and, like them, may be even greater after than during the febrile period. The changes in the carbon dioxide content of the blood run parallel to the output of ammonia in the urine. The carbon dioxide appears to bear no relation to chlorine excretion. In two unusual cases the carbon dioxide content of the blood was normal or above normal. This was associated with a very low oxygen content of the venous blood.


1985 ◽  
Vol 53 (01) ◽  
pp. 070-074 ◽  
Author(s):  
G Mallarkey ◽  
G M Smith

SummaryThe mechanism of collagen-induced sudden death in rabbits was studied by measuring blood pressure (BP), heart rate, ECG, the continuous platelet count and the plasma levels of thromboxane B2 (TxB2) and 6-keto prostaglandin Fia (6-keto PGF1α). Death was preceded by myocardial ischaemia and a sharp fall in BP which occurred before any fall in platelet count was observed. The calcium entry blockers (CEBs), verapamil, nifedipine and PY 108-068 protected the rabbits from sudden death without any significant effect on the decrease in the platelet count or increase in plasma TxB2 levels. 6-keto PGF1α could not be detected in any plasma samples. Indomethacin and tri-sodium citrate also protected the rabbits but significantly reduced the fall in platelet count and plasma TxB2. In vitro studies on isolated aortae indicated that verapamil non-specifically inhibited vasoconstriction induced by KC1, adrenaline and U46619 (a thromboxane agonist). It is concluded that CEBs physiologically antagonize the vasoconstricting actions of platelet-derived substances and that it is coronary vasoconstriction that is primarily the cause of death.


1985 ◽  
Vol 53 (01) ◽  
pp. 095-098 ◽  
Author(s):  
C R Jones ◽  
R McCabe ◽  
C A Hamilton ◽  
J L Reid

SummaryPaired blood samples were obtained from mothers (venous) and babies (cord venous blood) at the time of delivery by caesarean section under epidural anaesthetic. Fetal platelets failed to aggregate in response to adrenaline in vitro although adrenaline could potentiate the threshold response to adenosine diphosphate (1 μM). Fetal platelet responses to collagen and 8 Arg vasopressin did not differ significantly from maternal responses. Maternal and fetal platelets also showed similar inhibition of aggregation after activation of adenylate cyclase (PGE1 and parathormone), in contrast to the inhibition of adenylate cyclase by adrenaline.Alpha2 adrenoceptors were investigated using [3H] yohimbine binding receptor number and were reduced modestly but significantly on fetal compared to maternal platelets. The failure of fetal platelet aggregation in response to adrenaline appears to be related to a failure of receptor coupling and may represent a delayed maturation of fetal platelet alpha receptors or a response- to increased circulating catecholamines during birth.


2018 ◽  
Vol 14 (4) ◽  
pp. 329-334
Author(s):  
Ahmad Shanei ◽  
Neda Attaran ◽  
Marziyeh Mirzaeiyan ◽  
Mohammad Reza Salamat ◽  
Hossein Hejazi

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