Peripheral vasoconstriction

Acute intoxication with DHBs occurs mainly by the oral route symptoms are close to those induced by phenol poisoning including nausea, vomiting, diarrhea, tachypnea, pulmonary edema, and CNS excitation with possibiUty of seizures followed by CNS depression. Convulsions are more frequent with catechol as well as hypotension due to peripheral vasoconstriction. Hypotension and hepatitis seem more frequent with hydroquinone and resorcinol. Methemoglobinemia and hepatic injury may be noted within a few days after intoxication by DHBs. 

Hypoperfusion of skeletal muscles leads to fatigue, weakness, and exercise intolerance. Decreased perfusion of the central nervous system (CNS) is related to confusion, hallucinations, insomnia, and lethargy. Peripheral vasoconstriction due to SNS activity causes pallor, cool extremities, and cyanosis of the digits. Tachycardia is also common in these patients and may reflect increased SNS activity. Patients will often exhibit polyuria and nocturia. Polyuria is a result of increased release of natriuretic peptides caused by volume overload. Nocturia occurs due to increased renal perfusion as a consequence of reduced SNS renal vasoconstrictive effects at night. In chronic severe HF, unintentional weight loss can occur which leads to a syndrome of cardiac cachexia. This results from several factors, including loss of appetite, malabsorption due to gastrointestinal edema, elevated metabolic rate, and elevated levels of proinflammatory cytokines. 

Epinephrine is a nonspecific a- and P-adrenergic agonist. Epinephrine can increase cardiac index and produce significant peripheral vasoconstriction. However, it can also increase lactate levels and impair blood flow to the splanchnic system. Because of these undesirable effects, epinephrine should be reserved for patients who fail to respond to traditional therapies.24,27-28... 

Regardless of the etiology, fall in blood pressure (BP) is compensated by an increase in sympathetic outflow, activation of the renin-angiotensin system, and other humoral factors that stimulate peripheral vasoconstriction. Compensatory vasoconstriction redistributes blood away from the skin, skeletal muscles, kidneys, and GI tract toward vital organs (e.g., heart, brain) in an attempt to maintain oxygenation, nutrition, and organ function. 

Cardiovascular Effects. Peripheral vasoconstriction and gross plasma extravasation were reported in a man who accidentally fell into a cistern with hot copper cyanide (Dodds and McKnight 1985). Palpitations were recorded in 3 men who wore respiratory masks while working in an atmosphere containing 20,000 ppm hydrogen cyanide for 8-10 minutes (Drinker 1932). The masks were reported to give excellent respiratory protection. Therefore, the effects seen in these men may have been due to dermal exposure. 

Common side-effects associated with beta-adrenoceptor blockers, such as atenolol, include fatigue, bradycardia, sleep disturbances, and peripheral vasoconstriction leading to coldness of extremities. Water-soluble beta-blockers, such as atenolol, are less likely to cause sleep disturbances and nightmares than lipid-soluble beta-blockers, such as propranolol. 

Dopamine is an intermediate product in the biosynthesis of noradrenaline. Furthermore it is an active transmitter by itself in basal ganglia (caudate nucleus), the nucleus accumbens, the olfactory tubercle, the central nucleus of the amygdala, the median eminence and some areas in the frontal cortex. It is functionally important, for example in the extra-pyramidal system and the central regulation of emesis. In the periphery specific dopamine receptors (Di-receptors) can be found in the upper gastrointestinal tract, in which a reduction of motility is mediated, and on vascular smooth muscle cells of splanchnic and renal arteries. Beside its effect on specific D-receptors, dopamine activates, at higher concentrations, a- and -adrenoceptors as well. Since its clinical profile is different from adrenaline and noradrenaline there are particular indications for dopamine, like situations of circulatory shock with a reduced kidney perfusion. Dopamine can dose-dependently induce nausea, vomiting, tachyarrhythmia and peripheral vasoconstriction. Dopamine can worsen cardiac ischaemia. 

Vasoconstriction activity. Emit, administered to immature rats at a dose of 50% of the diet for 75 days after weaning, resulted in peripheral vasoconstriction leading to gangrene in the extremities within 40 days, and the loss of whole limbs in some cases . 

Ephedrine is an alkaloid obtained from Ephedra vulgaris plant. It act indirectly and directly on a and P receptors. It increases blood pressure both by peripheral vasoconstriction and by increasing the cardiac output. Ephedrine also relaxes the bronchial smooth muscles. 

Intestinal and peripheral vasoconstriction can follow prolonged infusion, resulting in gangrene of intestinal segments or of skin, fingers, or limbs. This has been fatal in several cases, and vasopressin should be withdrawn if skin necrosis occurs (SEDA-13,1310 7). 

Consequently, alpha antagonists are used in conditions where peripheral vasodilation would be beneficial. A principal application of these agents, for instance, is in treating hypertension.26 39 These drugs seem to attenuate the peripheral vasoconstriction me-... 

Fluid depletion may also be a serious problem during diuretic therapy. A decrease in blood volume may cause a reflex increase in cardiac output and peripheral vascular resistance because of activation of the baroreflex (see Chapter 18). This occurrence may produce an excessive demand on the myocardium, especially in patients with cardiac disease. Decreased blood volume may also activate the renin-angiotensin system, thereby causing further peripheral vasoconstriction and increased cardiac workload. Again, the effects of fluid depletion may be especially serious in patients with certain types of heart failure. 

Increased cardiac workload. The neurohumoral changes previously described contribute to peripheral vasoconstriction, as well as a general increase in sodium and water retention.15 These effects place additional strain on the heart by increasing cardiac preload (the volume of blood returning to the heart) and cardiac afterload (the pressure that the heart must pump against).13... 

Dopamine stimulates dopamine, a-, and [3-adrenergic receptors. The use of dopamine in congestive heart failure is limited because it causes nausea and vomiting, becomes inactive when given orally, increases afterload (a-adrenergic receptor-mediated peripheral vasoconstriction), and enhances oxygen demand on the left ventricle. 

Norepinephrine is used pharmacologically for its ability to cause peripheral vasoconstriction and increase blood pressure, which is useful to stem the effects of large drops in blood pressure as can occur in trauma or shock. Drugs affecting norepinephrine release and/or reuptake also have significant CNS utility, including the treatment of depression and attention deficit disorder. 

It is well established that increased sympathetic nerve activity is associated with chronic heart failure (CHF) (Porter et al. 1990 Singh 2000 Olshansky 2005 Brodde et al. 2006 Watson et al. 2006). The increase in sympathetic activity is a compensatory mechanism that provides inotropic support to the heart and peripheral vasoconstriction. However, it promotes disease progression and worsens prognosis (Watson et al. 2006). The autonomic nervous system (ANS) is a very complex, balanced system that influences the initiation, termination, and perpetuation of atrial fibrillation (AF), and the AF affects the ANS (Olshansky, 2005). At rest, sympathetic and parasympathetic outflows are related reciprocally heart failure patients had high sympathetic and low parasympathetic outflows, and healthy subjects had low sympathetic and high parasympathetic outflows (Porter et al. 1990). 

As emphasized above, since the 1930s, physiologists working on diving have looked at the problem of evolution of the diving response in very qualitative terms and assumed that all the key components of the diving response (apnea, bradycardia, and peripheral vasoconstriction with hypometabolism... 

Similarly, there was a lack of correlation between maximum heart rates and mean or modal dive durations (see Hochachka and Mottishaw, 1998). By implication, the same considerations apply for peripheral vasoconstriction, since the two reflexes are... 

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