Blood pressure decrease

Desflurane is less potent than the other fluorinated anesthetics having MAC values of 5.7 to 8.9% in animals (76,85), and 6% to 7.25% in surgical patients. The respiratory effects are similar to isoflurane. Heart rate is somewhat increased and blood pressure decreased with increasing concentrations. Cardiac output remains fairly stable. Desflurane does not sensitize the myocardium to epinephrine relative to isoflurane (86). EEG effects are similar to isoflurane and muscle relaxation is satisfactory (87). Desflurane is not metabolized to any significant extent (88,89) as levels of fluoride ion in the semm and urine are not increased even after prolonged exposure. Desflurane appears to offer advantages over sevoflurane and other inhaled anesthetics because of its limited solubiHty in blood and other tissues. It is the least metabolized of current agents. 

The principal mechanism of the hypotensive effect of diuretics (qv) is salt and fluid depletion, leading to reduction in blood volume (200,240). Acute effects lead to a decrease in cardiac output and an increase in total peripheral resistance. However, during chronic adrninistration, cardiac output and blood volume return toward normal and total peripheral resistance decreases to below pretreatment values. As a result, the blood pressure falls. The usual reduction in blood volume is about 5%. A certain degree of sustained blood volume contraction has to occur before the blood pressure decreases. The usual decrease in blood pressure achieved using a diuretic is about 20/10 mm Hg (2.7/1.3 kPa) (systoHc/diastoHc pressures. 

Ca2+ is an important intracellular second messenger that controls cellular functions including muscle contraction in smooth and cardiac muscle. Ca2+ channel blockers inhibit depolarization-induced Ca2+ entry into muscle cells in the cardiovascular system causing a decrease in blood pressure, decreased cardiac contractility, and antiarrhythmic effects. Therefore, these drugs are used clinically to treat hypertension, myocardial ischemia, and cardiac arrhythmias. 

Intravenous or oral doses of a P-blocker should be administered early in the care of a patient with STE ACS, and then oral agents should be continued indefinitely. Early administration of a P-blocker to patients lacking a contraindication within the first 24 hours of hospitalization is a quality care indicator.2,3 In ACS the benefit of P-blockers mainly results from the competitive blockade of P,-adrenergic receptors located on the myocardium. Pi-Blockade produces a reduction in heart rate, myocardial contractility, and blood pressure, decreasing myocardial oxygen demand. As a result of these effects, P-blockers reduce the risk for recurrent ischemia, increase in infarct size and risk of reinfarction, and occurrence of ventricular arrhythmias in the hours and days following MI.39... 

Figure 1.2 Negative feedback. These types of responses are employed throughout the body in order to maintain homeostasis. In this example, any change in blood pressure, which is monitored within the circulatory system and processed within the CNS, will cause reflex changes in heart rate. The change in heart rate will be in the opposite direction of the change in blood pressure if blood pressure increases, then heart rate decreases if blood pressure decreases, then heart rate increases. In this way, blood pressure is adjusted back to its normal value.

An example of this type of reflex is the baroreceptor reflex (see Figure 1.2). Baroreceptors located in some of the major systemic arteries are sensory receptors that monitor blood pressure. If blood pressure decreases, the number of sensory impulses sent from the baroreceptors to the cardiovascular control center in the brainstem also decreases. As a result of this change in baroreceptor stimulation and sensory input to the brainstem, ANS discharge to the heart and blood vessels is adjusted to increase heart rate and vascular resistance so that blood pressure increases to its normal value. 

The answer is d. (Hardman, pp 212—213.) Only isoproterenol will lower mean blood pressure, decrease peripheral vascular resistance, and increase heart rate. Methacholine decreases heart rate as does propranolol. Atropine has no action on peripheral resistance. Norepinephrine causes intense vasoconstriction and raises the mean blood pressure. 

The answer is F. (Katzung, p 167, Hardman, pp 237-2382 Labetalol has potent a and p antagonist actions, due to the specific components of its racemic mixture of four isomeric compounds. Cardiac output and heart rate change minimally, while blood pressure decreases due to a overall reduction in peripheral resistance. The combined a and p antagonism has been found to be of advantage in treating pheochromocytomas. 

Figure 15. Relationship between peripheral a-adrenoceptor activity, lipoid solubility, and centrally mediated cardiodepressor activity. Abscissa natural logarithms of the product of relative activity on peripheral a-adrenoceptors as derived from blood pressure decreases in spinal rats multiplied by percentage of distribution between octanol/buffer (Figure 4). Ordinate natural logarithms of the relative CNS activity as derived from bradycardia test in vagotomized...

CHEMICAL STRUCTURE blood pressure decrease mmHg ED20 mg/kg... 

The adrenergic neuron-blocking drugs are antihypertensive because they prevent the release of transmitters from peripheral postganglionic sympathetic nerves. The contraction of vascular smooth muscle due to sympathetic nerve stimulation is thereby reduced, and blood pressure decreases. Guanethidine is the prototypical member of this class. 

Mechanism of Action A smoking deterrent that inhibits acetylcholine at the auto-nomicganglia. Blocks central nicotinic cholinergic receptors, which inhibits effects of nicotine. Therapeutic Effect Reduces blood pressure decreases desire to smoke. Pharmacokinetics Completely absorbed following PO administration. Widely distributed. Excreted in urine. Half-life 24 hr. 

It is a clear, colourless, noninflammable liquid with a mild, sweet odour and considered to be a useful alternative to halothane. Induction of anaesthesia, appropriate for surgery may be achieved within 10 minutes after approximately 4 percent enflurane in inhaled. Arterial blood pressure decreases progressively as the depth of anaesthesia is increased with enflurane, about the same degree as it does with halothane inhalation. The anaesthesia produces rapid induction with quick recovery. 

Systemic arterial blood pressure decreases progressively with increasing depth of anaesthesia with isoflurane. It also increases heart rate but arrhythmias are not precipitated. Isoflurane depresses respiration as concentration is increased. Uterine and skeletal muscle relaxation is similar to enflurane. 

In the absence of heart failure, blood pressure decreases, owing to decreased vascular resistance, whereas cardiac output does not change or decreases slightly. In patients with heart failure and low cardiac output, output often increases owing to afterload reduction. 

Propranolol Nonselective competitive antagonist at adrenoceptors Decreased heart rate, cardiac output, and blood pressure decreases myocardial oxygen demand Prophylaxis of angina for other applications, see Chapters 10, 11, and 13 Oral and parenteral, 4-6 h duration of action Toxicity Asthma, atrioventricular block, acute heart failure, sedation Interactions Additive with all cardiac depressants... 

Increased biosynthesis of prostaglandins has been associated with one form of Bartter s syndrome. This is a rare disease characterized by low-to-normal blood pressure, decreased sensitivity to angiotensin, hyperreninemia, hyperaldosteronism, and... 

Anaesthetised animal not defined Basal blood pressure decrease Ea-Kim et al, 1993... 

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